Effects of nicardipine, a calcium antagonist, on myocardial salvage and high energy phosphate stores in reperfused myocardial injury

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The current study determined the effectiveness of nicardipine, a 1,4-dihydropyridine calcium antagonist, in preserving reperfused myocardium in a cat model of temporary coronary occlusion and ascertained if replenishment of myocardial phosphate stores during reperfusion as defined by phosphorus-31 nuclear magnetic resonance (NMR) spectroscopy was indicative of salvage.Twenty open chest, anesthetized cats were studied with use of a snare ligature around the proximal left anterior descending coronary artery, with a coil sutured to the epicardial surface overlying the distribution of the artery. Peak areas of phosphocreatine, inorganic phosphate and adenosine triphosphate (ATP) NMR signals were measured during 1 h of occlusion followed by 1.S h of reperfusion. Infarct size and jeopardy area were determined in vitro by simultaneous infusion of phthalocyanine Mue dye and triphenyltetrazolium chloride into the aorta and the left anterior descending corcnary artery, respectively, after 5 h of myocardial reperfusion.Nicardipine-treated and control groups had similar jeopardy area values (41.2 ± 1.6% versus 47.4 ± 3.1% of the left ventricle), but infant area was significantly reduced in the nkardipine-treated group (3.2 ± 1.1% versus 24.9 ± 7.5% of jeopardy area, p < 0.01). High energy phosphate compounds remained markedly altered during reperfusion in both groups. No significant improvement in phosphocreatine or inorganic phosphate recovery was observed in animals pretreated with nicrardipine despite an 87% reduction in infant size. Myocardial ATP was greater during reperfusion in the nicardipine-treated compared with the control group (average over initial 90 min of reperfusion 58 ± 6% versus 46 ± 3% of baseline values, p < 0.05), suggesting improved recovery of ATP. However, the measured levels of high energy phosphate compounds during reperfusion and their ratios did not correlate with infarct size and thus were not predictive of myocardial salvage.