AI Article Synopsis
- The study investigates how combining angiotensin-converting enzyme inhibitors (ACEI) with subthreshold preconditioning can protect the heart during ischemia by focusing on mitochondrial potassium channels.
- The experiment used isolated rat hearts to measure specific enzyme activities and observe the effects of the treatments on heart function during ischemia.
- Findings indicated that while neither treatment alone was effective, their combination improved heart function and delayed damage, suggesting that mitochondrial potassium channels play a crucial role in this protective mechanism.
Article Abstract
Aim: To determine mechanisms of cardioprotection induced by combination angiotensin-converting enzyme inhibitors (ACEI) with subthreshold preconditioning after activation of mitochondrial ATP-sensitive potassium (mitoK(ATP)) channel.
Methods: The Langendorff model of isolated rat heart was used. The time of the onset of uncoupling, the activities of sarcolemmal Na+/K+ -ATPase and Ca2+/Mg2+ -ATPase were measured.
Results: The subthreshold preconditioning (2 min of ischemia and 10 min reperfusion) or captopril (an ACEI) alone did not protect hearts against injury of sustained ischemia. However combination captopril with subthreshold preconditioning increased LVDP. Pretreatment hearts with mitoK(ATP) channel inhibitor 5-HD abolished the protection effect. Combination captopril with subthreshold preconditioning delayed the onset of uncoupling, and enhanced the activities of sarcolemmal Na+/K+ ATPase and Ca2+/Mg2+ -ATPase in ischemia/reperfusion hearts. But 5-HD cancelled these cardioprotection effects.
Conclusion: Combination ACEI with subthreshold preconditioning delays the onset of cellular uncoupling induced by acute ischemia, and promotes the stability of sarcolemmal ion channels, in which activation of the mitoK(ATP) channels may be involved.
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