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[Mitochondrial calcium uniporter participates in remote preconditioning induced cardioprotection in rat hearts subjected to ischemia and reperfusion].

Jian Xu, Ningfu Wang, Shizhong Zhang, Qin Gao, Qiang Xia

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Abstract

AIM: To investigate whether mitochondrial calcium uniporter participates in the cardioprotection of remote preconditioning in rat hearts subjected to ischemia and reperfusion in vivo. METHODS: Rat hearts were subjected to 30 min regional ischemia (occlusion of left anterior descending artery) and 120 min reperfusion in vivo. Remote preconditioning was induced by three cycles of 5 min of right femoral artery occlusion followed by 5 min of reperfusion. The mean arterial blood pressure, heart rate, infarct size, and lactate dehydrogenase (LDH) activity in plasma during reperfusion were measured. RESULTS: Remote preconditioning reduced both the infarct size and LDH release during reperfusion. Ruthenium red, an inhibitor of mitochondrial calcium uniporter, also decreased both the infarct size and LDH release. Administration of spermine, an activator of mitochondrial calcium uniporter, canceled the reduction of infarct size and LDH release induced by remote preconditioning. CONCLUSION: These results indicate that remote preconditioning protects myocardium against ischemia and reperfusion injury, that effect may be related to inhibiting mitochondrial calcium uniporter opening.

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AIM: To investigate whether mitochondrial calcium uniporter participates in the cardioprotection of remote preconditioning in rat hearts subjected to ischemia and reperfusion in vivo. METHODS: Rat hearts were subjected to 30 min regional ischemia (occlusion of left anterior descending artery) and 120 min reperfusion in vivo. Remote preconditioning was induced by three cycles of 5 min of right femoral artery occlusion followed by 5 min of reperfusion. The mean arterial blood pressure, heart rate, infarct size, and lactate dehydrogenase (LDH) activity in plasma during reperfusion were measured. RESULTS: Remote preconditioning reduced both the infarct size and LDH release during reperfusion. Ruthenium red, an inhibitor of mitochondrial calcium uniporter, also decreased both the infarct size and LDH release. Administration of spermine, an activator of mitochondrial calcium uniporter, canceled the reduction of infarct size and LDH release induced by remote preconditioning. CONCLUSION: These results indicate that remote preconditioning protects myocardium against ischemia and reperfusion injury, that effect may be related to inhibiting mitochondrial calcium uniporter opening.

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Available abstract

AIM: To investigate whether mitochondrial calcium uniporter participates in the cardioprotection of remote preconditioning in rat hearts subjected to ischemia and reperfusion in vivo. METHODS: Rat hearts were subjected to 30 min regional ischemia (occlusion of left anterior descending artery) and 120 min reperfusion in vivo. Remote preconditioning was induced by three cycles of 5 min of right femoral artery occlusion followed by 5 min of reperfusion. The mean arterial blood pressure, heart rate, infarct size, and lactate dehydrogenase (LDH) activity in plasma during reperfusion were measured. RESULTS: Remote preconditioning reduced both the infarct size and LDH release during reperfusion. Ruthenium red, an inhibitor of mitochondrial calcium uniporter, also decreased both the infarct size and LDH release. Administration of spermine, an activator of mitochondrial calcium uniporter, canceled the reduction of infarct size and LDH release induced by remote preconditioning. CONCLUSION: These results indicate that remote preconditioning protects myocardium against ischemia and reperfusion injury, that effect may be related to inhibiting mitochondrial calcium uniporter opening.

Key concepts: Uniporter, Cardioprotection, Ischemia, Ruthenium red, Ischemic preconditioning, Calcium, Lactate dehydrogenase, Cardiology

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[Mitochondrial calcium uniporter participates in remote preconditioning induced cardioprotection in rat hearts subjected to ischemia and reperfusion]. — Research Paper | ScholarLens