Inhibition of Na+–H+ exchange before resuscitation following hemorrhagic shock is cardioprotective in rats

Background: stimulation of the na+–h+ exchanger during resuscitation following hemorrhagic shock results in myocardial injury and dysfunction. inhibition of the na+–h+ exchanger appears to be a new pharmacological tool for myocardial protection following ischemia– reperfusion. our lab showed that inhibition of the na+–h+ exchanger, using amiloride and dimethyl amiloride, before ex vivo resuscitation of isolated perfused hearts protected the myocardium and improved the post-resuscitation myocardial function. the purpose of the present study was to examine the myocardial protective effects of treating the hemorrhagic shocked rats by intra-arterial injection of 20 lmdimethyl amiloride (dma), a specific na+–h+ exchanger blocker, before in vivo resuscitation. methods: sprague–dawley rats were assigned to hemorrhagic treated or untreated groups (n= 4 per group). after 60 min of hemorrhagic shock, rats were treated or not by injection of 20 lm 5- (n,n-dimethyl)-amiloride (dma) intra-arterially. rats were then resuscitated in vivo and monitored for 30 min. then hearts were harvested and perfused in the langendorff system for 60 min for measurements of hemodynamic function. results: administration of dma before in vivo resuscitation following 60 min of hemorrhagic shock and 30 min of in vivo resuscitation, 20 lm dma intra-arterially significantly improved post-resuscitation myocardial function.conclusion: our results suggest that dma protects the heart against post-resuscitation myocardialinjury.