Increased Activity in Left Ventricular Receptors during Hemorrhage or Occlusion of Caval Veins in the Cat. ‐ A Possible Cause of the Vaso‐vagal Reaction

Abstract

Impulse activity in vagal afferent fibres and changes in heart rate were simultaneously recorded during rapid hemorrhage or blood pooling in cats in order to elucidate whether the sudden reflex bradycardia, sometimes evoked with the mentioned interventions, was correlated to an increased activity in any type of heart receptors. The results show that the slowing of the heart, resulting from an emptying of the central blood reservoirs was correlated to, and preceded by, an increased activity in receptors located in the left ventricle and signalling in non‐medullated afferents. The receptors were found to be activated also by obstructions of the ascending aorta and mechanical stimulation of the heart, and therefore seem to operate as mechanorecepton, stimulated by a “distortion” of the myocardium. ‐ It is conceivable that with rapid bleeding or pooling of blood, the receptors are excited by an improper squeezing of the myocardium when the ventricles contract vigorously around an almost empty chamber, and then induce a reflex bradycardia. This reflex mechanism, resembling the so‐called vaso‐vagal syncope reaction in man, may therefore serve as a protective system causing a break on the heart and allowing for an improved diastolic filling in situations when venous return is critically reduced.

Cardiac Autonomic Patterns Preceding Occasional Vasovagal Reactions in Healthy Humans

“…16,18,21,22 The power of the LF and HF oscillatory components is computed both in absolute units (ms 2 ) and in normalized units (NU), obtained by dividing the absolute power of each oscillatory component by total power minus the very-low-frequency component and multiplying by 100. 16,18 The LF/HF values were calculated as a measure of the reciprocal changes of the sympathetic and vagal modulation of the sinoatrial node discharge (sympathovagal balance).…”

“…2 Indeed, in a group of fainters, Morillo et al 12 found reduced values of LF and LF/HF during the first 5 minutes of a 60°t ilt, suggestive of a failure in vagal withdrawal and a blunted sympathetic activation. Similarly, another study 11 based on time-frequency mapping of RR variability concluded that subjects prone to vasodepressor syncope were characterized by an elevated cardiac parasympathetic activity that persisted during orthostatic stress.…”

“…On the basis of experimental observations, 2 it has been hypothesized that a possible trigger mechanism in humans might be the inappropriate mechanical activation of ventricular vagal unmyelinated afferents in the presence of reduced ventricular filling. In particular, the stimulation of ventricular vagal receptors would be produced by an enhancement of heart contractility due to an exaggerated cardiac sympathetic activation.…”

Arterial baroreflex function in older adults with neurocardiogenic syncope

“…The classical explanation for NCS suggested that orthostatic stress produces reduced cardiac filling and increased sympathetic stimulation resulting in the stimulation of ventricular mechanoreceptors. 32 However, subsequent work has shown that even entirely empty dog hearts on bypass do not demonstrate a Bezold-Jarish response 6 , and NCS persists even after complete denervation of the heart. 33 Disproof of ventricular mechanoreceptor stimulation as the inciting event for NCS has consequently led investigators to examine central alterations in cardiovascular control, possibly involving either opiod 34 or serotonin pathways.…”

Role of Adenosine Receptors in the Paradoxic Bradycardia Response of Rats to Inferior Vena Cava Occlusion During an Infusion of Isoproterenol

“…When isoproterenol is administered, however, inferior vena cava occlusion causes paradoxic bradycardia. Bradycardia during hypotension is a major manifestation of clinical 1,2 and experimental 1,10 vasodepressor reactions. Although our previous work defined some of the neural pathways involved in reflex bradycardia, [6][7][8][9] we have not examined whether endogenous chemicals play a role in initiating the reaction.…”