Blood pressure is the lateral pressure exerted by blood on the vessel walls while flowing through it.
Four terms are in common use:
i. Systolic Pressure (S.P.):
The maximum pressure during systole.
ii. Diastolic Pressure (D.P.):
The minimum pressure during diastole.
iii. Pulse Pressure (P.P.):
The difference between systolic and accepted diastolic pressure.
iv. Mean Pressure (M.P.):
It is roughly the arithmetic mean of the diastolic and the systolic pressure.
But a close approximation to the mean pressure may be obtained by adding the diastolic pressure with one-third of the pulse pressure. In true sense it is the level of the line halving area between the pulse wave contour and the diastolic pressure level.
In adults the relation between the three pressures is as follows:
S.P/D.P./P.P = 3/2/1, viz., if systolic pressure be 120, diastolic pressure should be 80 and pulse pressure 40 mm of Hg.
Basal Blood Pressure:
As blood pressure differs from an individual to another one and under different circumstances it varies in the same individual, it is permissible to use the term normal range of blood pressure. When an individual is with the least possible amount of strain or stress, basal blood pressure is generally considered. It may also be regarded as the lowest pressure necessary in maintaining blood flow sufficient for needs of the body.
When a subject is in reclining state, 5 – 6 hours after last meal, in a comfortably warm room, after resting for at least 30 – 40 minutes and with a mind at possible ease, the basal pressure is obtained. In adult males, the average systolic pressure 125 – 130 mm of Hg ± 15 (viz., from 110 – 145 mm of Hg) and average diastolic pressure, 70 – 90 mm of Hg.
Although it is constant in a given individual, yet basal pressure varies in different ones with the following factors:
I. Physiological Variations:
Blood pressure rises with age. During infancy, the systolic pressure is from 70-90 mm of Hg; childhood, 90-110 mm of Hg; puberty, 110-120 mm of Hg; old age, 140-150 mm of Hg. At any age, a systolic pressure persistently above 150 mm of Hg and a diastolic pressure above 100 mm of Hg should be accepted as high. On the other hand, systolic pressure below 100 mm of Hg and diastolic below 50 should be taken as low in the adults. Recent observations indicate that the pressure which is reached in adolescence does not normally rise with age any more.
The average systolic pressure is 110-120 mm of Hg and diastolic pressure 70-80 mm of Hg. The normal upper limits of systolic and diastolic pressures are placed at 140 and 90 mm of Hg respectively.
Average blood pressure and standard deviations in apparently healthy persons (assuming diastolic end point is disappearance of sound) is listed in Table 7.7.
In females both systolic and diastolic pressures are slightly lower than in males up to the age of 45-50 years.
The systolic pressure is usually high in obese person. In most of the overweight persons the blood pressure is found to be high.
In strenuous exercise the systolic pressure rises and may reach even up to 180 mm of Hg. In moderate exercise there is slight rise of systolic blood pressure.
The diastolic pressure is slightly higher in the standing position. In the recumbent position the diastolic pressure is lower than in the standing or in the sitting position.
The systolic pressure falls by about 15 to 20 mm of Hg during sleep.
vii. After Ingestion of Meals:
There is a slight rise of systolic pressure.
viii. Emotion of Excitement:
It causes increase of systolic pressure.
II. Significance of Blood Pressure:
i. Systolic Pressure:
It undergoes considerable fluctuations. Excitements, exercise, males, etc., increase it, while sleep, rest etc., and diminish it.
The height of systolic pressure indicates:
(a) The extent of work done by heart,
(b) The force with which the heart is working, and
(c) The degree of pressure which the arterial walls have to withstand.
ii. Diastolic Pressure:
It undergoes much less fluctuations in health and remains within a limited range. Increase of diastolic pressure indicates that the heart is approaching towards its failure. Consequently, variations of diastolic pressure are of greater prognostic importance than those of systolic. Diastolic pressure is the measure of peripheral resistance. It indicates the constant load against which heart has to work.
iii. Pulse Pressure:
It generally varies directly as the stroke volume. But this quantitative relation may not be true in all cases.
III. Normal Function of Blood Pressure:
i. To maintain a sufficient pressure head to keep the blood flowing.
ii. To provide for the motive force of filtration at the capillary bed, thus assuring nutrition to the tissue cells, formation of urine, lymph and so on.
From the above considerations, it is seen that, the height of blood pressure gives correct information’s about the state of the circulatory system as a whole and also about the functional condition of the tissue cells and organs.
IV. Measurement and Recording of Blood Pressure:
A. Arterial Blood Pressure:
This can be measured by two methods:
(a) Direct, and
(a) Direct Method:
The artery is exposed and an arterial cannula of which one tapering end is inserted directly into the lumen of the exposed vessel and the other end is connected to the U-shaped mercury manometer that shows the actual blood pressure in mm of Hg. As the mercury column in one limb (that has direct contact with the blood vessel) descends and the other limb of the U-tube ascends, the value in the scale will be doubled so as to get the actual blood pressure. For convenience it is generally considered to be 1 mm in the scale equivalent to 2 mm of Hg of pressure.
