BACKGROUND: The cardioprotection of ischemic post-conditioning (IPO) has been well demonstrated after a short period of reperfusion. However, little is known about the long-term effects of IPO. This study aimed to investigate the long term cardioprotection of IPO in a rat myocardial ischemia/reperfusion model and to explore the potential mechanism. METHODS AND RESULTS: Rats were either sham-operated (Sham group) or underwent 30-min left anterior descending coronary artery ischemia followed by immediate reperfusion (I/R group) or post-conditioning with 5 cycles of 10-s ischemia and 10-s reperfusion (IPO group). At 24 h after reperfusion, infarct size reduced from 34.7±1.1% in I/R group to 24.9±1.3% in IPO group (P<0.05) and the iNOS expression in IPO group was 4.7-fold higher than in I/R group. iNOS inhibitor 1400 W (1 mg/kg, 5 min before postconditioning or reperfusion) prevented the increase in iNOS expression and abolished IPO-induced protection (34.4±1.0%, P>0.05 vs. I/R group). When rats were treated with PI3K inhibitor LY294002 5 min before reperfusion (0.3 mg/kg), p-Akt expression at R 3 h and iNOS expression at R 24 h were significantly inhibited. Moreover, the delayed infarct-sparing effect of IPO was absent in the presence of LY294002. CONCLUSION: IPO has prolonged cardioprotective effects and iNOS as an important downstream effector of PI3K-Akt pathway contributes to the delayed phase cardioprotection of IPO.
BACKGROUND: The cardioprotection of ischemic post-conditioning (IPO) has been well demonstrated after a short period of reperfusion. However, little is known about the long-term effects of IPO. This study aimed to investigate the long term cardioprotection of IPO in a ratmyocardial ischemia/reperfusion model and to explore the potential mechanism. METHODS AND RESULTS:Rats were either sham-operated (Sham group) or underwent 30-min left anterior descending coronary artery ischemia followed by immediate reperfusion (I/R group) or post-conditioning with 5 cycles of 10-s ischemia and 10-s reperfusion (IPO group). At 24 h after reperfusion, infarct size reduced from 34.7±1.1% in I/R group to 24.9±1.3% in IPO group (P<0.05) and the iNOS expression in IPO group was 4.7-fold higher than in I/R group. iNOS inhibitor 1400 W (1 mg/kg, 5 min before postconditioning or reperfusion) prevented the increase in iNOS expression and abolished IPO-induced protection (34.4±1.0%, P>0.05 vs. I/R group). When rats were treated with PI3K inhibitor LY294002 5 min before reperfusion (0.3 mg/kg), p-Akt expression at R 3 h and iNOS expression at R 24 h were significantly inhibited. Moreover, the delayed infarct-sparing effect of IPO was absent in the presence of LY294002. CONCLUSION: IPO has prolonged cardioprotective effects and iNOS as an important downstream effector of PI3K-Akt pathway contributes to the delayed phase cardioprotection of IPO.
Authors: C Duilio; G Ambrosio; P Kuppusamy; A DiPaula; L C Becker; J L Zweier Journal: Am J Physiol Heart Circ Physiol Date: 2001-06 Impact factor: 4.733
Authors: Jacob Lønborg; Henning Kelbaek; Niels Vejlstrup; Erik Jørgensen; Steffen Helqvist; Kari Saunamäki; Peter Clemmensen; Lene Holmvang; Marek Treiman; Jan S Jensen; Thomas Engstrøm Journal: Circ Cardiovasc Interv Date: 2010-01-26 Impact factor: 6.546
Authors: Rhaí André Arriel; Jéssica Ferreira Rodrigues; Hiago Leandro Rodrigues de Souza; Anderson Meireles; Luís Filipe Moutinho Leitão; Antonio Crisafulli; Moacir Marocolo Journal: Int J Environ Res Public Health Date: 2020-11-04 Impact factor: 3.390