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Beta-adrenergic dilator interaction with the constrictor response in resistance vessels of skeletal muscle during
A marked beta-adrenergic dilator interaction with the vasoconstrictor response in skeletal muscle during hemorrhage is described. The dilator influence corresponded to some 40% of the constrictor response both at mild and moderate as well as at large bleeding. In absolute resistance units, the beta-adrenergic dilator influence averaged no less than 14 mmHg/ml X min-1 X 100 g-1) at large bleeding (hemorrhagic hypotension of 50 mmHg). 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, which is known to be secreted in large amounts during hemorrhage. The described beta-adrenergic dilator mechanism may serve to maintain nutritional blood flow by counteracting the constrictor response. It deserves consideration also from the point of view that it obviously has to be taken into account for proper evaluation of other vascular control mechanisms brought into action in hemorrhage.
A marked beta-adrenergic dilator interaction with the vasoconstrictor response in skeletal muscle during hemorrhage is described. The dilator influence corresponded to some 40% of the constrictor response both at mild and moderate as well as at large bleeding. In absolute resistance units, the beta-adrenergic dilator influence averaged no less than 14 mmHg/ml X min-1 X 100 g-1) at large bleeding (hemorrhagic hypotension of 50 mmHg). 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, which is known to be secreted in large amounts during hemorrhage. The described beta-adrenergic dilator mechanism may serve to maintain nutritional blood flow by counteracting the constrictor response. It deserves consideration also from the point of view that it obviously has to be taken into account for proper evaluation of other vascular control mechanisms brought into action in hemorrhage.
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