The role of beta-adrenergic receptors in the cardiac output response during carbon monoxide hypoxia.

Abstract

Cardiac output increases during carbon monoxide hypoxia (COH) in anesthetized dogs when the level of carboxyhemoglobin exceeds 40% (Einzig et al., 1980; King et al., 1984; King et al., 1985; Sylvester et al., 1979). This compensatory response partially offsets the decrease in whole body oxygen delivery which results from the reduced oxygen content; oxygen uptake is maintained in spontaneously breathing anesthetized dogs at both 50 and 65% carboxyhemoglobin (King et al., 1984). The mechanisms underlying the cardiac output response during COH are not fully understood. It has been shown that nonselective β1 and β2-adrenergic blockade with propranolol resulted in lower values for cardiac output at 30 minutes of COH than in unblocked animals (King et al., 1985; Villeneuve et al., 1985). The effect of propranolol could have resulted from blockade of β1, β2 or a combination of the β1 and β2-adrenergic receptor sub-types. In the present study, the effects of the selective β2 blocker ICI 118,551 on cardiac output and whole body oxygen uptake responses were observed during severe COH (62% decrease in arterial oxygen concentration) in anesthetized, spontaneously breathing dogs. The data were compared to our earlier results obtained during COH in dogs treated with propranolol.KeywordsCardiac OutputUntreated GroupTotal Peripheral ResistanceBody OxygenArterial Oxygen ContentThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.