Contrasting reflex influences of cardiac afferent nerves during coronary occlusion

Abstract

Afferent neurons contained within cardiac sympathetic nerves may have important influences on the circulation when activated during myocardial ischemia. Although such activation is known to reflexly excite upper thoracic sympathetic efferent neurons, effects on other components of sympathetic outflow are unknown. Therefore, cardiac sympathetic afferent nerves were stimulated by occlusion of coronary arteries to investigate their reflex influences on renal sympathetic nerve activity and systemic arterial blood pressure. Responses were observed in anesthetized cats in which sympathetic and/or vagal cardiac afferent nerves remained intact and arterial baroreceptors remained intact or had been denervated. Stimulating sympathetic afferent neurons caused excitation of renal nerve activity, which was accompanied by variable changes in arterial pressure. Stimulation of vagal afferents by coronary occlusion consistently produced inhibition of renal nerve activity and marked depressor responses. When both components of cardiac innervation remained intact, increases or decreases in renal nerve activity and blood pressure were elicited by coronary artery occlusion in the presence or absence of arterial baroreceptors. These results illustrate that cardiac sympathetic afferent nerves can contribute significantly to cardiovascular control during myocardial ischemia.

Neural control of sympathetic nerve response to cardiogenic hypotension in anesthetized cat.

“…Occlusion of the left coronary artery also activates receptors innervated by afferent cardiac sympathetic nerves. These cardiac sympathetic afferent nerves can initiate excitatory sympathetic reflexes leading to increased blood pressure (BROWN, 1967;BROWN and MALLIANI, 1971;MALLIANI et al, 1969;UCHIDA and MURAO, 1974;FELDER and THAMES, 1979;WEAVER et a!., 1981).…”

“…In experimental myocardial infarction, however, COSTANTIN (1963) found that a decrease in sympathetic nerve activity occurred, while MALLIANI and LOMBARDI (1978) and UCHIDA and MURAO (1974) reported an increase in sympathetic nerve activity during coronary occlusion. It has been also reported that myocardial ischemia produced reflexly activated sympathetic nerve activity due to an excitation of cardiac sympathetic afferents and an inhibition mediated by vagal afferents arising from the heart (BROWN and MALLIANI, 1971;FELDER and THAMES, 1979;WEAVER et al, 1981;LOMBARDI et al, 1984). The occurrence of an excitatory cardiocardiac sympathetic reflex response to coronary occlusion, in addition, has been investigated after spinal cord section (MALLIANI et al, 1969;BROWN, 1967;FELDER and THAMES, 1981), which interrupts the supraspinal inhibitory influences on preganglionic sympathetic activity (DEMBOWSKY et al, 1980).…”

The bezold‐jarisch reflex in acute inferior myocardial infarction: Clinical and sympathovagal spectral correlates

“…[1][2][3] Both experimental and early clinical reports with intracoronary thrombolysis demonstrated a similar sympathoinhibitory reflex response after occlusion and recanalization of the right coronary artery. [4][5][6][7] Although there are only a few clinical studies relative to BJR after intravenous thrombolysis in acute myocardial infarction (MI), this reflex response has earned a reputation as indicator of successful thrombolysis, particularly in the setting of an inferior MI. [7][8][9] However, the pathophysiologic neural mechanisms underlying this phenomenon remain largely unknown.…”

“…1 Besides Jarisch and Zotterman, 2 who confirmed these results, a host of other investigators contributed greatly to increase our knowledge about the coronary BJR, involving receptors, couched in different terminologies, as ventricular mechanosensitive or chemosensitive neuroreceptors, mostly located in the inferioposterior left ventricular wall, which discharge irregularly and sporadically into small nonmyelinated afferent C-fibers in the vagi. [2][3][4][5] Although these receptors have not been described anatomically or histologically, and the precise mechanisms and the natural stimulus to the cardioinhibitory reflex response are insufficiently understood, stimulation by stretch, distension of an infarcted area, or chemical substances are thought to modulate the arterial baroreflex mediating efferent vagal activation. 17 Fundamental experimental evidence suggests that locally released mediators that occur within minutes after the onset of ischemia, and particularly during reperfusion, such as prostaglandins, serotonin, and oxygenderived free radicals, may activate the cardiac vagal afferent pathways.…”

“…3,4,17 Reflex bradycardia and hypotension has been observed to occur in animal models after prolonged coronary occlusion and reperfusion, and in humans, in the laboratory, after intracoronary injection of contrast material. 3,4,18 In clinical practice, BJR responses are observed in patients with inferior ischemia in association with coronary spasm and might account for most of the bradyarrhythmias in up to 61%, occurring within the first hour of posterior MI. 19,20 Clinical Relevance of Reperfusion-Induced Bezold-Jarisch Reflex…”