Before recording the blood pressure, the mercury levels in both limbs of the U-tube must be adjusted to the 0 mark of the scale. For recording pressure a floating stylus with a writing pointer that marks on the smoked paper may be used (Fig. 7.85). This method is only suitable in animals and gives the idea about mean pressure. Due to high inertia of the mercury, the blood pressure changes associated with cardiac cycle are damped. Respiratory undulation of mean pressure waves are clearly seen in this direct method.
(b) Indirect Method:
In indirect method, the pressure may be measured without any surgical procedure and thus it is very convenient clinically in human being. Riva-Roci (1896) first introduced this indirect method and afterwards Korotkoff (1905) introduced a convenient method by which the systolic and diastolic pressure could be ascertained only through listening to a sound. This is the standard method of recording blood pressure all through-out the world.
In this method commonly the pressure of the brachial artery is measured. The instrument used is known as Sphygmomanometer.
2. Palpatory, and
1. Oscillatory Method:
Inspection of oscillation in spring gauge or mercury manometer is the basis of this method. In this method a pressure cuff is wrapped over the brachial artery and the oscillations that are produced by the pulsations are observed. The instrument is always kept at the heart level. When the cuff pressure is increased and raised above the systolic pressure, the oscillations disappear, but on releasing the pressure gradually, the oscillations become larger and prominent.
The pressure head, at which the larger oscillations are seen, is considered as systolic pressure. But on further release of pressure, the oscillations become smaller and disappeared. The pressure, at which the oscillation just becomes smaller or disappears, is known as diastolic pressure.
2. Palpatory Method:
The instrument is kept at the level of the heart and the cuff is tied round the upper arm. Pressure is raised to 200 mm of Hg and then gradually released. When the pulse just appears at the wrist, the pressure is noted. This is the systolic pressure. This method is not accurate. By this method the diastolic pressure cannot be determined.
3. Auscultatory Method:
The instrument is kept at the level of the heart and the cuff is tied round the upper arm. Pressure is raised to 200 mm of Hg and then gradually released. Variations of sounds are heard with a Stethoscope placing its chest piece on the brachial artery, a little below the cuff.
The sounds are heard due to occurrence of turbulence in the flow of blood through the narrowed blood vessels when the manometric pressure just coincides with the systolic blood pressure. Due to giving air pressure in the cuff, the vessel is pressed and blood flow is obliterated.
But while releasing the air pressure gradually, blood just begins to flow through the narrowed blood vessels and the pattern of flow is changed from streamline flow (silent) to turbulent flow (noisy). When the pressure is further released, normal streamline flow sets in and the sound is no longer heard. At this point manometric pressure coincides with the diastolic blood pressure.
So as the pressure is released the following variations of sounds are heard:
i. First Phase:
Sudden appearance of a clear tapping sound. This indicates systolic pressure. It persists while the pressure falls through 15 mm of Hg.
ii. Second Phase:
The tap sound is replaced by a murmur persisting for another 15 mm of Hg.
iii. Third Phase:
The murmur is replaced by a clear loud gong sound lasting for the next 20 mm of Hg.
iv. Fourth Phase:
The loud sound suddenly becomes muffled and rapidly begins to fade. This point indicates diastolic pressure.
v. Fifth Phase:
Absence of all sounds.
Factors Controlling Arterial Blood Pressure:
i. Pumping Action of the Heart:
Effectual contraction of the heart is the main factor for controlling the cardiac output, blood pressure and flow within the blood vessel. Because in each effectual contraction of the ventricle certain amount of blood is ejected out into the aorta. The driving force of blood is mainly created by the pumping action of the heart. The efficiency of the heart is considered upon how much amount of blood is driven out by the heart into the aorta in each beat.
ii. Cardiac Output:
Alterations of cardiac output will alter blood pressure. Cardiac output depends upon venous return, force and frequency of heart beat. Blood volume affects blood pressure directly, by mainly modifying the cardiac output.
iii. Peripheral Resistance:
It is the resistance which blood has to overcome while passing through the periphery. The chief seat of peripheral resistance is the arterioles and to a smaller extent the capillaries (vide below).
Peripheral resistance depends on the following:
(a) Velocity of blood,
(b) Viscosity of blood,
(c) Elasticity of arterial walls, and
(d) Lumen of blood vessels.
Resistance is directly proportional to the first two and inversely to the last two factors:
A rapidly flowing stream will have more frictional effect than a slower one. Hence, pressure is high in the aorta but low in the capillaries.
Other factors remaining constant, a more viscid blood will have a higher friction than a lesser one. For this reason, plasma transfusion is sometimes more effective to maintain blood pressure than ordinary saline.
