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Ann Thorac Surg 1994;58:1631-1636
© 1994 The Society of Thoracic Surgeons
Department of Thoracic-Cardiovascular Surgery, Tokyo Medical and Dental University, School of Medicine, Tokyo, Japan
Accepted for publication May 3, 1994.
* Address reprint requests to Dr Sunamori, Department of Thoracic-Cardiovascular Surgery, Tokyo Medical and Dental University, School of Medicine, 1-5-45, Yushima, Bunkyo-ku, Tokyo, 113, Japan.
We studied the effect of pinacidil, a potassium-channel opener, on the hemodynamic, biochemical, and ultra-structural changes in rat hearts undergoing hypothermic cardioplegia. Fifty-four male Wistar rats weighing 250 to 300 g were used. Isolated hearts were prepared for modified Langendorff circulation in the working mode using modified Krebs-Henseleit bicarbonate solution bubbled with a 95% O2 and 5% CO2 gas mixture. Eighty minutes of cardioplegia at 25 °C was followed by normothermic reperfusion for 30 mimutes. Pinacidil, 5, 10, or 50 µmol/L added to the cardioplegic solution, did not affect heart rate, but it significantly improved the recovery of aortic flow as compared with controls (88.1% ± 4.3 [5 µmol/L]; 83.2% ± 8.5% [10 µmol/L]; 90.3% ± 5.3% [50 µmol/L]compared with 55.6 ± 4.3% [control]; p < 0.05). Administration of pinacidil during repertasion did not further enhance the recovery of aortic flow. The doseresponse curve of aortic flow to the pinacidil concentrations was flat from 5 to 50 µmol/L. However, preservation of myocardial adenosine triphosphate and calcium concentrations and mitochondrial morphology suggested that the optimal concentration of pinacidil cardioplegia is 10 µmol/L.
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