Abstract
A marked .beta.-adrenergic [propranolol] dilator interaction with the vasoconstrictor response in cat skeletal muscle during hemorrhage is described. The dilator influence corresponded to some 40% of the constrictor response at mild, moderate and extensive bleeding. In absolute resistance units, the .beta.-adrenergic dilator influence averaged no less than 14 mm Hg/(ml/min 100 g) at extensive bleeding (hemorrhagic hypotension of 50 mm Hg). Comparison of the hemorrhage-induced resistance effects in the autoperfused innervated muscle, in the autoperfused denervated muscle and in the innervated muscle cross-circulated from a donor animal, showed that the .beta.-adrenergic dilator influence more or less completely was caused by blood-borne catecholamines, in all likelihood by adrenaline [epinephrine], which is secreted in large amounts during hemorrhage. The described .beta.-adrenergic dilator mechanism may maintain nutritional blood flow by counteracting the constrictor response. It obviously has to be taken into account for proper evaluation of other vascular control mechanisms brought into action in hemorrhage.