Due to elastic properties in the arteries can dilate and accommodate considerable amount of blood with relatively less rise of blood pressure. In old age, the arterial walls become stiff. Hence, blood pressure rises.
(d) Lumen of the Vessel:
Peripheral resistance is inversely proportional to the lumen of the vessel. In other words, smaller the vessel, higher will be the resistance. One should expect therefore that the capillaries, having the smallest lumen, should have the highest pressure.
But this is not the case. Because the velocity of blood being lowest in the capillaries, the frictional effect is very low. Hence, the pressure is also low. The seat of peripheral resistance is found to be chiefly in the arterioles, where the velocity is fairly high and the lumen is narrow.
Mean arterial pressure can be expressed in dynes per square centimetre by multiplying the pressure in mm of Hg by 1,332.
iv. Elasticity of the Arterial Walls:
In normal diastolic pressure arterial walls are stretched but due to the presence of elastic tissues in their walls, they tend to recoil. Due to elasticity of the arterial walls the blood flow is pulsatile in the arteries. In the capillaries and venules the flow is continuous. In old age the expansion of the arterial walls becomes limited due to sclerotic changes and the blood pressure rises.
v. Blood Volume:
Increase in blood volume will raise both the systolic and diastolic blood pressures due to the increased quantity of blood in the arterial system and greater stretching of the arterial walls.
vi. Viscosity of the Blood:
Alteration in blood viscosity will affect the diastolic pressure by its effect on the peripheral resistance. The intramolecular friction is greater when the viscosity is high.
B. Venous Pressure:
It is the pressure which is exerted by the blood within the veins. Average venous pressure of human being in recumbent position is about 60-120 cm of H2O. The venous pressure can be measured by inserting a needle directly into the anticubital vein and by connecting the needle to a water manometer (Fig. 7.87). Venous pressure is a valuable index in determining the efficiency of the heart.
In 1841 the French Physician J.L.M. Poiseuille studied the factors regulating the flow of viscous fluid through the capillary tubes. He showed that resistance to blood flow in any blood vessel proportionally varies directly with the viscosity of the blood and also with the length of the blood vessel, and inversely with the fourth power of the radius of the blood vessel.
It can be represented by the following formula:
R = ƞl/r4 × 8/π, where R stands for resistance to blood flow, ƞ for viscosity of blood, l for length of blood vessels, r for radius of the blood vessel, 8 for Hagen’s integration and π factor for a cylindrical tube.
Taking this value for resistance in the formula it is found that blood flow proportionally varies directly with the blood pressure and the fourth power of the radius of the blood vessel, and inversely with the viscosity of the blood and length of the blood vessel.
The following formula, known as poiseuille’s law, expresses the above relations:
BF = K BP/R or BF = BP × (π/8) × (1/ƞ) × (r4/l), where BF stands for blood flow, BP for blood pressure, r for radius of the blood Vessel, ƞ for viscosity of blood, l for length of the blood vessel and π for 3.14. This law is not applicable when the arterial pressure falls below 20 mm of Hg.
Adjustment of Blood Pressure:
In normal individual the constancy of the internal environment is being adjusted by the well-organised controlling system—which is called Milieu interieur after Claude Bernard and Homoeostasis after Cannon. Adjustment of blood pressure, according to the needs of the body, may be carried out by the several complex reflexes whose centres are lying in the cerebral cortex formatio reticularis, hypothalamus, medullary and spinal vasomotor centres. The (I) efferent and (II) afferent pathways constituting the above reflexes are lying within the sympathetic and parasympathetic nervous systems whose activities are modified by the hypothalamus and other centres.
I. Efferent Pathways of this Self-adjustment or Homoeostasis of Blood Pressure:
These are the vagi and the sympathetic nerves which control the blood pressure by:
(a) Modifying the cardiac activity,
(b) Altering the cardiac output, and
(c) Altering the lumen of the blood vessels.
The relative activities of the vagi and the sympathetic of the efferent pathways are under the control of vasomotor systems, which are described below:
This system consists of:
i. Vasomotor centre,
ii. Vasoconstrictor nerves, and
iii. Vasodilator nerves.
They supply vasomotor nerves—mainly to the arterioles but to some extent to the capillaries and venules. This vasomotor centre is highly developed in higher animals and human beings. In infants and children it is imperfect. By regulating the radius of the blood vessels this system takes part in adjusting blood pressure and blood supply to a particular part. It also plays an immense role in heart regulation.
i. Vasomotor Centre (V.M.C.):
Vasomotor centre is situated on the floor of the fourth ventricle in the reticular formation at the level of the calamus scriptorius. It extends from the lower part of the pons to the obex and forms a diffuse network of neurones. After section of the brain stem at the level of the calamus scriptorius there is fall of blood pressure.
There are practically two areas in the reticular formation of the medulla:
a. Pressor centre—which causes rise of blood pressure.
b. Depressor centre—which causes fall of blood pressure.
