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• W2049288512 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, α 1 -blocked, α 1 + α 2 -blocked, and β 2 -blocked). Cardiac output increased, but hindlimb blood flow [Formula: see text] and resistance (R L ) remained at prehypoxic levels during COH (O 2 content reduced 50%) in untreated animals. When activity in the sciatic nerve was reversibly cold blocked, [Formula: see text] doubled and R L 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 α 1 -blocked), R L dropped (~50%) during COH, an indication that catecholamines played a significant role in maintaining tone to skeletal muscle. Animals with both α 1 + α 2 -adrenergic blockade (phenoxybenzamine and yohimbine added) did not survive COH. R L was higher in β 2 -block than in the untreated group during COH, but nerve cooling indicated that β 2 -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 R L during COH, but they were not activated by sympathetic nerve stimulation to the limb muscles.Key words: α 1 -adrenoreceptor blockade, α 2 -adrenoreceptor blockade, peripheral vascular resistance, skeletal muscle, blood flow." @default.
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• W2049288512 date "1991-10-01" @default.
• W2049288512 modified "2023-09-23" @default.
• W2049288512 title "Adrenoceptor regulation of canine skeletal muscle blood flow during carbon monoxide hypoxia" @default.
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• W2049288512 doi "https://doi.org/10.1139/y91-209" @default.
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