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Summary  In the assessment of classical haemorrhagic shock in twenty-two dogs, thirteen of them treated with Nylidrin HC1, ten survived extended episodes of arterial hypotension down to a mean arterial pressure of 40 mm.Hg. Of nine control animals (untreated), five survived the re-infusion period. In the course of our study, Nylidrin HC1 displayed two important pharmacodynamic effects:   1.  It stimulated peripheral tissue arterial inflow, thus assisting metabolic exchange and reducing the peripheral anoxia of circulatory failure which aggravates metabolic acidosis.    2.  It significantly increased cardiac output. Nylidrin HC1 improves myocardial contractility and reduces peripheral arterial resistance. Slight increases in cardiac rate were also noted, along with a moderate decrease in arterial blood pressure. However, neither change proved to be statistically significant. Both groups were compared during and after shock to evaluate contributions to therapy afforded by a Beta stimulatory sympathomimetic. agent.

Nylidrin HCL: A beta-sympathetic stimulant in the management of haemorrhagic shock