The depressor centre is not the vasodilator centre. This centre causes inhibition of the vasoconstrictor tone. The depressor centre relays the inhibitory impulses to the pressor centre. Pressor and depressor centres form one functional unit and it is defined as the vasomotor centre. The vasomotor centre discharges impulses which pass down the lateral white column of the spinal cord in the cervical, thoracic and lumbar segments of the spinal cord and form synaptic connections with the lateral horn cells of the spinal cord.
a. Depressor Reflex:
Blood pressure falls due to diffuse dilatation of the arterioles. Rise of blood pressure stimulates the baroreceptors of the carotid sinuses and aortic arch, and causes slowing of the heart and arteriolar dilatation. The vasodilatation is due to inhibition of vasoconstrictor effect of the sympathetic.
b. Pressor Reflex:
Blood pressure rises due to diffuse constriction of the arterioles. Diminution of blood pressure fails to stimulate the baroreceptors of the carotid sinuses and aortic arch, and the parasympathetic inhibitory tone over the heart and blood vessels is withdrawn. Blood pressure is raised reflexly through overactivity of the sympathetic. Vasoconstriction of the arterioles is due to activity of the vasoconstrictor centre. Reflex vasoconstriction also occurs due to stimulation of chemoreceptors during the fall of blood pressure.
Control of V.M.C:
Vasomotor centre is under the superior control of cerebral cortex and hypothalamus (Fig. 7.88).
Factors influencing V.M.C. have been described as follows:
a. Higher Centre (Including Hypothalamus):
Emotion generally stimulates, causing vasoconstriction. But shock may depress the centre—leading to a sudden fall of blood pressure and fainting (vasovagal attacks).
During inspiration systemic blood pressure is generally decreased but increased during expiration. This is due to the decrease of left ventricular cardiac output during inspiration. Reverse is the effect during expiration. There is no evidence of direct respiratory centre—effect on vasomotor centre.
c. CO2 Excess:
Excess stimulates. The action is mainly on the centre but partly reflexly through the sino-aortic nerves.
d. O2 Lack:
Generally stimulates V.M.C. The effect is mainly reflex through the sino-aortic nerves and slightly direct on the centre.
e. Sino-Aortic Nerves:
Variations of blood pressure, CO2 tension, O2 tension, etc., reflexly regulate the activity of the vasomotor centre through the sino-aortic nerves. Normally, a stream of inhibitory impulses is carried up by these nerves depressing the vasomotor centre. When blood pressure rises, V.M.C. is depressed, vasodilatation occurs and further rise of blood pressure is checked. When blood pressure falls, the centre is released causing vasoconstriction and raising blood pressure. [Sino-aortic nerves also control cardiac centre, respiratory centre and adrenaline secretion]
f. Other Afferents:
Local vasomotor tone is altered by afferent nerves originating from different baroreceptor and chemoreceptor areas, distributed all throughout the body. The baroreceptors are located in the right atrium, in the left atrium and left ventricle, in the pulmonary arch of aorta, in the junction of the superior thyroid artery and common carotied artery, junction of the subclavian artery and common carotid artery, and all throughout common carotid artery in between the superior thyroid artery and subclavian artery, mesenteric blood vessels (Pacinian corpuscles), thoracic arch of the aorta and in the central vein (venous receptor).
The chemoreceptors are located in the ventricular cavity and all throughout the blood vessels wall. Reactive hyperaemia is the consequence of local chemoreceptor activity on the blood vessels wall by the accumulated metabolites. Heat dilates and cold constricts the skin vessels, reflexly.
ii. Vasoconstrictor Nerves:
The fibres pass along the sympathetic outflow from the first thoracic to the second lumbar segments.
Brief details are as follows:
a. To the Skin and Muscles:
Pass out through the grey rami communicants—to the mixed spinal nerves— and finally distributed through ordinary motor and sensory nerves. The distribution is strictly unilateral, stopping sharply at the midline.
b. To the Head and Neck:
Come from the first to the fourth thoracic segments—enter the superior cervical ganglion from which postganglionic fibres arise and pass along the carotid artery and its branches.
c. To the Fore Limbs:
Arise from the fourth to tenth thoracic segments—enter the stellate ganglion from which the postganglionic fibres arise and pass along the spinal nerves and supply the blood vessels.
d. To the Hind Limbs:
Arise from the eleventh thoracic to the second lumbar segments—relay in the lower lumbar and upper sacral ganglia, the postganglionic fibres accompany the nerves of the sacral plexus.
e. To the Abdominal Viscera:
From the lower thoracic and upper two lumbar segments—pass through the splanchnic nerves to coeliac ganglion-the postganglionic fibres pass along the blood vessels.
f. To the Thoracic Viscera:
Heart receives constrictor fibres through the vagus; lungs form the sympathetic.
iii. Vasodilator Nerves:
There are three types of vasodilator nerves:
1. Parasympathetic (Craniosacral) Vasodilators:
a. Chorda tympani—to the sub-maxillary or sub-mandibular gland,
b. Lesser superficial petrosal-to the parotid gland, and
c. Lingual—to the vessels of tongue.
