Adrenoceptor regulation of canine skeletal muscle blood flow during carbon monoxide hypoxia

Abstract

We questioned whether carbon monoxide hypoxia (COH) would affect peripheral blood flow by neural activation of adrenoceptors to the extent we had found in other forms of hypoxia. We studied this problem in hindlimb muscles of four groups of anesthetized dogs (untreated, α1-blocked, α1 + α2-blocked, and β2-blocked). Cardiac output increased, but hindlimb blood flow [Formula: see text] and resistance (RL) remained at prehypoxic levels during COH (O2 content reduced 50%) in untreated animals. When activity in the sciatic nerve was reversibly cold blocked, [Formula: see text] doubled and RL decreased 50%. These changes with nerve block were the same during COH, suggesting that neural activity to hindlimb vasculature was not increased by COH. In animals treated with phenoxybenzamine (primarily α1-blocked), RL dropped (~50%) during COH, an indication that catecholamines played a significant role in maintaining tone to skeletal muscle. Animals with both α1 + α2-adrenergic blockade (phenoxybenzamine and yohimbine added) did not survive COH. RL was higher in β2-block than in the untreated group during COH, but nerve cooling indicated that β2-adrenoceptor vasodilation was accomplished primarily by humoral means. The above findings demonstrated that adrenergic receptors were important in the regulation of [Formula: see text] and RL during COH, but they were not activated by sympathetic nerve stimulation to the limb muscles.Key words: α1-adrenoreceptor blockade, α2-adrenoreceptor blockade, peripheral vascular resistance, skeletal muscle, blood flow.