Transient acidosis during early reperfusion attenuates myocardium ischemia reperfusion injury via PI3k-Akt-eNOS signaling pathway

Xin Qiao; Jinjin Xu; Qing-Jun Yang; Yun Du; Shaoqing Lei; Zhi-Hong Liu; Xinwei Liu; Huimin Liu

doi:10.1155/2013/126083

Transient acidosis during early reperfusion attenuates myocardium ischemia reperfusion injury via PI3k-Akt-eNOS signaling pathway

Oxid Med Cell Longev. 2013:2013:126083. doi: 10.1155/2013/126083. Epub 2013 Nov 7.

Authors

Xin Qiao¹, Jinjin Xu, Qing-Jun Yang, Yun Du, Shaoqing Lei, Zhi-Hong Liu, Xinwei Liu, Huimin Liu

Affiliation

¹ Department of Anesthesiology, Chongqing Zhoushan Hospital, Chongqing 404100, China ; Department of Anesthesiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 404100, China.

Abstract

In this paper, we concluded that transient acidosis reperfusion conferred cardioprotection against myocardial ischemia reperfusion injury in isolated rat hearts through activating PI3K-Akt-eNOS pathway.

MeSH terms

Acidosis / complications*
Acidosis / enzymology*
Acidosis / pathology
Acidosis / physiopathology
Animals
Dinoprost / analogs & derivatives
Enzyme Activation
Heart Function Tests
Ischemic Postconditioning
Isoprostanes / metabolism
Male
Myocardial Reperfusion Injury / complications*
Myocardial Reperfusion Injury / enzymology*
Myocardial Reperfusion Injury / pathology
Myocardial Reperfusion Injury / physiopathology
Nitric Oxide / metabolism
Nitric Oxide Synthase Type III / metabolism*
Perfusion
Phosphatidylinositol 3-Kinases / metabolism*
Proto-Oncogene Proteins c-akt / metabolism*
Rats
Rats, Sprague-Dawley
Signal Transduction

Substances

Isoprostanes
8-epi-prostaglandin F2alpha
Nitric Oxide
Dinoprost
Nitric Oxide Synthase Type III
Phosphatidylinositol 3-Kinases
Proto-Oncogene Proteins c-akt