Nervi erigentes—to the vessels of genitalia.
2. Sympathetic Vasodilators:
Sympathetic fibres are mostly vasoconstrictor in nature. But some vasodilators are also present.
i. The dilator fibres of the coronary vessels come through the sympathetic.
ii. Sympathetic dilator fibres have been demonstrated in the peripheral nerves in human beings.
iii. Stimulation of the last anterior thoracic root produces dilatation of the kidney vessels.
iv. Stimulation of the right splanchnic nerve sometimes causes vasodilatation and fall of blood pressure.
3. Antidromic Vasodilators:
Antidromic vasodilators in the posterior spinal root (Fig. 7.89). When posterior spinal root is cut, distal to the ganglion and the peripheral end is stimulated—although the nerve is afferent, yet the vessels in the periphery-both skin and muscles, dilate (axon reflex). In the skin, it is due to liberation of histamine and as such produces the typical triple response; dilatation, flare and wheal. In the muscle it liberates acetylcholine and thereby causes vasodilatation.
II. Afferent Pathways:
They are lying in two sets of receptors that carry information of the instantaneous circulatory status to the centre.
These sensory receptors are:
(1) Chemoreceptors, and
(2) Baroreceptors distributed all throughout the cardiovascular system.
The relative roles of the different afferent pathways have been described under separate headings, viz.:
(a) Sino-aortic mechanisms controlling systemic blood pressure and flow, and
(b) Vasocular receptors other than Sino-aortic—controlling mostly the local blood pressure and flow.
(a) Role of Sino-Aortic Mechanism in the Regulation of Normal Blood Pressure:
From the above, it is evident that blood pressure can be adjusted according to the needs of the body in various ways. Of all the factors, the Sino-aortic mechanism plays the chief role. The Sino-aortic mechanism is carried on by baroreceptors and chemoreceptors. This mechanism regulates blood pressure by adjusting the heart rate, vasomotor centre, and secretion of adrenaline and noradrenaline. It also adjusts respiratory centre in such a way that the functions of heart and respiration may run parallel.
This includes carotid sinus and aortic arch (Fig. 7.90).
i. Carotid Sinus:
It is a dilatation at the root of internal carotid artery, often involving the common carotid. The exact location varies in different species. The wall of the sinus is thinner due to less muscle fibres in the media. In the deeper parts of adventitia, an extensive network of afferent nerve fibres is present. The fibres end in free nerve terminals and characteristic minisci. These pressor receptors are sensitive to stretch (distortion effect) being stimulated by rise of blood pressure.
The sinus nerve (afferent) arises from the carotid sinus and carotid body, passes along the glossopharyngeal nerve and ends in the medulla in close relation with respiratory, cardiac and vasomotor centres.
ii. Aortic Arch:
Afferent nerves and stretch receptors—similar to those in the carotid sinus—are also present in the adventitia of aortic arch, the roots of great vessels and even the adjoining parts of left ventricle. They serve the same function as the carotid sinus.
This nerve arises from the arotic body, the aortic arch and the basal part of left ventricle. It is a purely afferent nerve. Its course varies in different species but in human beings it mostly passes in the vagus. Like the sinus nerve it ends in medulla being closely related to cardiac, vasomotor and respiratory centres.
This includes carotid (G.karas =sleep) body and arotic bodies (Fig. 7.92).
i. Carotid Body (Fig. 7.91):
It is a small nodule situated on the occipital artery, a branch of the external carotid artery very close to the carotid sinus. It consists of clumps of large polyhedral cells (Glomus cells), richly supplied with blood vessels and nerves. The vessels arise from the carotid artery. Some of the cells stain with chromic acid and belong to the chromaffin system but do not contain adrenaline. Numerous afferent nerve fibres surround the cell clumps and even the individual cells, and terminate in special chemoreceptors. They are sensitive to chemical changes in blood.
ii. Aortic Bodies:
Four groups of aortic bodies have been shown in cat.
These are small nodular structures, supplied by a special blood vessel and situated:
(a) On the thorax between the pulmonary trunk and ascending aorta,
(b) On the ventral surface of the root of the right subclavian artery,
(c) On the ventral surface of the root of the left subclavian artery, and also
(d) On the ventral surface of the aortic arch (Fig. 7.92). Afferent pathways from these chemoreceptor areas are lying in the arotic nerves and vagi. Their structures, nerve endings and functions are similar to those of carotid body.
By perfusion experiments, the effects of chemical changes in blood, as brought about through the Sino-aortic chemoreceptors. It is seen that CO2 excess, O2 lack and increased H-ion concentration stimulate respiration (mainly), increase heart rate, produce vasoconstriction and raise blood pressure.
