New Na(+)-H+ exchange inhibitor HOE 694 improves postischemic function and high-energy phosphate resynthesis and reduces Ca2+ overload in isolated perfused rabbit heart.

摘要: BACKGROUND Experiments were carried out using the new Na(+)-H+ exchange inhibitor (3-methylsulfonyl-4-piperidinobenzoyl)guanidine methanesulfonate (HOE 694) to assess role of in myocardial ischemic and reperfusion injury. METHODS AND RESULTS Three groups rabbit hearts (n = 5 each) perfused with blood subjected 45 minutes global normothermic (37 degrees C) ischemia, followed by 1 hour reperfusion. Group was control group (vehicle only); 2, HOE 694 (1 mumol/L) administered before ischemia (pretreatment group); 3, given only during separate actions exerted from those specifically obtained End-diastolic pressure rise at reduced administration starting (from 52.2 +/- 8.5 mm Hg 17.6 4.5 P CONCLUSIONS Postischemic dysfunction associated a end-diastolic pressure. This effectively blocked 694. The drug most effective when treated although partial protection observed started on action strengthens idea that both contributes contractile dysfunction.