The Cardiovascular Effects of Nitrous Oxide-Halothane Anesthesia in Man

Bahlman, Steven H.; Eger, E. I.; Smith, N. Ty; Stevens, Wendell C.; Shakespeare, Thomas F.; Sawyer, Donald C.; Halsey, Michael J.; Cromwell, Thomas H.

doi:10.1097/00000542-197109000-00010

Cited by 45 publications

(19 citation statements)

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“…[1][2][3][4][5][6][7] Briefly, studies were made on healthy volunteers between 21 and 30 years of age. Blood and voided urine specimens were obtained immediately prior to anaesthesia.…”

Section: Methodsmentioning

confidence: 99%

Comparative toxicity of isoflurane, halothane, fluroxene and diethyl ether in human volunteers

Stevens

Eger

Joas

et al. 1973

Canad. Anaesth. Soc. J.

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“…[1][2][3][4][5][6][7] Briefly, studies were made on healthy volunteers between 21 and 30 years of age. Blood and voided urine specimens were obtained immediately prior to anaesthesia.…”

Section: Methodsmentioning

confidence: 99%

Comparative toxicity of isoflurane, halothane, fluroxene and diethyl ether in human volunteers

Stevens

Eger

Joas

et al. 1973

Canad. Anaesth. Soc. J.

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“…In the present investigation one might expect cardiac output to be reduced by the combination of halothane and controlled ventilation, especially as normocapnia was maintained. The divergent results could be explained by the sympathomimetic effects of nitrous oxide [4,20]. Although there was a significant reduction in MAP, systemic vascular resistance did not change during anaesthesia.…”

Section: Discussionmentioning

confidence: 96%

“…Bahlman et al [4] have shown that nitrous oxide plus halothane produce less depression on myocardial function, cardiac output and mean arterial pressure in man, than does halothane alone at the same minimum alveolar concentration (MAC).…”

Section: Discussionmentioning

confidence: 99%

Central haemodynamics and regional blood flow during halothane-nitrous oxide anaesthesia and controlled ventilation

et al. 1983

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The haemodynamic effects of halothane-N2O/O2 anaesthesia with controlled ventilation were studied in rats, using the microsphere method. Mean arterial blood pressure was significantly reduced but only minor effects on cardiac output (CO), heart rate, and systemic vascular resistance were seen. During anaesthesia, there were significantly increased fractions of CO delivered to brain, lungs, small intestine and liver (hepatic artery), while the fractions to spleen, stomach and carcass were decreased. Fractional distribution and regional blood flow to heart, kidneys, adrenals and preportal area remained unchanged. When anaesthesia was prolonged from 60 to 90 min, no further changes in central or regional haemodynamics were seen. Considering the minor effects on central haemodynamics and the absence of changes in central and regional haemodynamics at 60 and 90 min, this anaesthesia model should be useful in experimental research.

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“…Because halothane is known to produce changes in the circulatory system, 14 the question arises as to whether the 5-hour recovery time alloted was adequate for complete recovery from the effects of this anesthetic agent. Previous studies from this laboratory 9 have shown that rabbits anesthetized with halothane plus nitrous oxide to surgical levels had decreases in arterial pressure and cardiac output, with elevated values for PR A.…”

Section: Discussionmentioning

confidence: 99%

Pressor responses to norepinephrine during captopril in renal prehypertensive rabbits.

Koivunen¹,

Johnson²,

Nichols³

et al. 1983

Hypertension

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SUMMARY The role of angiotensin II (All) in pressor hyperresponsiveness was examined in conscious one-kidney, one clip rabbits with renal artery stenosis 01 3-days' duration (renal prehypertensive rabbits). Conscious one-kidney rabbits without renal artery stenosis served as controls. Two experiments were performed. The first experiment used four groups of six rabbits each, to examine the pressor responses to intravenous (i.v.) infusions of norepinephrine (NE) at several doses, ranging from 25 to 1200 ng/min/kg body weight, in 3-day renal artery stenosis and in 3-day control rabbits, receiving NE plus the angiotensin-converting enzyme inhibitor, captoprii (SQ 14,225), or receiving NE alone. The arterial pressure and values for plasma renin activity (PRA) were the same in the renal artery stenosis rabbits as in the controls. The exaggerated pressor responses to NE in the renal artery stenosis rabbits were restored to normal by captoprii administration.The second experiment investigated the pressor responses to i.v. infusions of NE at 800 ng/min/kg in six rabbits with renal artery stenosis and in six control rabbits before captoprii, during captoprii administration, and during the administration of captoprii plus the i.v. infusion of AH at 0.5,1.0, and 2.0 ng/min/kg body weight. Plasma concentrations of All were determined at each point in this experiment. The renal artery stenosis rabbits had the same values for arterial pressure and PRA as the control rabbits. The renal artery stenosis rabbits had increased pressor responses to NE, and this pressor hyperresponsiveness was abolished by captoprii. The i.v. infusion of All during captoprii treatment in the renal artery stenosis rabbits increased the pressor responses to NE, and All infusion at 2.0 ng/min/kg completely restored the pressor hyperresponsiveness in these rabbits. The control rabbits had no changes in the pressor responses to NE with captoprii or with captoprii plus any of the AH doses. Before captoprii, the control and renal artery stenosis rabbits had the same plasma concentrations of AH. With captoprii, plasma concentrations of All in the renal artery stenosis rabbits decreased to undetectably low levels and remained so during the infusions of AH at all doses. This study provided strong evidence that plasma All plays an important role in the enhanced pressor responses to NE in 3-day renal artery stenosis rabbits, and that this effect is not due to elevated plasma levels of AH.

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The Cardiovascular Effects of Nitrous Oxide-Halothane Anesthesia in Man

Cited by 45 publications

References 0 publications

Comparative toxicity of isoflurane, halothane, fluroxene and diethyl ether in human volunteers

Comparative toxicity of isoflurane, halothane, fluroxene and diethyl ether in human volunteers

Central haemodynamics and regional blood flow during halothane-nitrous oxide anaesthesia and controlled ventilation

Pressor responses to norepinephrine during captopril in renal prehypertensive rabbits.

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