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.