Abstract
Summary
Lactic acidosis was produced in the dog by controlled arterial hemorrhage to a sustained mean arterial pressure of 50 mmHg. A stable metabolic acidosis with increased arterial lactate concentration, increased arterial lactate to pyruvate ratio and increased excess lactate occurred. Intravenous sodium nitroprusside at both low (0.27 μg/kg/min) and high (2.23 μg/kg/min) doses produced regional and systemic vasodilatation but failed to produce a statistically significant or clinically important change in arterial acid-base status or lactate/pyruvate metabolism. It is concluded that stable lactic acidosis can be produced in dogs by graded arterial hemorrhage with sustained hypotension. Vasodilator therapy with sodium nitroprusside is without significant effect on lactic acidosis associated with hypotension in the dog.
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