Baroreflex control of heart rate during and after propofol infusion in humans

Abstract

We conclude that heart rate responses to both lowering and elevating blood pressure were depressed by propofol anaesthesia, and 60 min was required for their full recovery after discontinuation of propofol infusion.

Cortisol Lowering Action and Cardiovascular Stability of Etomidate: A Comparison With Propofol in Controlled Hypertensives

“…15 Propofol has been shown to decrease the baroreceptor reflex relating to blood pressure in human beings. 16 In contrast, etomidate preserves baroreceptor reflex mechanism. 17 An induction dose of etomidate given to cardiac patients results in very stable haemodynamics with almost no change in heart rate, mean arterial pressure, mean pulmonary artery pressure, pulmonary capillary wedge pressure, central venous pressure, stroke volume, cardiac index, or pulmonary and systemic vascular resistance.…”

Brainstem Adenosine A1 Receptor Signaling Masks Phosphorylated Extracellular Signal-Regulated Kinase 1/2-Dependent Hypotensive Action of Clonidine in Conscious Normotensive Rats

“…In contrast, central A 1 R blockade had no influence on the hypotensive response or the increase in RVLM pERK1/2 elicited by clonidine in ABD rats. These findings support the hypothesis that central adenosine A 1 R signaling opposes the adenosine A 2A R-mediated (pERK1/ 2-dependent) hypotensive response and yield insight into a cellular mechanism that explains the absence of clonidineevoked hypotension in conscious normotensive rats.Clonidine-evoked hypotension is minimal or absent in conscious normotensive rats (Abdel-Rahman, 1992;Ricci et al, 1992;Medvedev et al, 1998) in contrast to animal preparations that exhibit baroreflex dysfunction such as anesthetized (Borkowski and Finch, 1979;Sannajust et al, 1992;Su et al, 2002;Sato et al, 2005) and hypertensive (Judy et al, 1976Judy and Farrell, 1979;Prados et al, 1998) rats and after surgically induced baroreceptor dysfunction [aortic barodenervation (ABD)] (Abdel-Rahman, 1992; Nassar and Abdel-Rahman, 2006, 2008. However, the cellular mechanisms that explain these findings remain unclear.…”

“…Clonidine-evoked hypotension is minimal or absent in conscious normotensive rats (Abdel-Rahman, 1992;Ricci et al, 1992;Medvedev et al, 1998) in contrast to animal preparations that exhibit baroreflex dysfunction such as anesthetized (Borkowski and Finch, 1979;Sannajust et al, 1992;Su et al, 2002;Sato et al, 2005) and hypertensive (Judy et al, 1976Judy and Farrell, 1979;Prados et al, 1998) rats and after surgically induced baroreceptor dysfunction [aortic barodenervation (ABD)] (Abdel-Rahman, 1992; Abdel-Rahman, 2006, 2008). However, the cellular mechanisms that explain these findings remain unclear.…”

Comparison of the Macro-circulatory Effects of the New Generation Plasma Expander EAF-HexaPEGylated Albumin (EAF-PEG-BSA) in a Rabbit Hemorrhagic Shock Model: a Comparison with Conventional Crystalloid and Colloid Solutions

“…The HR remained essentially at the baseline in all 25% hemorrhagic shock experiments but in 75% hemorrhagic shock studies where it returned to a value higher than the baseline value; propofol may have altered the natural HR response [4,5]. CO did not return to the baseline values when resuscitated with saline or 25% albumin, but returned close to the baseline with PEG-albumin both with the 25% hemorrhagic shock experiments and exceeded the baseline value in the 75% hemorrhagicshock resuscitation model.…”