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Abstract
The involvement of the phospholipid-arachidonic acid pathway and of a pertussis toxin-sensitive G protein in the myocardial depressant effect of volatile anesthetics was examined in the rat heart left papillary muscle and atria. Neither phospholipase A 2, cyclooxygenase or lipoxygenase antagonists altered the potency or the efficacy of clinically used concentrations of halothane and isoflurane in decreasing the contractile force of the muscles. Pretreatment of the rats with pertussis toxin (50 μg/kg i.v., 72 h before sacrifice), which abolished the myocardial depressant effect of muscarinic agonists, did not prevent the decrease in contractile force induced by the anesthetics. The results of this study indicate that the cellular mechanism of the myocardial depressant effect of volatile anesthetics does not involve a metabolite of the phospholipid-arachidonic acid pathway, does not require a functional pertussis toxin-sensitive G protein, and differs from that of muscarinic agonists.
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