AJP - Heart and Circulatory Physiology, Vol 243, Issue 6 1010-H1017, Copyright © 1982 by American Physiological Society
Hindlimb resistance in hypoxic dogs after adrenergic blockade or denervation
S. M. Cain and C. K. Chapler
Blood flow (Q) and O2 uptake (Vo2) were measured in the intact autoperfused
left hindlimb (less paw) of anesthetized paralyzed dogs ventilated at
constant rate with either room air (normoxia) or 9.1% O2 in N2 (hypoxia)
for 20-min periods. One group of 10 dogs was given 3.0 mg/kg
phenoxybenzamine (alpha-block) and was subjected to the sequence of
normoxia, hypoxia, normoxia. The sequence was repeated after 1.0 mg/kg
propranolol (beta-block). A second group of 10 was treated the same but was
not given adrenergic blockers (no block). A third group of 10 was made
hypoxic only once after the sciatic and femoral nerves to the prepared limb
were severed (denervated). Decreased O2 availability during hypoxia limited
both total and limb V02 in all cases. Limb Q did not change, but vascular
resistance increased in the no-block group with onset of hypoxia and a
brisk transient hyperemia occurred with reoxygenation. After both alpha-
and beta-block no change occurred in limb resistance with reoxygenation. A
similar result was obtained in the denervated limb. These results indicated
that the transient hyperemia following hypoxia was the result of altered
states of neurally mediated vascular tone, mostly sympathetic, and was not
due to local metabolic vasodilation or altered blood levels of
catecholamines during a 20-min period of hypoxia.
