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The regulation of the heart is effected through the afferent (centripetal) and efferent (centrifugal) nerves of the heart (Fig. 7.79).
The afferent nerves are:
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i. From the heart through the vagus nerve and from the aortic arch, the aortic nerve.
ii. From the heart through the inferior cervical and first four thoracic ganglia and first four thoracic nerve roots into the spinal cord.
iii. From the carotid sinus through the sinus nerve, a branch of glossopharyngeal nerve.
The efferent nerves are:
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i. Vagus.
ii. Sympathetic (Fig. 7.78).
i. Vagus Nerves:
The preganglionic fibres of the vagus nerves arise from the dorsal nuclei of the vagus situated in the floor of the fourth ventricle in the medulla (Fig. 7.78). After their origin they descend downwards. The cardiac fibres separate from the main nerve trunk in the neck and proceed towards the heart and form deep and superficial cardiac plexuses with the fibres of the sympathetic.
The fibres reach the atrial muscle and make synaptic connections with intraganglionic cells situated near the Sino-atrial and atrioventricular nodes. From here the postganglionic fibres arise and supply the specialised tissue of the Sino-atrial and atrioventricular nodes and also extend between the muscle fibres. The postganglionic fibres do not extend beyond the upper part of the bundle of His and the base of the ventricles. Ventricular myocardium of the apex is said not to receive any vagal fibres. The vagus nerves also supply fibres to the coronary vessels.
Tonic Action of the Vagus Nerves:
The vagus exerts a tonic inhibitory control over all parts of heart. Acetylcholine is released by the postganglionic fibres on stimulation. Atropine prevents action of acetylcholine on the cardiac muscle and the heart rate is increased even up to 150 per minute in human beings. This proves that a constant inhibitory influence is exerted by the vagus on heart. The vagal tone is of reflex in origin, being produced by the sino-aortic nerves. Section of these nerves reduces the vagal tone and increases the heart rate.
Stimulation of the Vagus Nerves causes the following effects:
i. The heart rate is slowed down even it may stop. This is caused by reducing the rhythmicity of the S.A. node. This is known as the negative chronotropic effect of the vagus.
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ii. The conductivity of the bundle is reduced thus producing various degrees of heart block. This effect is known as negative dromotropic effect. This may be an additional cause for slowing.
iii. The force of contraction is diminished. In the frog the vagus directly depresses the ventricular muscle. This is known as the negative inotropic effect of the vagus.
iv. The duration of systole is diminished, but the duration of diastole is increased.
v. The length of refractory period (which depends upon the systolic length) is diminished.
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vi. Excitability of the heart is also reduced and this condition is known as negative bathmotropic effect. On the whole, the vagus acts as the inhibitor of heart.
Vagus Escape:
In animals (frogs, etc.), stimulation of the vagus by a tetanising current causes slowing or stoppage of heart rate. But after a little while heart starts beating again even if the stimulation is continued. This phenomenon is called vagus escape—meaning by that the heart escapes from inhibitory influence of the vagus.
Four explanations have been advanced:
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1. Bainbridge Reflex:
Due to slowing or stoppage of the heart rate, engorgement of the great veins and right atrium takes place. This may mobilise this reflex hence the heart starts beating. This reflex takes place only in normal animal but not in pithed animal or in animals whose brain has been damaged. However this effects has been contradicted by many.
2. Sino-Aortic Reflex:
The fall of blood pressure in the aorta reflexly increases the heart rate through Sino-aortic mechanism in animal with intact central nervous system. The chemoreceptors which are present in carotid bodies and aortic bodies are stimulated and reflexly stimulate the heart by depressing the vagi but exciting the sympathetic.
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3. Idioventricular Rhythm:
Due to complete heart block, ventricle originates its own rhythm. In the mammalian heart, the vagal fibres are not extended beyond the upper part of the bundle. So the vagus nerves exert their effect upon the heart through their action on atrial muscle and the slowing or stoppage of heart rate following vagal stimulation is due to the depression of conduction in the atrioventricular connections.
So the ventricular stoppage is due to an indirect effect of atrial slowing. If this effect is prolonged then atrioventricular dissociation may take place and ventricles escape from the Sino-atrial control and beat at its own rhythm (idioventricular rhythm).
Sometimes shifting of pacemaker is taken place if the normal pacemaker function is totally depressed and subsequently impulse formation is totally suppressed due to vagal stimulation. In such case pacemaker regions, next to the S.A. node or A.V. node, become developed and maintain the heartbeat.
