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Optimal Pressure for Low Pressure Controlled Reperfusion to Efficiently Protect Ischemic Heart: An Experimental Study in Rats
Abstract Recent work has demonstrated the benefit of low pressure (LP) reperfusion to protect the heart undergoing an ischemic insult. The goal of the present study was to determine the optimal pressure for the application of LP reperfusion. Isolated rats hearts (n = 30) were exposed to 40 minutes o...
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Published in: | Transplantation proceedings 2009-03, Vol.41 (2), p.703-704 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Abstract Recent work has demonstrated the benefit of low pressure (LP) reperfusion to protect the heart undergoing an ischemic insult. The goal of the present study was to determine the optimal pressure for the application of LP reperfusion. Isolated rats hearts (n = 30) were exposed to 40 minutes of global warm ischemia followed by 70 minutes of reperfusion with a pressure fixed at 100 cm H2 O (normal pressure [NP] = control group), 85 cm (group LP [low pressure]-85), 70 cm (group LP-70), or 55 cm (group LP-55). Cardiac function was assessed during reperfusion using the Langendorff model. Myocardial necrosis was assessed by measuring lactate dehydrogenase (LDH) and creatine kinase (CK) leakage in the coronary effluents. Functional recovery was progressively and significantly improved with decreased perfusion pressure. Rate-pressure product (RPP) averaged 3765 ± 408, 6824 ± 439, and 12,036 ± 664 mm Hg/min, respectively, among the control, LP-85, and LP-70 groups ( P < .001, LP-70 vs other groups). However, RPP collapsed in the LP-55 group. Similarly, necrosis as measured by LDH and CK leakage progressively reduced between LP-100 and LP-70 hearts ( P < .01), with a drastic increase in enzyme in the LP-55 group. In conclusion, this study demonstrated that 70 cm H2 O is an optimal LP to improve postischemic contractile dysfunction and attenuate necrosis during reperfusion. |
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ISSN: | 0041-1345 1873-2623 |
DOI: | 10.1016/j.transproceed.2008.12.005 |