After haemorrhage or in enfeebled circulation a rhythmic blood pressure wave (vasomotor wave) is often encountered. These vasomotor waves are due to chemoreceptor activities under such state. These waves were observed by Mayer (1876) and known as Mayer’s wave. Following inactivation of chemoreceptors, these waves disappear completely.
Mechanisms of Stimulation of Chemoreceptors:
It has been claimed that for the stimulation of chemoreceptor nerve endings, the liberation of acetylcholine plays as the chemical intermediary (vide Chemical regulation of respiration)
To study the functions of the Sino-aortic nerves various experiments have been performed.
i. Section and Stimulation:
Section and stimulation of the sinus and carotid nerves.
ii. Perfusion Experiments:
Perfusion experiments in which the carotid sinus region Is isolated and perfused with blood or other fluids whose pressure and composition can be varied at will.
iii. Electrophysiological Study:
Electrophysiological study shows that in normal arterial pressure the sinus nerves discharge impulses, the frequency of which rises with systolic pressure and diminishes with diastolic pressure. Rise in systolic pressure increases, the frequency of impulse discharge.
iii. Cross-Circulation Experiments:
Heymans and his associates have studied the functions of the carotid sinus and sinus nerve by cross-circulation experiments (Fig. 7.93).
The carotid sinus of the second dog B was isolated (the nerve supply remaining intact) and perfused with the blood of the first dog A. When the arterial pressure of the dog A was raised the arterial pressure of the dog B was diminished. Again when the arterial pressure of the dog A was lowered, the arterial pressure of the dog B was increased by secretion of adrenaline as evidenced from splenic contraction in dog C which got adrenaline from dog B through anastomoses of the suprarenal vein and the jugular vein.
The followings are the complete observations:
On raising the pressure in the carotid sinus, the following reflex effects are produced:
i. Slowing of the heart rate.
ii. Peripheral vasodilatation preferably in the splanchnic bed so as to increase the total vascular capacity.
iii. Fall of blood pressure.
iv. Diminished adrenaline secretion.
v. Slowing or stoppage of respiration.
vi. Diminished tone in voluntary muscles.
vii. Various changes in the viscera, viz., increased volume and movement of the stomach, decreased tone of urinary bladder, etc., caused by disturbed activity of the autonomic system. Fall of sinus pressure or section of the sinus nerve produces opposite effects. Stimulation of the central cut end of the sinus nerve also produces similar effects.
Raising the aortic pressure causes the following effects:
i. Slowing of the heart rate—mainly due to the stimulation of cardio-inhibitory centre and partly to the inhibition of accelerator centre.
ii. Inhibition of the vasomotor centre causing vasodilatation.
iii. Depressed adrenaline secretion.
iv. Fall of blood pressure.
v. Depressed respiration.
Fall of aortic pressure of section of the aortic nerve—produces reverse effects. Stimulation of the central cut end of the aortic nerve produces similar effects. Sometimes stimulation of the central cut end of vagus or aortic nerve may raise blood pressure by reflex cardiac acceleration and vasoconstriction. This proves that these nerves also carry some pressor fibres.
For the last few years there is considerable progress regarding the studies in connection with changes in the circulation and arteriolar resistance in blood pressure. In hypertension of the Sino-aortic origin there occurs vasoconstriction and stimulation of the sympathetic nerves of the heart. After occlusion of the common carotid arteries, hypertension occurs with decrease in the volume of spleen, kidney, limbs, etc.
Thus, it is evident that the functions of the sinus and aortic nerves (Buffer nerves) are very similar.
The effects of the various factors are summarised as follows:
From the above observations, the functions of Sino-aortic nerves may be described as follows:
i. Reflexly maintain the vagal tone and thus exert tonic inhibitory control on the heart.
ii. Reflexly maintain the inverse relation between blood pressure and heart rate and thus keep the variations of blood pressure within an optimum range (hence called Buffer nerves).
iii. Exert tonic inhibitory action on respiratory centre and vasomotor centre (vasoconstrictor).
iv. Reflexly regulate the activity of the respiratory, cardiac, vasomotor centres and adrenaline secretion and thus bring about a perfect coordination among them.
v. Changes in viscera, viz., variations of movement, tone, etc., may be reflexly produced through autonomic nerves.
The Sino-aortic mechanisms are meant for the maintenance of systemic blood pressure and flow. But the vascular receptors other than Sino-aortic are responsible mostly for control of local blood pressure and blood flow.
