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- W2056554737 abstract "This study was designed to investigate whether a cardioprotective intervention could delay the completion of necrosis so that subsequent reperfusion would be more useful. Thirty-six pigs were randomly allocated to treatment with diltiazem (15 μ g/kg per min) or saline solution and to a 60 or 120 minute coronary occlusion period followed by reperfusion. The treatment was begun 15 minutes before coronary occlusion and terminated 75 minutes after reperfusion. Twenty-four hours after the procedure, the heart was sliced and incubated in triphenyltetrazolium chloride. The infarct area and the maximal transmural area of extension of the infarct were calculated by planimetry. The total number of red blood cells in a transmural section was also counted. In the pigs with a 60 minute coronary occlusion, diltiazem (compared with saline solution) significantly reduced infarct size from 9.7 ± 1.5% of left ventricular mass to 5.9 ± 0.6% (p < 0.05) and the percent transmural extension from 0.72 ± 0.05 to 0.61 ± 0.05% (p < 0.05). Red blood cell extravasation in the infarcted area was reduced from 161,934 ± 59,905 to 78,525 ± 46,484 cells/mm3 (p < 0.05) with diltiazem and the percent transmural extension of the hemorrhagic necrosis from 70 ± 10 to 36 ± 15% (p < 0.05). No such differences were observed in the 120 minute coronary occlusion groups. Mean red blood cell counts and the extent of hemorrhagic necrosis did not correlate with either infarct size or transmural extension. These results document increased myocardial salvage by diltiazem when reperfusion is performed 1 hour but not 2 hours after occlusion and suggest a transient and time-related protective effect of diltiazem against ischemic damage in myocytes and the vessel wall." @default.
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- W2056554737 date "1987-10-01" @default.
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- W2056554737 title "Diltiazem and progression of myocardial ischemic damage during coronary artery occlusion and reperfusion in porcine hearts" @default.
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- W2056554737 doi "https://doi.org/10.1016/s0735-1097(87)80287-5" @default.
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