Effect of Calcium Channel Blocking Agents on Infarct Size After Ischaemia-Reperfusion in Anaesthetised Pigs

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Abstract
Summary: We compared the abilities of verapamil and nicardipine to protect the porcine myocardium from the consequences of ischaemia-reperfusion in vivo. Infusion of verapamil (50 μg/kg) into the left anterior descending coronary artery LAD (i.c.a.), in 15 min immediately be-fore ligation depressed regional contractile function, reduced infarct size by 80% and enabled contractile function to recover partially during reperfusion. Verapamil (10 μg/kg i.c.a.) did not depress contractile function be-fore ligation or permit its recovery during reperfusion, despite reducing infarct size by 80%. Lower doses of verapamil were not cardioprotective. Nicardipine (It) and 30 μg/kg i.c.a.) depressed contractile function before ligation but did not permit its recovery during reperfusion. Nicardipine did not reduce infarct size development. Thus, drug-induced negative inotropic activity (which presumably reflects myocardial calcium channel blockade) and cardioprotection are not linked. Verapamil can markedly reduce infarct size development at a dose that exerts no detectable negative inotropic activity. This cardioprotective effect of verapamil was greatly reduced by intravenous (i.v.) pretreatment with aspirin (30 mg/kg). which alone did not alter infarct size development. Thus, the cardioprotective effect of verapamil (10 μg/kg i.c.a.) appears to be mediated by a cyclooxygenase product, possibly prostacyclin.

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