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Ann Thorac Surg 2001;72:107-112
© 2001 The Society of Thoracic Surgeons
Accepted for publication January 26, 2001.
Address reprint requests to Dr Menasché, Service de Chirurgie Cardiovasculaire B, Hôpital Bichat Claude Bernard, 46, rue Henri-Huchard, 75018 Paris, France
e-mail: ccv-bloc.sec3{at}bch.ap-hop-paris.fr
Background. Cardiac harvest teams are usually committed to immediately transfer the explanted donor heart into its cold storage solution. We tested the opposite hypothesis that a brief prestorage episode of heat-enhanced ischemic preconditioning could be protective.
Methods. Fifty-three isolated isovolumic rat hearts underwent 4 hours of cold (4°C) storage in the Celsior preservation solution and 2 hours of reperfusion. Control hearts were immediately immersed after arrest. In the 3 treated groups, 2 customized thermal probes were first applied onto the left ventricular free wall of the explanted heart at 22°C, 37°C or 42.5°C for 15 minutes before immersion. Each of the selected temperatures were monitored at the probe-tissue interface by a thermocouple.
Results. Whereas base line end-diastolic pressure was set at 
8 mm Hg in all groups, it increased during reperfusion (mean ± SEM) to 28 ± 3, 27 ± 3, 17 ± 1, and 18 ± 2 mm Hg in control, 22°C, 37°C and 42.5°C-heated hearts, respectively (37°C and 42.5°C: p < 0.05 versus controls and 22°C). Slopes of pressure-volume curves featured similar patterns. Likewise, reperfusion dP/dT (mm Hg/s-1) was significantly lower in control and 22°C hearts (1,119 ± 114 and 1,076 ± 125, respectively) than in those undergoing prestorage heating to 37°C and 42.5°C (1,545 ± 109 and 1,719 ± 111, p < 0.05 and p < 0.01 versus controls and 22°C, respectively). Western blot analysis of LV samples did not demonstrate any upregulation of HSP 72 in either group. Conversely, the involvement of preconditioning was evidenced by the loss of protection in the 42.5°C-heated hearts when, in 2 additional groups, the storage solution was supplemented with either the protein kinase C and tyrosine kinase inhibitors chelerythrine (5 µmol/L) and genistein (50 µmol/L) or the mitochondrial KATP channel inhibitor 5-hydroxydecanoate (200 µmol/L).
Conclusions. A brief period of postexplant ischemia with enhancement by topical heating ("backtable preconditioning") could be a simple and effective means of improving the functional recovery of heart transplants.
This article has been cited by other articles:
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  D. Ramzy, V. Rao, and R. D. Weisel Clinical applicability of preconditioning and postconditioning: The cardiothoracic surgeons's view Cardiovasc Res, May 1, 2006; 70(2): 174 - 180. [Full Text] [PDF]
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N. C Chi and J. S Karliner Molecular determinants of responses to myocardial ischemia/reperfusion injury: focus on hypoxia-inducible and heat shock factors Cardiovasc Res, February 15, 2004; 61(3): 437 - 447. [Abstract] [Full Text] [PDF]
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R. A Kloner, M. T Speakman, and K. Przyklenk Ischemic preconditioning: a plea for rationally targeted clinical trials Cardiovasc Res, August 15, 2002; 55(3): 526 - 533. [Full Text] [PDF]
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