These are as follows:
A. As Baroreceptors:
i. At the Junction of Superior Thyroid Artery and Common Carotid Artery:
These baroreceptors mainly control the pressure and flow of the thyroid gland. When the systemic pressure is raised, these baroreceptors may be stimulated and impulse is carried through the common carotid nerve (C. C. N.) and is reflexly produced dilatation of the thyroid blood vessels. The presence of these baroreceptors has been demonstrated by Green (1956) in cats.
ii. Several Baroreceptor Areas in the Wall of Right and Left Common Carotid Arteries:
Several baroreceptor areas in the wall of right and left common carotid arteries between the level of the superior thyroid artery and subclavian bifurcation—have been demonstrated by Green (1956). Afferent impulses from these areas are carried through the branches of the aortic nerves.
iii. Baroreceptor Areas at the Junction of the Right Subclavian Artery and Common Carotid Artery:
These baroreceptor areas have been demonstrated by Heyman’s (1956) in cats and also in other mammals. Rise of pressure in these areas produces reflex systemic hypotension and hypopnoea. Afferent impulses are carried from these areas via the branch of the aortic nerves.
iv. Baroreceptors of the Pulmonary Arch of Aorta:
These baroreceptors are present in the pulmonary conus of bifurcation. It has been claimed by Aviado and Schmidt (1955) that reflex bradycardia and hypotension are produced if these receptors are stimulated due to rise of pressure.
v. Receptors in Thoracic Aorta:
The presence of baroreceptors has been claimed by Gruhzit and Moe (1953) and also others. Rise of blood pressure may produce reflex vasodilatation in the innervated limb through the stimulation of these baroreceptors.
vi. Mesenteric Baroreceptors:
Gammon and Bronk (1935) first detmonstrated the presence of mesenteric baroreceptors. The Pacinian corpuscles are the actual baroreceptors of the mesenteric blood vessels. These receptors are not directly related to the level of systemic blood pressure, but to a degree of distention of the mesenteric blood vessels.
It has been observed by Heymans and his colleagues (1937) under isolated cross-circulation technique that increases pressure in mesenteric blood vessels produces reflex vaso-dilatation of the spleen. But the specific functions of these baroreceptors are not yet clear. These receptors do not play any important role in the regulation of systemic blood pressure but they may play in the regulation of blood flow in the abdominal viscera.
vii. Peripheral Vascular Receptors:
Presence of other peripheral vascular receptors has been observed by many. Yamado and Burton (1954) have observed decrease of flow in the finger if negative pressure is exerted on it. It is claimed that this reflex decrease of blood flow is through venous-arteriolar reflex—causing constriction of the arterioles due to (a) distention and (b) increase of transmural pressure of the veins.
In congestive heart failure there is general occurrence of peripheral vasoconstriction (in the fingers and nose) is mostly due to reflex effect of increased central venous pressure. Ganglionic blocking agents and sympatholytic drugs relieve these conditions. The venous-arteriolar reflexes may play an important role in relieving the venous congestion because with the increase of venous congestion, the arterioles are constricted so that the outflow from the veins will exceed inflow from the constricted arterioles.
The presence of veni-venimotor reflexes have also been described by Wallis and others (1963). They have observed vasoconstriction in the haemodynamically isolated venous segment due to venous congestion produced by blowing up a cuff on the arm. Local anaesthesia abolishes this response.
viii. Lӧven Reflex:
This is nothing but axon reflex. If any portion of the vessel is dilated then the neighbouring vessel is constricted. This was first observed by Lovett.
ix. Bainbridge Reflex:
Bainbridge (1915) showed that intravenous administration of saline or blood produced reflex acceleration of the heart. He claimed this to be reflex arising from the stretch receptors present in the venous side of the heart (great vein and also right atrium) and bilateral sectioning of the vagi abolished the response.
His observation has been criticised by many but Jones (1962) has observed that reflex acceleration of the heart rate due to venous engorgement following infusion of saline or blood is dependent upon pre-existing heart rate of the animal. He claimed that if the heart rate is initially high (above 130 per min) then the reflex effect will be bradycardia instead of tachycardia.
x. Right Atrial Receptors (A and B):
Aviado and Schmidt have claimed that increasing the perfusion pressure in the right atrium produces bradycardia. This reflex effect is abolished by atropine or vagotomy. They suggest that the Bainbridge effect is the cause of stimulation of chemoreceptors supplied by the vago-depressor trunk which might well be activated by the changes in gas content, acidity, tonic balance and viscosity of the blood associated with the massive intravenous infusion.
xi. Pulmonary Deflation Receptors:
Paintal (1955a) has claimed that these receptors are stimulated by congestion of lungs during rapid venous return and produce reflex bradycardia. These receptors are also a part of pulmonary depressor chemo-reflex.
xii. Reflexes from the Inflation of the Lungs:
The physiology of these reflexes has been studied by Irving (1939) and Scholander (1963). They have described these reflexes to be an important line of defense against death due to asphyxia of the divers. They observed bradycardia and selective vasoconstrictions in non-vital organs (limbs, kidneys and mesenteries) after diving. They claimed that these reflex effects are due to stimulation of stretch receptors in the lungs.
xiii. Left Atrial and Left Ventricular Receptors:
Paintal (1955b) has shown that these receptors are excited by the increased pressure in the left side of the heart and produce bradycardia.
