Abstract
It was shown that perfusion of the isolated heart of rat with solution containing the CB1- and CB2-receptor agonist HU-210 at concentrations of 0.1 or 1.0 μM/L for a duration of 10 min at 20 min before global ischemia (45 min) and reperfusion (30 min) promotes a twofold decrease in creatine kinase levels in coronary effluent. It was established that K ATP channel blockade by glibenclamide (1 μM/L) or inhibition of protein kinase C (2 μM/L) by chelerythrine abolishes the cardioprotective effect of HU-210. The inhibitor of NO synthase L-NAME (1 μM/L) had no effect on the anti-necrotic effect of HU-210. Thus, the intracellular signaling mechanism of the cardioprotective effect of the CB-agonist HU-210 involves the activation of K ATP channels and protein kinase C without the participation of NO-synthase.
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