Carotid sinus baroceptor modifications associated with endotoxin shock

Abstract

Carotid sinus baroceptor responses were studied in dogs before and after administration of shock-producing quantities of E. coli endotoxin. Responses were characterized as the relationship between intrasinusal stimulus pressure and baroceptor nerve discharge frequency. Both constant and pulsating pressure stimuli were used. After endotoxin administration and the onset of endotoxin shock it was found that postendotoxin discharge frequencies exceeded control discharge frequencies for most pressures. These response shifts result in a resetting of the hemoregulatory barostatic mechanism to regulate blood pressure to a new and hypotensive level. It is concluded that in the later phases of endotoxin shock, the reflex modification may play the predominant role in maintaining hypotension and that barostatic resetting partially explains the poor compensatory response to the initial profound hypotension after endotoxin administration.

Comparison of the reflex vasomotor responses to separate and combined stimulation of the carotid sinus and aortic arch baroreceptors by pulsatile and non‐pulsatile pressures in the dog

“…During pulsatile perfusion, however, some fibres show a phasic discharge even although the mean pressure may be below the threshold pressure for a steady discharge (Ead et al 1952;Landgren, 1952). Trank & Visscher (1962) and Spickler & Kezdi (1967) found that for the same mean pressure the averaged discharge frequency in the carotid sinus nerve was greater during pulsatile than non-pulsatile pressure perfusion. It might be anticipated therefore that at low sinus pressures the curve for pulsatile pressure perfusion would reach a plateau at a lower level of systemic arterial pressure than that for non-pulsatile pressure.…”

“…On the assumption that the vasomotor centre responds to the total number of impulses it receives per unit time, its inhibition by substituting in the carotid sinuses a pulsatile pressure for a non-pulsatile pressure at the same mean pressure must result from an increased discharge. Evidence from averaged whole nerve recordings from the carotid sinus nerve indicates that this is so (Trank & Visscher, 1962;Spickler & 290 CAROTID AND AORTIC BARORECEPTOR REFLEXES 291 Kezdi, 1967;Koushanpour & McGee, 1969). This increased total nerve activity is not the result of an alteration in the number of impulses per cycle in individual baroreceptor units firing throughout the cycle (Ead et al 1952) but is presumably due to recruitment of additional fibres.…”

Effects of Bradykinin and Autonomic Nervous System Inhibition on Systemic and Regional Hemodynamics in the Unanesthetized Rhesus Monkey

“…An alternative mechanism for the sustained decrease of peripheral resistance during early endotoxemia is lack of effective reflex cardiovascular response to hypotension (14). To test this possibility, we also examined the regional and systemic hemodynamic changes occurring during autonomic ganglionic blockade before and during bradykinin infusion.…”

Baroreflex participation of cardiovascular response to E. coli endotoxin.

“…HALINEN et al (1977) reported that peripheral sympathetic nerve discharges increase reflexly during their 15-min observation periods after the injection of endotoxin, as in the case of acute hemorrhagic hypotension but they did not report what happened later. TRANK and VISSCHER (1962) found that carotid sinus baroreceptor mechanisms do not function normally when endotoxin was present for longer observation periods of over 30 min. KOYAMA and MANNING (1985) reported that hypotenslon caused by endotoxin occurred in parallel with a decrease in efferent splanchnic nerve activity, and KOYAMA (1986) showed that an intravenous injection of endotoxin causes a hypotensive effect simultaneous with a reduction in spontaneous renal sympathetic nerve activity.…”

“…conflicting reports about the participation of the baroreceptor reflex system in endotoxlc hypotenslon (TRANK and VISSCHER, 1962;BLATTBARG and LEVY, 1969;HALINEN et al, 1977). HALINEN et al (1977) reported that peripheral sympathetic nerve discharges increase reflexly during their 15-min observation periods after the injection of endotoxin, as in the case of acute hemorrhagic hypotension but they did not report what happened later.…”