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

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.