Hydrogen peroxide induced impairment of post-ischemic ventricular function is prevented by the sodium-hydrogen exchange inhibitor HOE 642 (cariporide).

摘要: Objective: Sodium–hydrogen exchange (NHE) activation is a major mechanism of cardiac injury produced by ischemia and reperfusion. In addition, NHE may mediate the direct effects hydrogen peroxide (H2O2) in normally perfused hearts. The present study was done to determine whether H2O2 at low concentrations producing mild myocardial depression affects post-ischemic recovery function ability inhibitor HOE 642 modulate this effect. Methods : Isolated Langendorff-perfused rat hearts with left ventricular balloon inflated an initial end-diastolic pressure 5 mmHg were subjected 90 min global zero-flow followed 60 Study 1, randomized for perfusion or without (20 μM) 15 before throughout 2, identical experiments except that pretreated (5 μM). Function assessed determining intraventricular pressures. Results: Recovery developed 1 after 10 reperfusion 60.3±8% pre-ischemic values control whereas reduced 29.9±10% treated ( P <0.05). After 80.3±5.2% 60.7±7% H2O2-treated hearts, respectively rates development (+d /d t ) relaxation (−d paralleled seen pressure. Moreover, these associated significantly elevated during last 20 completely prevented deleterious effect H2O2, both respect elevation Conclusions Our results show very impair model ischemia–reperfusion. our suggest likely dependent on activity can be treatment 642.