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  • Title: Mechanism for the cardioprotective effects of the calcium channel blocker clentiazem during ischemia and reperfusion.
    Author: Kusuoka H, Corretti MC, Koretsune Y, Marban E.
    Journal: Jpn Circ J; 1998 Aug; 62(8):611-6. PubMed ID: 9741740.
    Abstract:
    To elucidate whether or not Ca channel blockers have an intrinsic benefit that cannot be attributed to the reduction of Ca2+ entry by pretreatment, time-averaged intracellular Ca2+ concentration ([Ca2+]i) and energy-related phosphates were measured in isolated ferret hearts using nuclear magnetic resonance. In the drug-free ischemic group, [Ca2+]i increased significantly during 30 min of global ischemia at 30 degrees C and during 0-5 min of reperfusion. After 30 min of reperfusion, isovolumic left ventricular developed pressure recovered only to 63+/-7% of the pre-ischemic level (mean+/-SEM; N=5). Pretreatment with the Ca channel blocker clentiazem (10(-7) mol/L) itself depressed developed pressure by 53+/-9%. In the clentiazem group, [Ca2+]i showed no significant changes during ischemia or reperfusion. Recovery of developed pressure (87+/-8% of untreated level) was significantly higher than in the non-treated group (p<0.05). Nevertheless, when the negative inotropism of clentiazem was offset by increasing [Ca]o from 2 to 3 mmol/L, no beneficial effects of clentiazem were observed; [Ca2+]i increased significantly during 0-5 min of reperfusion, and developed pressure recovered only 60+/-7% of untreated level. These results indicate that reduction of Ca2+ entry from the extracellular space to the myocyte, as reflected by negative inotropism during pretreatment, is required for clentiazem to protect myocardium in a model of global ischemia and reperfusion.
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