Taurine-mediated cardioprotection is greater when administered upon reperfusion than prior to ischemia

Taurine (TA) administered exogenously before the induction of myocardial ischemia decreases lactic acid production and increases pyruvic acid production during ischemia. It also preserves the activity of GOT, GPT, LDH and CPK during ischemia and enhances recovery of CKMB synthesis as early as 5 minutes after onset of reperfusion. The aim of the study was to determine the optimal conditions for administering TA in order to reduce myocardial ischemia-reperfusion injury. Left ventricular (LV) function, creatine kinase (CK) and lipid peroxide products (LPOP = oxidant stress), as well as the area at risk (AAR), and infarct size (IS) after reperfusion were studied in 3 groups of isolated rat hearts perfused with Krebs Henseleit Buffer (KHB)-stabilized isolated rat hearts that were subjected to 20 minutes(') of global ischemia at 37 degrees C followed by 60' of reperfusion with KHB: Hearts were perfused with TA containing KHB for 10' just prior to ischemia or during the first 10' of reperfusion.

Taurine before ischemia or during reperfusion was equally effective in preventing infarction; however, when administered at reperfusion, taurine reduced lipid peroxidation and myocardial injury more, thereby providing improved early recovery of function.