Hemodynamics and arterial catecholamines during hypoxic hypoxia (HH) and carbon monoxide hypoxia (COH)

J. Sylvester, S. Scharf, R. Gilbert, R. Fitzgerald

Research output: Contribution to journalArticle

Abstract

Anesthetized paralyzed dogs with constant ventilation were subjected to severe HH and COH (ΔCaO2 = -10 vol%) before and after bilateral carotid body resection (CBR). Before CBR, HH caused increases in cardiac output (ΔQ = +86% of control) and mean arterial pressure (ΔPa = +23%) and a decrease in total peripheral resistance (ΔTPR = -33%), whereas COH caused a smaller increase in Q (+50%), a decrease in Pa (-21%) and a greater decrease in TPR (-48%). Arterial catecholamine concentration ([CA]a) increased equally with both types of hypoxia (Δ[CA]a = +0.8 ng/ml). After CBR, the hemodynamic responses to HH and COH were the same and were characterized by an increase in Q (+47%) and decreases in Pa (-28%) and TPR (-54%). These changes were not different from those seen during COH before CBR. Again, the observed increases in [CA]a were equal, but were 2.5 times greater than before CBR (Δ[CA]a = +2.0 ng/ml). It is concluded that during HH and COH before CBR the differences in hemodynamic response were due to stimulation of carotid chemoreceptors by the reduction in arterial PO2 that occurred during HH but not COH; the carotid chemo and baroreceptor complex inhibited production and/or enhanced elimination of catecholamines; and arterial catecholamines either had little to do with the differences in hemodynamic response or contributed to them via alteration of the epinephrine:norepinephrine concentration ratio.

Original languageEnglish (US)
Pages (from-to)No. 1128
JournalFederation Proceedings
Volume34
Issue number3
StatePublished - Jan 1 1975

ASJC Scopus subject areas

  • Medicine(all)

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