Mark Kollai

Effect of cardiac vagal and sympathetic nerve activity on heart rate in rhythmic fluctuations

Beat-to-beat changes observed in cardiac vagal and sympathetic nerve activity and their effects on cardiac cycle length were studied during slow wave blood pressure and heart rate fluctuations (third order rhythm) and during respiratory sinus arrhythmia. Recordings were made from both nerves simultaneously in chloralose anesthetized and artificially ventilated dogs. During slow wave fluctuations in heart rate, a linear relationship was found to exist between the number of spikes per pulse interval recorded from vagal and sympathetic nerves and the length of pulse intervals. During respiratory sinus arrhythmia the time course of rhythmic changes in nerve activity and in cardiac cycle length was analyzed. Comparison of time courses indicated that vagal discharges affected the timing of not the following beat, but the one after; while the sympathetic effect was further delayed, affecting the third beat after the discharge. Baroreceptor stimulation, which resulted in lengthening the cardiac cycle, shifted this relationship by one cycle, i.e. vagal discharges affecting the occurrence of the following beat, while sympathetic discharges affecting the beat after. These results provide evidence for the conclusion that in dogs both vagal and sympathetic nerve activity contribute to the control of cardiac cycle length, however, with different time relations and effectiveness.

Cardiovascular reflexes and interrelationships between sympathetic and parasympathetic activity

Simultaneous recordings from vagal and sympathetic nerve fibers innervating the heart have enabled us to study relationships between activity in these two autonomic nerves. Our recent studies, as well as those of others, are reviewed with respect to tonic activity and reflex actions in these two autonomic efferents. Discharges of the two nerves in relation to blood pressure pulses and to respiratory cycles are reciprocal. During slower fluctuations of hemodynamic changes which occur spontaneously, such as during Mayer waves, a reciprocal relationship between activity in the two autonomic nerves is also observed. On the other hand, in reflex responses both reciprocal and non-reciprocal patterns of reactions produced by stimulations of the hypothalamus showed varied relationships between responses in the two autonomic outflows. The functional significance of the interrelationships of the activity pattern observed in vagal and sympathetic nerves is discussed with respect to control of cardiac functions.

Study of cardiac sympathetic and vagal efferent activity during reflex responses produced by stretch of the atria.

(1) In chloralose anesthetized dogs, effects of the left and the right atrial stretch were studied in the same animal. Stretch of the sino-atrial region of the right atrium produced acceleration of the heart rate during, and reversal of response at the termination of, the stretch. Stretch of the left pulmonary vein-atrial junctional region evoked an initial decrease followed by an increase in heart rate. The responses were similar in all animals, despite initial heart rates ranging from 120 to 200 beats per minute. (2) Activity in vagal and sympathetic nerve branches innervating the heart was recorded simultaneously. Care was taken to identify the vagal fibers innervating the heart, and record their activity without contamination of sympathetic impulses. The right atrial stretch evoked an augmentation of sympathetic activity which reached its peak at 20 sec after the beginning of stimulus. The stimulus slightly increased the vagal activity; this change occurred slowly and reached its peak in about 40-60 sec after stretch. At the release of stretch, sympathetic activity generally showed a reversal of response, i.e. activity was inhibited for 30 sec. (3) Stretch of the left atrium produced biphasic changes in cardiac sympathetic nerves; their activity was strongly inhibited for the first 15 sec, then augmented throughout the remainder of the stretch. This effect lasted 30 sec after the cessation of stimulus. Effects on vagal cardiac nerve fibers were smaller; mild augmentation in activity was produced. The onset of this effect was faster than that seen in case of the right atrium stretch. (4) Reciprocal action between vagal and sympathetic cardiac nerves was obvious only in the early phase of left atrium stretch. Effects on the heart were determined by balances in activity of these antagonistic nerves. In contrast with what occurred in cardiac reflexes, carotid sinus distension even in the same animal produced a large increase in vagal activity, and near complete inhibition of sympathetic nerve activity. Thus, good reciprocal action between the two sets of nerves was demonstrated. A difference in the two types of reflexes was thus revealed. (5) Stretch of the right atrium evoked during carotid sinus distension caused an increase in heart rate from the new low level which was produced by baroreceptor activation. Vagal activity which was greatly augmented by sinus distension was decreased by atrial stretch, while previously inhibited sympathetic activity due to sinus distension was augmented by stretch of the atrium. The effect of stretch on vagal activity seems to depend to a degree on the prestimulus level. It is of interest that the powerful baroreceptor reflexes do not mask the cardiac reflexes studied. (6) The relative importance of sympathetic and vagal efferents to atrial stretch reflexes was discussed.

Differential responses in sympathetic outflow evoked by chemoreceptor activation.

It is well established that excitation of arterial chemoreceptors results in an elevation of blood pressure due to increased sympathetic vasoconstrictor activitya,lL Skeletal muscle vascular resistance is particularly increased and muscle blood flow decreases greatly4,11. Parallel with the pressor response heart rate decreases in animals with controlled ventilation1,4,6, is, although it has been reported by some that the direct effect of chemoreceptor stimulation is a moderate tachycardia14,1L Such reflex reactions to chemoreceptor activation, i.e. the vasoconstriction in skeletal muscle accompanied by bradycardia, suggest that opposite changes in activity occur between sympathetic cardiac and vasoconstrictor nerves; the cardiac vagus may also contribute to bradycardia. In contrast to the chemoreceptor reflex, activation of arterial baroreceptors is known to inhibit activity of all sympathetic outflows, though to different degrees19, z°. There have been numerous studies of the cardiovascular responses involved in chemoreceptor reflexes. However, in only a few studies 9 has use been made of simultaneous recordings from various sympathetic nerves involved and comparisons made between activities in these outflows. The aim of this study was to compare changes in activity caused by chemoreceptor stimulation in cardiac sympathetic and vertebral nerves, those sympathetic fibers innervating mainly blood vessels of forearm a, and to examine the mechanism involved in the differential response produced. The experiments to be described were performed on 14 cats, anesthetized with chloralose (70 mg/kg, i.p.) and artificially ventilated after paralysis with Flaxedil (4 mg/kg, i.v.). The femoral artery and vein were cannulated, arterial blood pressure was measured by use of a Statham transducer. Heart rate was recorded by a tachometer triggered by the pressure pulse. Blood flow through the axillary artery was recorded with electromagnetic flow meter in the right, skinned forearm with the paw occluded. The vertebral and cardiac sympathetic nerves and phrenic nerve on the left side were exposed and placed on bipolar platinum electrodes for recording. The activities

Cardiac vagal and sympathetic nerve responses to baroreceptor stimulation in the dog

The effects of ascending stepwise pressure changes in the isolated carotid sinuses on cardiac vagal and sympathetic nerve activities were studied in anesthetized, open chest dogs. The steady state responses of the cardiac vagal and the sympathetic nerve activity and arterial blood pressure were plotted against the sinus pressure and the relations were approximated by the normal distribution function (response curve). The sinus pressure- vs. “reflex gain” relations (reflex gain curve) were approximated by the normal density function. The maximum gain and the “range of change” were found to be greater for the vagal than for the sympathetic and arterial pressure responses. The sinus pressure values derived from “response curves” and “reflex gain curves” for vagal and sympathetic nerve responses were close to each other, while these values and those obtained from arterial pressure responses were considerably apart. It was concluded that: (1) The cardiac vagal neurons are more sensitive to the baroreceptor input than the sympathetic neurons; (2) The similar type of baroreceptor afferent inputs reach the cardiac vagal and the sympathetic structures which are controlling the autonomic outflows.