Protective effect of pretreatment with the @entity460 antagonist @entity50233 on the ischemic-reperfused XXXX myocardium: a @entity9715 nuclear magnetic resonance study.

@entity50233 @entity1734 @entity63 @entity9715 @entity1391 @entity460 @entity35 @entity855
To assess whether the prophylactic administration of @entity50233 , a new @entity460 antagonist, protects the heart against the effects of @entity63 and reperfusion, @entity35 were injected intraperitoneally twice daily for 5 days with 5 mg/kg body weight of this drug. The heart was then isolated and perfused by the Langendorff technique. @entity9715 nuclear magnetic resonance spectroscopy was used to monitor myocardial energy metabolism and intracellular pH during control perfusion and 30 min of total @entity63 (37 degrees C), followed by 30 min of reperfusion. Pretreatment with @entity50233 altered neither left ventricular developed pressure under normoxic conditions nor the rate and extent of depletion of @entity855 ( @entity855 ) and @entity1734 during @entity63 . Intracellular acidification, however, was attenuated. On reperfusion, hearts from @entity50233 -pretreated animals recovered significantly better than untreated hearts with respect to replenishment of @entity855 and @entity1734 stores, restitution of low levels of intracellular inorganic @entity1391 and recovery of left ventricular function and coronary flow. Intracellular pH recovered rapidly to preischemic levels, whereas in untreated hearts a complex intracellular inorganic @entity1391 peak indicated the existence of areas of different pH within the myocardium. It is concluded that @entity50233 pretreatment protects the heart against some of the deleterious effects of @entity63 and reperfusion. Because this protection occurred in the absence of a negative inotropic effect during normoxia, it cannot be attributed to an energy-sparing effect during @entity63 . Therefore, alternative mechanisms of action are to be considered.
