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J Thorac Cardiovasc Surg 1995;110:523-531
© 1995 Mosby, Inc.

CARDIAC AND PULMONARY REPLACEMENT

IMPROVED HYPOTHERMIC PRESERVATION OF RAT HEARTS BY FUROSEMIDE

Tel Aviv, Israel

Supported by the Israeli Ministry of Health and the Emerico Letay Foundation.

Received for publication April 8, 1994. Accepted for publication Dec. 8, 1994. Address for reprints: Professor G. Navon, School of Chemistry, Tel Aviv University, Tel Aviv 69978, Israel.

Abstract

The effect of furosemide, a blocker of the Na⁺/K⁺/Cl^-cotransporter, on hypothermic preservation of rat hearts was studied with use of the Langendorff perfusion system and electron microscopy. Furosemide significantly improved the mechanical recovery and the coronary flow of the hearts preserved for 8 hours in St. Thomas' Hospital cardioplegic solution at a temperature of 4 ° C. Furosemide at the concentration of 100µmol/L was found to have an optimal effect, whereas at high concentrations (1000µmol/L) it was found to have toxic effects. In addition, furosemide reduces the time elapsed between the end of the preservation time and the resumption of myocardial contractions. Ultrastructural evaluations were done in which the presence of swollen mitochondria was chosen as a criterion of hypothermic ischemic damage to the myocardium. Morphometric analysis indicated that the mitochondrial volume of hearts stored for 8 hours in St. Thomas' Hospital cardioplegic solution increased by 72% as compared with the mitochondrial volume of hearts that were not exposed to the hypothermic ischemic conditions (control group). The addition of 100µmol/L furosemide to the cardioplegic solution resulted in a significant reduction of mitochondrial swelling during the period of 8 hours' storage, which amounted only to 28% as compared with the figure for the control group. The reduction of mitochondrial swelling by furosemide and the improved mechanical and coronary flow recoveries are thought to be related to the blocking of the sarcolemmal Na⁺/K⁺/Cl^-cotransporter and consequently the reduction of the Na⁺influx during hypothermic ischemic storage.(J THORACCARDIOVASCSURG1995;110:523-31)

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