TY - JOUR
T1 - Optimal Time Duration for Low-Pressure Controlled Reperfusion to Efficiently Protect Ischemic Rat Heart
AU - Bopassa, J. C.
AU - Nemlin, C.
AU - Sebbag, L.
AU - Rodriguez, C.
AU - Ovize, M.
AU - Ferrera, R.
N1 - Funding Information:
This work was supported by the Agence de la Biomédecine, France.
Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2007/10
Y1 - 2007/10
N2 - Previous studies have shown the capacity of low-pressure (LP) reperfusion to protect the ischemic heart. The present study sought to determine the optimal time for the application of LP reperfusion. Isolated rat hearts (n = 30) were exposed to 40 minutes of global warm ischemia followed by 70 minutes of reperfusion. Reperfusion was performed under LP (LP = 70 cm H2O) for 0 (control group), 5 (group LP-5), 10 (group LP-10), 30 (group LP-30), or 60 (group LP-60) minutes. Following the LP period the hearts were reperfused with normal pressure (100 cm H2O) until the end of reperfusion. Cardiac function was assessed during reperfusion using the Langendorff model. Myocardial necrosis was assessed by measuring LDH leakage in the coronary effluents. Functional recovery was reduced among the control and LP-5 groups with rate-pressure products (RPP) averaging 3788 ± 499 and 5333 ± 892 mm Hg/min, respectively. RPP was significantly improved in other groups with RPP averaging 7363 ± 1159, 7441 ± 863, and 7269 ± 692 mm Hg/min in LP-10, LP-30, and LP-60 (P < .01). Similarly, necrosis measured by LDH leakage was significantly reduced in LP-10, LP-30, and LP-60 hearts (P < .01). This study demonstrated that LP reperfusion improves postischemic contractile dysfunction and attenuates necrosis when applied for at least 10 minutes.
AB - Previous studies have shown the capacity of low-pressure (LP) reperfusion to protect the ischemic heart. The present study sought to determine the optimal time for the application of LP reperfusion. Isolated rat hearts (n = 30) were exposed to 40 minutes of global warm ischemia followed by 70 minutes of reperfusion. Reperfusion was performed under LP (LP = 70 cm H2O) for 0 (control group), 5 (group LP-5), 10 (group LP-10), 30 (group LP-30), or 60 (group LP-60) minutes. Following the LP period the hearts were reperfused with normal pressure (100 cm H2O) until the end of reperfusion. Cardiac function was assessed during reperfusion using the Langendorff model. Myocardial necrosis was assessed by measuring LDH leakage in the coronary effluents. Functional recovery was reduced among the control and LP-5 groups with rate-pressure products (RPP) averaging 3788 ± 499 and 5333 ± 892 mm Hg/min, respectively. RPP was significantly improved in other groups with RPP averaging 7363 ± 1159, 7441 ± 863, and 7269 ± 692 mm Hg/min in LP-10, LP-30, and LP-60 (P < .01). Similarly, necrosis measured by LDH leakage was significantly reduced in LP-10, LP-30, and LP-60 hearts (P < .01). This study demonstrated that LP reperfusion improves postischemic contractile dysfunction and attenuates necrosis when applied for at least 10 minutes.
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U2 - 10.1016/j.transproceed.2007.08.024
DO - 10.1016/j.transproceed.2007.08.024
M3 - Article
C2 - 17954191
AN - SCOPUS:35348829783
SN - 0041-1345
VL - 39
SP - 2615
EP - 2616
JO - Transplantation Proceedings
JF - Transplantation Proceedings
IS - 8
ER -