Circulatory Reflex Responses during the Initial Stage of Feline Endotoxin Shock

Halinen, Matti; Hakumäki, M. O. K.; Sarajas, H. S. S.

doi:10.1111/j.1748-1716.1977.tb06007.x

Cited by 7 publications

(3 citation statements)

References 20 publications

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“…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.…”

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“…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.…”

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Baroreflex participation of cardiovascular response to E. coli endotoxin.

et al. 1986

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The purpose of this experiment was to evaluate the effects of the arterial baroreceptor buffering capacity on cardiovascular parameters during hypotension caused by E. coli endotoxin in anesthetized dogs. In the control group, mean blood pressure and cardiac output fell significantly from 104 + 10 mmHg to 63±7 mmHg and 1.17 + 0.16 l/min to 0.67 + 0.08 l/min, respectively, 60 min after intravenous injection of endotoxin (1 mg/kg). Central venous pressure also decreased significantly after the injection. Total peripheral resistance and portal vein pressure increased significantly immediately after the injection, and then returned toward baseline levels. The time course of changes in these five cardiovascular parameters after the injection of endotoxin was the same as that in dogs with sino-aortic denervation. Following the injection of endotoxin, stroke volume and left ventricular dP/dt fell significantly in both control and denervated dogs; however, these decreases in the denervated group were significantly greater. These findings suggest that the arterial baroreceptors may play a role in the poor compensatory response to hypotension induced by endotoxin, at least, in the cases of mean blood pressure, cardiac output, total peripheral resistance, central venous pressure, and portal vein pressure.

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Baroreflex participation of cardiovascular response to E. coli endotoxin.

et al. 1986

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“…Coincidental to the increase in plasma catecholamines, is an increase in the postganglionic sympathetic nerve firing rates to the heart and spleen in cats (Halinen et. al., 1977) and to the kidney of rats (Palsson et.…”

Section: Alterations In Beta Adrenoceptor Signal Transduction In Sepsismentioning

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Alterations in intrinsic heart rate in endotoxemia

Wearden¹

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After much early debate, it is now well recognized that the origin of the heart beat is myogenic, or intrinsic, to the heart. It has been felt that the intrinsic heart rate (IHR) is constant and that the observed heart rate is controlled by tonal alterations in the activity of the autonomic nervous system in response to various stimuli. Some investigators have recognized, however, that the intrinsic heart rate (IHR) can be altered in certain conditions. Sepsis, or the host response to bacterial infection, is recognized as a stress to the host that results in decreased myocardial contractility and tachycardia. Some previous work has suggested that this tachycardia may exist outside the tonal regulation of the autonomic nervous system, raising the possibility of an elevation of the IHR. Utilizing an E. coli lipopolysaccharide (LPS) endotoxin model of sepsis in the rat, this work demonstrates an elevation of the IHR in sepsis. The experimental evidence further suggests that the β-adrenoceptor participates in the induction of the elevation in IHR early in the septic process. By sixteen hours after LPS administration the β-adrenoceptor is, however, no longer required for the ongoing elevation of IHR. It is also demonstrated that the elevation in IHR is more prolonged than the contractile dysfunction induced by LPS. iii Dedication To Andrea, Andrew, Mara and Luke Without your support this would not have been possible Without your unconditional love this would all be meaningless

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