B. As Chemoreceptors:
i. Bezold and Jarisch Reflex:
Bezold and Hirt (1868) and Jarisch (1938) observed profound bradycardia, hypotension and apnoea following intravenous injection of veratrine alkaloid. They considered to be the direct effect of the drug on this cardiac receptors in left ventricle (mostly) that causes reflex cardiac and respiratory effects.
Jarisch has claimed that these are proprioceptive receptors and are normally responsive to stretch of the ventricular wall. Paintal (1955b) has shown that veratrine and related substances may stimulate the ventricular receptors and also some of atrial receptors (‘A’ and ‘B’). He also claimed that these drugs do not act directly on these receptors but act through changing the ionic status of the receptor areas.
ii. Pulmonary Depressor Chemoreflex and Pulmonary Respiratory Chemoreflex:
Brodie (1900) observed bradycardia and hypotension following intravenous administration of egg-white and serum into cats. He claimed that these effects are due to stimulation of receptors of the pulmonary vascular bed. These have been investigated by many. Dawes and Mott (1950) also observed bradycardia and hypotension after administration of phenyl diguamide.
They claimed that these effects were due to direct stimulation of the pulmonary vascular receptors. Paintal (1955a) has claimed these pulmonary depressor chemoreflex, pulmonary respiratory chemoreflex to be responsible for the stimulation of the pulmonary deflation receptors.
iii. Reactive Hyperaemia:
Chemoreceptors are present all throughout the vascular wall and are stimulated by the local accumulation of metabolites. Hyperaemia caused by locally accumulated metabolites acting on the blood vessels are called reactive hyperaemia. It is a kind of auto-regulation of blood circulation of the organ itself.
iv. Abdominal Chemoreceptors:
It has been described by a group of workers that certain peripheral (abdominal) vascular chemoreceptors are present which, when stimulated by strongly irritant chemicals, may produce reflex respiratory effects. But the presence of these receptors has not yet been substantiated and Heymans and his colleagues have shown that these effects are not observed if the drugs are administered in the isolated organs.
Summarily, it can be argued that nature’s mission is to protect the vital organs like heart and brain from any un-physiological conditions. Whenever there is any rise of blood pressure or fall of pressure, the normal range of blood pressure and blood flow of the vital organs are maintained by redistribution of blood. This redistribution of blood is made by withdrawing or heightening the vasomotor tone.
In condition of increased blood pressure, there is depression of sympathetic tone along with activation of parasympathetic tone—causing peripheral vasodilatation so as to shift the blood to the splanchnic bed (peripheral bed); but in condition of decreased blood pressure, there is increase of sympathetic tone along with decrease of para-sympathetic tone—causing profound vasoconstriction in the splanchnic bed (other peripheral bed) so as to shift the blood to the vital organs.
Chemical Control of Blood Pressure Influenced by Vasomotor Mechanism:
Many substances produced in the body are known to increase or decrease blood pressure by influencing the vasomotor mechanism.
Some of these are:
Tonic activity of the vasoconstrictor area may be due to stimulating action of CO2 in blood. During early stage of asphyxiation this may bring about a great increase in blood pressure. It is observed that over-ventilation of lungs, as by voluntary deep inspiration and expiration for 3 or 4 minutes, causes a feeling of giddiness. As large amounts of CO2 are expelled from blood by over-ventilation, the vasoconstrictor area is derived from proper stimulation by CO2. As a result, a fall in blood pressure and vasodilatation in splanchnic area occur.
If it is injected into blood, epinephrine constricts the cutaneous and abdominal arterioles, and this result in a very sharp rise of blood pressure, but the elevated pressure does not stand for a long time. By application locally, it is used in minor operation on the eye, nose, etc. In contrast, there is a dilatation of the coronary and skeletal muscle arterioles.
It is much weaker in action than in that of epinephrine. It is much used in bad colds and hay fever because of its constricting action. When inhaled or applied locally by drops or a spray, it brings about an immediate shrinkage of the congested blood vessels of the nasal mucosa. After 3 or 4 hours, the opening of nasal passages by vasoconstriction becomes freer and more comfortable for breathing.
It causes a marked dilatation of capillaries and arterioles in lowering of blood pressure.
It causes a marked dilatation of blood vessels as a depressant on the vasomotor centre. On a cold day after consuming alcohol the cutaneous vessels are especially affected.
Smoking increases both systolic and diastolic blood pressure. There is an increase of pulse rate materially and a decrease of temperature of extremities. So the use of tobacco may be injurious in arteriosclerosis and also in .cardiac diseases associated with arteriosclerosis or even high blood pressure.
Though it is an internal secretion of the posterior pituitary, it causes an increase of blood pressure. But this rise in pressure is not as great as that of epinephrine, yet this pressure continues for a long time.
Direct action of acetylcholine on coronary blood vessels is dilatation.