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J Cardiovasc Transl Res. 2019 Apr 12. doi: 10.1007/s12265-019-09886-1. [Epub ahead of print]

Protection of Myocardial Ischemia-Reperfusion by Therapeutic Hypercapnia: a Mechanism Involving Improvements in Mitochondrial Biogenesis and Function.

Author information

1
Department of Anesthesiology, The Heilongjiang Province Key Lab of Research on Anesthesiology and Critical Care Medicine, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
2
Department of Anesthesiology, The Heilongjiang Province Key Lab of Research on Anesthesiology and Critical Care Medicine, Second Affiliated Hospital of Harbin Medical University, Harbin, China. wenzhili9@126.com.

Abstract

Previous studies proposed that acidic reperfusion may be a protective strategy for myocardial ischemia-reperfusion therapy with potential of clinical transformation. In this study, we investigated whether therapeutic hypercapnia could mimic acidosis postconditioning in isolated hearts with a 30-min left coronary artery ligation-reperfusion model in rats. Therapeutic hypercapnia (inhalation 20% CO2 for 10 min) is cardioprotective with a strict therapeutic time window and acidity: it reduced the infarct ratio and serum myocardial enzyme and increased the myocardial ATP content. Furthermore, mitochondrial morphology damage, the loss of mitochondrial membrane potential, and the formation of mitochondrial permeability transition pore were effectively inhibited, indicating the improvements in mitochondrial function. The expression of the mitochondrial biogenesis regulators was upregulated simultaneously. These findings indicated therapeutic hypercapnia in animals can mimic ex vivo acidosis postconditioning to alleviate myocardial ischemia-reperfusion injury. The effect is related to improvement in mitochondrial function and regulation of the mitochondrial biogenesis pathway.

KEYWORDS:

Acidosis; Hypercapnia; Mitochondrial biogenesis; Myocardial ischemia–reperfusion; Postconditioning

PMID:
30980235
DOI:
10.1007/s12265-019-09886-1

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