IMPROVED HYPOTHERMIC PRESERVATION OF RAT HEARTS BY FUROSEMIDE

Citation
Y. Rubin et al., IMPROVED HYPOTHERMIC PRESERVATION OF RAT HEARTS BY FUROSEMIDE, Journal of thoracic and cardiovascular surgery, 110(2), 1995, pp. 523-531
Citations number
20
Categorie Soggetti
Respiratory System","Cardiac & Cardiovascular System",Surgery
ISSN journal
00225223
Volume
110
Issue
2
Year of publication
1995
Pages
523 - 531
Database
ISI
SICI code
0022-5223(1995)110:2<523:IHPORH>2.0.ZU;2-P
Abstract
The effect of furosemide, a blocker of the Na+/K+/Cl- cotransporter, o n hypothermic preservation of rat hearts was studied with use of the L angendorff perfusion system and electron microscopy, Furosemide signif icantly improved the mechanical recovery and the coronary flow of the hearts preserved for 8 hours in St, Thomas' Hospital cardioplegic solu tion at a temperature of 4 degrees C, Furosemide at the concentration of 100 mu mol/L was found to have an optimal effect, whereas at high c oncentrations (1000 mu mol/L) it was found to have toxic effects, In a ddition, furosemide reduces the time elapsed between the end of the pr eservation time and the resumption of myocardial contractions, Ultrast ructural evaluations were done in which the presence of swollen mitoch ondria was chosen as a criterion of hypothermic ischemic damage to the myocardium, Morphometric analysis indicated that the mitochondrial vo lume of hearts stored for 8 hours in St, Thomas' Hospital cardioplegic solution increased by 72% as compared with the mitochondrial volume o f hearts that were not exposed to the hypothermic ischemic conditions (control group), The addition of 100 mu mol/L furosemide to the cardio plegic solution resulted in a significant reduction of mitochondrial s welling during the period of 8 hours' storage, which amounted only to 28% as compared with the figure for the control group, The reduction o f 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 reducti on of the Na+ influx during hypothermic ischemic storage.