Effects of Anesthesia on Baroreflex Control of Heart Rate in Man

Bristow, James; Prys‐Roberts, C.; Fisher, Anthony; Pickering, Thomas G.; Sleight, Peter

doi:10.1097/00000542-196911000-00009

Cited by 107 publications

(33 citation statements)

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“…Baroreceptor reflexes have been demonstrated in pigs but their sensitivity is lower than that observed in other less sedentary species (Booth et al, 1966). Barbiturate anaesthesia is known to depress baroreceptor reflexes (Bristow et al, 1969) and this may have contributed to their variable sensitivity in our experiments. We conclude that the baroreceptor-mediated response to hypertension does not adequately account for the observed fall in cardiac output that follows L-NAME.…”

Section: Discussionmentioning

confidence: 58%

Comparison of the ability of nicardipine, theophylline and zaprinast to restore cardiovascular haemodynamics following inhibition of nitric oxide synthesis

Herity

Allen

Silke

et al. 1994

British J Pharmacology

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1 The use of pharmacological inhibitors of nitric oxide (NO) synthesis to treat patients with septic shock is limited by the observation that they cause a fall in cardiac output in some subjects. The aim of this work was to investigate this fall and to test whether it was reversible by subsequent administration of nicardipine, theophylline or the cyclic GMP-selective phosphodiesterase inhibitor, zaprinast (M&B 22948). 2 In pentobarbitone-anaesthetized pigs, haemodynamic indices were measured before and after intravenous administration of NG-nitro-L-arginine methyl ester (L-NAME) in a dose-response protocol (0.2-20 mg kg-'; n = 6) and as a single bolus of 10 mg kg-' either alone or followed by increasing doses of nicardipine, theophylline or zaprinast (n = 8 in each group). 3 L-NAME caused a dose-dependent rise in systemic vascular resistance and mean systemic arterial pressure and a dose-dependent fall in cardiac output. A single bolus of L-NAME (10 mg kg-') produced these effects within 15 min. 4 Subsequent administration of nicardipine (0.05-0.2 mg kg-') caused complete reversal of systemic vasoconstriction and hypertension and in doing so completely restored cardiac output. Theophylline (7.5-1O mg kg-') partially reversed the rise in systemic vascular resistance and partially restored cardiac output but the effect was small compared to that of nicardipine. Zaprinast (1-5 mg kg-') had no significant effect on any of these variables. 5 These results suggest that reduced cardiac output following inhibition of NO synthesis is an effect of increased afterload on the heart and is reversible by nicardipine and to a lesser extent by theophylline. These findings may have potential value for those using NO synthase inhibitors to treat patients with septic shock.

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Section: Discussionmentioning

confidence: 58%

Comparison of the ability of nicardipine, theophylline and zaprinast to restore cardiovascular haemodynamics following inhibition of nitric oxide synthesis

Herity

Allen

Silke

et al. 1994

British J Pharmacology

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“…The observation in the present study that the animals with hypertrophy but without overt heart failure had less reduction of sensitivity than the group with overt heart failure suggests that the severity of this dysfunction of the baroreceptor reflex arc may be a function of the severity of the cardiac abnormality. Apparently, the sensitivity of this reflex is altered under other circumstances as well, since it has been shown to be accentuated during natural sleep (11) and depressed in hypertension in experimental animals (20) and man (21) and during anesthesia (13) and exercise (22,23) . 1 Baroreceptor Reflex in Heart Failure in man; resetting of the threshold without a change in sensitivity of the reflex has been produced by hypercapnia in normal subjects (24).…”

Section: Discussionmentioning

confidence: 99%

“…In order to study the sensitivity of this reflex in heart failure, we compared some of the systemic and regional hemodynamic effects of induced baroreceptor hyper-and hypotension in normal healthy dogs and in dogs with experimentally produced cardiac hypertrophy and heart failure. Since the sensitivity of this reflex is known to be affected profoundly by the level of consciousness (11,12) and by various anesthetic agents (12,13), this study was conducted in the conscious unsedated dog.…”

Section: Introductionmentioning

confidence: 99%

Alterations in the Baroreceptor Reflex in Conscious Dogs with Heart Failure

Higgins¹,

Vatner²,

Eckberg³

et al. 1972

J. Clin. Invest.

220

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A B S T R A C T The effectiveness of the baroreceptor reflex in conscious dogs with experimental cardiac hypertrophy and heart failure was compared with that in a group of normal conscious dogs. Cardiac hypertrophy and heart failure were produced by tricuspid avulsion and progressive pulmonary stenosis. The sensitivity of the baroreceptor reflex to transient hypertension was assessed by determining the slope of the regression line relating the prolongation of the R-R interval to the rise in systolic arterial pressure during the transient elevation of arterial pressure induced by an intravenous injection of 1-phenylephrine. The mean slope averaged 22.4 +2.3 msec/mm Hg in 16 normal animals, 23.1 ±1.5 in five sham-operated animals, and was significantly reduced to 8.3 ±0.8 in 10 dogs with hypertrophy alone (P < 0.001), and to 3.3 ±0.5 in nine dogs with heart failure (P < 0.001). The response to baroreceptor hypotension was compared during bilateral carotid artery occlusion (BCO) in six normal and six heart failure dogs previously instrumented with Doppler flow transducers on the superior mesenteric and renal arteries. During BCO, in normal dogs arterial pressure increased 52 ±4 mm Hg, heart rate 33 ±2 beats/min, mesenteric resistance 0.17 ±0.03 mm Hg/ml per min, and renal resistance 0.37 ±0.10 mm Hg/ml per min. In the heart failure group all of these variables increased significantly less (P < 0.01 ); arterial pressure rose 25 ±3 mm Hg, heart rate 13 ±4 beats/min, mesenteric resistance 0.04 ±0.007 mm Hg/ ml per min, and renal resistance 0.18 ±0.09 mm Hg/ ml per min.

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“…Fritze, Dittmar & Pfluderer (1968), reported that the pressor response to dopamine in the conscious rabbit was converted to a hypotensive response under urethane anaesthesia. In man, the cardiovascular responses to phenylephrine (Bristow, Prys-Roberts, Fisher, Pickering & Sleight, 1969) and mephentermine (Andersen, Perkins & Gravenstein, 1963) have been shown to be inhibited by certain anaesthetics, including ether and thiopental.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular responses to noradrenaline in the rat before and after administration of various anaesthetics

Brezenoff

1973

British J Pharmacology

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Summary1. Cardiovascular responses to intravenously administered noradrenaline were monitored in the rat in the conscious state and again following anaesthesia. Injections and pressure recordings were made via permanently implanted venous and arterial catheters. 2. The pressor response to noradrenaline was inhibited by diethyl ether, urethane and deep pentobarbitone anaesthesia. It was unchanged by ketamine and was potentiated by chloralose and light pentobarbitone anaesthesia. 3. Reflex bradycardia was potentiated by chloralose, blocked by ketamine and reduced by pentobarbitone. It was either reduced or unchanged by ether or urethane.

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Effects of Anesthesia on Baroreflex Control of Heart Rate in Man

Cited by 107 publications

References 0 publications

Comparison of the ability of nicardipine, theophylline and zaprinast to restore cardiovascular haemodynamics following inhibition of nitric oxide synthesis

Comparison of the ability of nicardipine, theophylline and zaprinast to restore cardiovascular haemodynamics following inhibition of nitric oxide synthesis

Alterations in the Baroreceptor Reflex in Conscious Dogs with Heart Failure

Cardiovascular responses to noradrenaline in the rat before and after administration of various anaesthetics

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