The role of alpha-adrenergic receptors in carbon monoxide hypoxia.
The importance of alpha-adrenergic receptors in the cardiac output and peripheral circulatory responses to carbon monoxide (CO) hypoxia was studied in anesthetized dogs. Phenoxybenzamine (3 mg/kg i.v.) was injected to block alpha-receptor activity and the data obtained were then compared with those from a previous study of CO hypoxia in unblocked animals. Values for cardiac output, hindlimb blood flow, vascular resistance, and oxygen uptake were obtained prior to and at 30 and 60 min of CO hypoxia which reduced arterial oxygen content by approximately 50%. alpha-Adrenergic blockade resulted in a lower (p less than 0.05) control value for cardiac output than observed in unblocked animals, but no differences were present between the two groups at 30 or 60 min of CO hypoxia. Similarly, limb blood flow was lower (p less than 0.05) during the control period in the alpha-blocked group but rose to the same level as that in the unblocked animals at 60 min of COH. No change in limb blood flow occurred during CO hypoxia in the unblocked group. These findings demonstrated that during CO hypoxia alpha-receptor mediated venoconstriction does not contribute to the cardiac output response and alpha-receptor mediated vasoconstriction probably does prevent a rise in hindlimb skeletal muscle blood flow.
D000818:Animals; D001784:Blood Gas Analysis; D001794:Blood Pressure; D002249:Carbon Monoxide Poisoning / Q000503:physiopathology*; D002302:Cardiac Output; D004285:Dogs; D005121:Extremities / Q000098:blood supply; D000860:Hypoxia / Q000503:physiopathology*; D010101:Oxygen Consumption; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D012039:Regional Blood Flow
D011942:Receptors, Adrenergic, alpha