TY - JOUR
T1 - Enhanced tolerance of the rat myocardium to ischemia and reperfusion injury earlyafter acute myocardial infarction
AU - Pantos, C.
AU - Mourouzis, I.
AU - Dimopoulos, A.
AU - Markakis, K.
AU - Panagiotou, M.
AU - Xinaris, C.
AU - Tzeis, S.
AU - Kokkinos, A. D.
AU - Cokkinos, D. V.
PY - 2007/7
Y1 - 2007/7
N2 - It is now recognized that changes occurring during cardiac remodelingmay influence the tolerance of the myocardium to ischemic stress. Therefore, the present study investigated the response of the post-infarcted heart to ischemia in an experimental model of ischemia and reperfusion injury and the possible underlying mechanisms. Acute myocardial infarction (AMI) was induced in Wistar male rats by ligating the left coronary artery (AMI, n = 13), while sham-operated rats were used as controls (SHAM, n = 11). At 2 weeks, cardiac dysfunction was observed in AMI, as indicated by the reduction of the left ventricular EF%. Isolated hearts were then subjected to 30 min of zero-flow global ischemia followed by 45 min of reperfusion. Ischemic contracture was significantly depressed in AMI hearts. Postischemicleft ventricular end diastolic pressure (LVEDP45) in mmHg and LDH release in IU/g were markedly decreased; LVEDP45 was 52.1 (7.5) for AMI vs 96.6 (7.5),P < 0.05 and LDH release was 7.5 (1.0) in AMI vs 11.4 (0.56)in SHAM, P < 0.05. This response was associated with 2-fold increase in HSP70 expression in AMI hearts (noninfarcted segment), P < 0.05 vs SHAM and 1.7 fold increase in the expression of the phospho-HSP27, P < 0.05, while the expression of PKCε was shown to be 1.4-fold less in AMI, P < 0.05. In conclusion,the post-infarcted heart seems to be resistant to ischemiareperfusion injury and heat shock protein 70 and 27 may be involved in this response.
AB - It is now recognized that changes occurring during cardiac remodelingmay influence the tolerance of the myocardium to ischemic stress. Therefore, the present study investigated the response of the post-infarcted heart to ischemia in an experimental model of ischemia and reperfusion injury and the possible underlying mechanisms. Acute myocardial infarction (AMI) was induced in Wistar male rats by ligating the left coronary artery (AMI, n = 13), while sham-operated rats were used as controls (SHAM, n = 11). At 2 weeks, cardiac dysfunction was observed in AMI, as indicated by the reduction of the left ventricular EF%. Isolated hearts were then subjected to 30 min of zero-flow global ischemia followed by 45 min of reperfusion. Ischemic contracture was significantly depressed in AMI hearts. Postischemicleft ventricular end diastolic pressure (LVEDP45) in mmHg and LDH release in IU/g were markedly decreased; LVEDP45 was 52.1 (7.5) for AMI vs 96.6 (7.5),P < 0.05 and LDH release was 7.5 (1.0) in AMI vs 11.4 (0.56)in SHAM, P < 0.05. This response was associated with 2-fold increase in HSP70 expression in AMI hearts (noninfarcted segment), P < 0.05 vs SHAM and 1.7 fold increase in the expression of the phospho-HSP27, P < 0.05, while the expression of PKCε was shown to be 1.4-fold less in AMI, P < 0.05. In conclusion,the post-infarcted heart seems to be resistant to ischemiareperfusion injury and heat shock protein 70 and 27 may be involved in this response.
KW - Acute myocardial infarction
KW - Cardiac remodeling
KW - Cardioprotection
KW - Heat shock proteins
KW - Myocardial ischemia
UR - https://www.scopus.com/pages/publications/34250329900
U2 - 10.1007/s00395-007-0645-4
DO - 10.1007/s00395-007-0645-4
M3 - Article
C2 - 17285351
AN - SCOPUS:34250329900
SN - 0300-8428
VL - 102
SP - 327
EP - 333
JO - Basic Research in Cardiology
JF - Basic Research in Cardiology
IS - 4
ER -