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Journal of Pharmacology And Experimental Therapeutics, Vol. 161, Issue 1, 98-110, 1968
Copyright © 1968 by American Society for Pharmacology and Experimental Therapeutics


PROTECTIVE EFFECTS OF NYLIDRIN AND ISOPROTERENOL AGAINST HEMORRHAGIC SHOCK

George J. Grega 1 and William J. Kinnard 1

1 Department of Pharmacology, University of Pittsburgh School of Pharmacy, Pittsburgh, Pennaylvania

The effects of beta adrenergic stimulants (nylidrin and isoproterenol) on the course of hemorrhagic shock were determined and compared with those of phenoxybenzamine, an alpha adrenergic blocking agent. Anesthetized dogs were subjected to 3 hr of hypovolemia followed by the return of the shed blood. Saline, nylidrin, isoproterenol (continuous infusion) or phenoxybenzamine were administered 1 hr after bleeding 45 to 50 ml/kg of blood from the animal. Nylidrin and isoproterenol afforded significant protection against shock deaths, lessened the degree of metabolic acidosis, prevented blood and plasma volume loss and prevented cardiovascular and gastrointestinal deterioration. Phenoxybenzamine did not prevent shock deaths despite considerable blood volume replacement during the hypovolemic period. The return of these additional quantities of blood did not increase cardiac output or the circulating blood volume; hence it is concluded that phenoxybenzamine induces a significant pooling of blood. Cardiac output, mesenteric and renal blood flows and the circulating blood volume were significantly below prehemorrhage levels in the phenoxybenzamine-treated animals after the return of the shed blood; thus it appears that this agent increases the peripheral vascular capacity at the expense of impairing blood flow. In contrast, nylidrin maintained cardiac output and renal and mesenteric flows in the presence. of hypotension and hypovolemia and following the return of the withdrawn blood while markedly reducing systemic vascular resistance. The beta adrenergic stimulants probably protect against shock deaths by maintaining cardiac output, lowering vascular resistance and causing a more favorable distribution of blood flow without expanding the vascular capacity.

Submitted on September 18, 1967
Accepted on January 9, 1968







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Copyright © 1968 by the American Society for Pharmacology and Experimental Therapeutics.