4. Differential Effect of the Vagus and Sympathetic:
In frogs or other animals, sympathetic fibres pass through the vagus (vagosympathetic). Stimulation of the trunk produces vagal effect first, but if the stimulation is continued further, the vagal effect is possibly ineffective and when the sympathetic becomes effective. This ineffectiveness of the vagus is either due to exhaustion of acetylcholine for continued stimulation or the heart muscle becomes refractory to the effect of acetylcholine.
ii. Sympathetic Nerves (Fig. 7.78):
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Connector cells of the sympathetic nerves are situated in the lateral horn cells of the upper thoracic segments of the spinal cord (T.1-5 or 6). Excitor cells are situated in the superior, middle and inferior cervical ganglia from where the postganglionic or excitor fibres take origin and pass directly to the heart. Cardiac branches from the sympathetic chain also runs from the upper thoracic ganglia, to the heart (Fig. 7.78).
The fibres supply the specialised tissues of the sinoatrial and atrioventricular nodes, atrial and ventricular muscles. Nonidez has described that middle cardiac nerves supply efferent fibres to the heart; and superior cardiac nerves supply nerve to large arteries at the base of the heart, while the inferior cardiac nerves supply only afferent fibres to the heart. The sympathetic fibres carry vasodilator fibres to the coronary vessels.
The sympathetic exerts a light tonic accelerating action on the human heart. Noradrenaline is released by the postganglionic fibres of the sympathetic on stimulation. Slowing of the heart rate occurs after bilateral excision of the first to sixth thoracic ganglia.
Action potential, recorded in the sympathetic nerves of the heart of cat, has demonstrated the existence of accelerator tone. [Of the two nerves—vagus and sympathetic -the former exerts a much stronger influence on the heart than the latter.]
Effects of Stimulation of the Sympathetic Nerves:
i. Increases the Frequency of Heart Rate (Accelerator):
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It is due to its effect on Sino-atrial node. This is known as (positive) chronotropic effect of the sympathetic.
ii. Increases the Force of Contraction (Augmentor):
It is due to its effect on atrial and ventricular muscles. This is known as (positive) inotropic effect of the sympathetic.
iii. Increases the Excitability:
Increases the excitability (positive bathmotropic) and irritability of heart and thereby may cause extra- systoles (ectopic beats).
iv. Increases the Conductivity:
Increases the conductivity (positive dromotropic) of the myocardium and the bundle of His.
On the whole the sympathetic is taken as the accelerator and augmenter of heart.
Cardiac Centres (Fig. 7.79):
Though the existence of separate centres (areas) for each vagus and sympathetic has been described by many, yet their anatomical positions particularly of the latter one has been a point of much dispute and it requires further study.
The dorsal motor nucleus of vagus in the medulla is the cardiac-inhibitory centre and it transmits continuous tonic inhibitory vagal impulse to the heart. This centre has got direct connection with the afferent nerves coming from the baroreceptors or chemoreceptors.
Reflex bradycardia during the rise of systemic blood pressure is due to stimulation of the cardio-inhibitory centre. On the other hand, tachycardia is observed during the fall of blood pressure—which is due to inhibition or depression of the cardio-inhibitory centre along with the withdrawal of vagal tone from the heart. Under such state sympathetic cardiac centres get the upper hand.
The sympathetic cardiac centres or cardio-accelerator centres are situated in the lateral horn cells of the upper thoracic segments of the spinal cord (T.1-5 or 6). The preganglionic fibres enter the sympathetic ganglia to connect with the cells of thoracic ganglia and inferior, middle and superior cervical ganglia.
In animals and even in human beings the first thoracic ganglion and inferior cervical ganglion are fused to form the stellate ganglion from which postganglionic fibres (accelerator fibres) run directly to the heart. The function of the cardio-accelerator centre of the spinal cord is modified by the higher centres. The exact location of the higher cardio-accelerator centre is not yet fully known and the probable existence of the same in the medulla cannot be denied.
Some are of opinion that there is no separate cardio-accelerator centre in the medulla and in addition to the cardio-inhibitory centre, there are pressor and depressor centres (areas) in the medulla. With the increase in the activity of the pressor centre along with the rise of blood pressure, heart rate and stroke volume are also increased. This pressor centre possibly functions with the superior control of the same in the hypothalamus and cerebral cortex.
The posterior hypothalamic nuclei have been indicated to be the cardio-accelerator centres by Beattie, Brow and Long. Sympathetic activities on the heart are increased following stimulation of these centres. These centres have got connections with motor and premotor areas (centres) of the cerebral cortex.
If these cortical areas are stimulated, the increase of heart rate is encountered. The middle groups of nuclei of the hypothalamus are related with the parasympathetic – whose stimulation causes the slowing of heart rate.
