Hypoxic and CO hypoxia in dogs: hemodynamics, carotid reflexes, and catecholamines

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Abstract
The effects of severe hypoxic hypoxia (HH) and carbon monoxide hypoxia (COH) of 15-20 min duration were compared in 2 groups of anesthetized, paralyzed dogs receiving constant ventilation. In the 1st group, cardiac output (.ovrhdot.Q) and stroke volume (SV) increased during both HH and COH. Heart rate (HR) changed variably. The ratio of stroke work (SW) to mean left atrial pressure (.hivin.PLA) was not significantly altered. Mean arterial pressure (.hivin.Pa) increased during HH and decreased during COH. Total peripheral resistance (TPR = .hivin.Pa/.ovrhdot.Q) fell during both types of hypoxia, but the fall during COH was significantly greater than that during HH. After carotid body resection (CBR), the circulatory effects of HH and COH were the same and were characterized by decreases in .hivin.Pa and TPR and increases in .ovrhdot.Q and SV; HR and SW/.hivin.PLA did not change. In the 2nd group, HH and COH caused equal increases in arterial total catecholamine concentration before CBR. After carotid body resection, HH and COH again increased catecholamines equally, but the magnitude of the increase was double that observed before CBR. The circulatory effects of HH and COH were different in the anesthetized, paralyzed dog. These differences depended on the presence of the carotid chemo- and baroreflexes and upon differences in arterial O2 tension, but not on differences in total catecholamine concentration or ventilatory response.

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