Acetate fails to reverse myocardial depression in dogs anesthetized with halothane.
Sodium acetate has been shown to reverse the myocardial depression induced by halothane in vitro. The biochemical basis for this restoration of contractility has been located in the glycolytic pathway. The present study was designed to determine whether this antagonistic property of acetate also occurs in vivo. Dogs autonomically blocked with guanethidine, phenoxybenzamine, and atropine were sequentially anesthetized with halothane in O2 and N2O-O2-succinylcholine in a random pattern. All animals were given sodium acetate IV in amounts adequate to produce pharmacologically active levels. Myocardial performance was measured by LVdP/dtmax, LVPDP/dt/KPmax, and Vmax. Halothane effected a significant depression of these myocardial parameters. Acetate did not reverse this depressant effect of halothane. Acetate, a well-established peripheral vascular vasodilator, did decrease left ventricular and aortic pressures.
D000085:Acetates / Q000097:blood / Q000494:pharmacology*; D000769:Anesthesia, Inhalation; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001774:Blood Chemical Analysis; D001794:Blood Pressure / Q000187:drug effects; D004285:Dogs; D006145:Guanethidine / Q000494:pharmacology; D006221:Halothane / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D006321:Heart / Q000187:drug effects*; D010643:Phenoxybenzamine / Q000494:pharmacology
D000085:Acetates; D010643:Phenoxybenzamine; D001285:Atropine; D006221:Halothane; D006145:Guanethidine