TY - JOUR
T1 - One hour reperfusion is enough to assess function and infarct size with ttc staining in langendorff rat model
AU - Ferrera, R.
AU - Benhabbouche, S.
AU - Bopassa, J. C.
AU - Li, B.
AU - Ovize, M.
PY - 2009/8
Y1 - 2009/8
N2 - Background: There is not general agreement concerning the optimal time of reperfusion necessary to assess myocardial function and necrosis on isolated perfused heart model. Nevertheless, the study of cardioprotection (especially, pre- and postconditioning) requires a reliable and standardized assessment of myocardial necrosis. Objective: The objective of this study was thus to evaluate whether 1 h of reperfusion was sufficient to assess rat heart viability on Langendorff preparation. Isolated rat hearts (n=30) underwent 40 min of global normothermic ischemia followed by 60 or 120 min Langendorff reperfusion. In each group, hearts were also randomly assigned into the 2 following sub-groups: postconditioning (PostC, consisting in 2 episodes of 30 s ischemia and 30 s reperfusion at the onset of reperfusion), and control (no intervention). Coronary flow, heart rate, dP/dt and rate-pressure-product were measured. Myocardial necrosis was assessed by TTC staining and LDH, CK release analysis. Results: Our results indicated that heart function tended to slightly decrease between 60 min and 120 min reperfusion. Infarct size was identical at 60 min and 120 min reperfusion, averaging 33-34% of total LV area in controls versus 17% in PostC (p<0.001 between control and PostC groups). Similarly, the maximum of enzymatic releases (CK and LDH) measured in coronary effluents was at 60 min of reperfusion, followed by a progressive decrease at 90 min and 120 min. As expected, postconditioning limited enzymatic releases whatever the studied time of reperfusion. Conclusion: In conclusion, we showed that prolonged reperfusion beyond 60 min was not useful for function assessment and did not change infarct size measurement, on Langendorff rat model of ischemia-reperfusion.
AB - Background: There is not general agreement concerning the optimal time of reperfusion necessary to assess myocardial function and necrosis on isolated perfused heart model. Nevertheless, the study of cardioprotection (especially, pre- and postconditioning) requires a reliable and standardized assessment of myocardial necrosis. Objective: The objective of this study was thus to evaluate whether 1 h of reperfusion was sufficient to assess rat heart viability on Langendorff preparation. Isolated rat hearts (n=30) underwent 40 min of global normothermic ischemia followed by 60 or 120 min Langendorff reperfusion. In each group, hearts were also randomly assigned into the 2 following sub-groups: postconditioning (PostC, consisting in 2 episodes of 30 s ischemia and 30 s reperfusion at the onset of reperfusion), and control (no intervention). Coronary flow, heart rate, dP/dt and rate-pressure-product were measured. Myocardial necrosis was assessed by TTC staining and LDH, CK release analysis. Results: Our results indicated that heart function tended to slightly decrease between 60 min and 120 min reperfusion. Infarct size was identical at 60 min and 120 min reperfusion, averaging 33-34% of total LV area in controls versus 17% in PostC (p<0.001 between control and PostC groups). Similarly, the maximum of enzymatic releases (CK and LDH) measured in coronary effluents was at 60 min of reperfusion, followed by a progressive decrease at 90 min and 120 min. As expected, postconditioning limited enzymatic releases whatever the studied time of reperfusion. Conclusion: In conclusion, we showed that prolonged reperfusion beyond 60 min was not useful for function assessment and did not change infarct size measurement, on Langendorff rat model of ischemia-reperfusion.
KW - Infarct size
KW - Langendorff preparation
KW - Reperfusion
KW - Triphenyltetrazolium
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U2 - 10.1007/s10557-009-6176-5
DO - 10.1007/s10557-009-6176-5
M3 - Article
C2 - 19466533
AN - SCOPUS:69249206798
SN - 0920-3206
VL - 23
SP - 327
EP - 331
JO - Cardiovascular Drugs and Therapy
JF - Cardiovascular Drugs and Therapy
IS - 4
ER -