O₂ Transport and Uptake in Dogs during CO Hypoxia with and without β-Block

Abstract

At levels of carboxyhemoglobin greater than 40% (CO hypoxia), cardiac output increases in anesthetized dogs (Einzig et al., 1980; Sylvester et al., 1979). At the same time, both sympathetic activity (Fitzgerald et al., 1976) and circulating levels of catecholamines are increased (Sylvester et al., 1979). In addition to these facts, Scharf et al. (1975) reported that left ventricular contractile performance, as measured by dp/dt, increase when isolated dog hearts were perfused with blood from donor dogs that had inhaled carbon monoxide. The increased ventricular dp/dt was abolished following β-adrenergic blockade; These findings suggest that β-adrenergic receptor activity is an important component in the cardiac response to CO hypoxia. With respect to the peripheral circulation, Cain and Chapler (1979) showed that β-adrenergic vasodilation contributed to the rise in hindlimb skeletal muscle blood flow which occurred in both anemic and hypoxic hypxia. To identify the role of β-adrenergic receptors during CO hypoxia, we have measured some of the cardiovascular and metabolic responses of the whole body and hindlimb skeletal muscle with and without propranolol to block β-adrenergic receptors.

Research supported by grants from the Medical Research Council of Canada and National Institutes of Health (Grant No. HL-14693).