Abstract

To compare with earlier studies of anemic hypoxia obtained by hemodilution, O2 carring capacity was decreased by carbon monoxide (CO) hypoxia. Arterial O2 content was reduced either 50% (moderate CO) or 65% (severe CO). In two groups of anesthetized dogs (moderate and severe CO) hindlimb innervation remained intact while in a third group (moderate CO) the hindlimb was denervated. Measurements were obtained prior to and at 30 and 60 min of CO hypoxia. Cardiac output was elevated at 30 min of CO hypoxia in all groups (p less than 0.01) and in the severe CO group at 60 min (p less than 0.01). Hindlimb blood flow remained unchanged during CO hypoxia in the intact groups. In the denervated group, hindlimb blood flow was greater (p less than 0.05) than that in the intact groups throughout the experiment. A decrease in mean arterial pressure (p less than 0.01) in all groups was associated with a fall in total resistance (p less than 0.01). Hindlimb resistance remained unchanged during moderate CO hypoxia in the intact group but increased (p less than 0.05) in the denervated group. In the severe CO group hindlimb resistance was decreased (p less than 0.05) at 60 min. The results indicate that the increase in cardiac output during CO hypoxia was directed to nonmuscle areas of the body and that intact sympathetic innervation was required to achieve this redistribution.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call