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Updated: Jun 2, 2026
Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia
Published on: July 31, 2017
Acidic buffer or plus cyclosporine A post-conditioning protects isolated rat hearts against ischemia-reperfusion
Xin Duan1, Bingyang Ji, Kun Yu
1Fuwai Hospital & Cardiovascular Institute, Chinese Academy of Medical Science, Peking Union Medical College, 167 Bei li shi Road, Fuwai Da Jie, Xi Cheng, Beijing, Peoples Republic of China.
Background:
It is well documented that transient acidosis during reperfusion is protective. The aim of this study was to evaluate the cardioprotection of acidic buffer or plus cyclosporine A in isolated rat hearts after cardioplegic arrest.
Methods:
Langendorff-perfused Sprague-Dawley rat hearts were perfused for 20 min with Krebs-Henseleit (K-H) buffer followed by 30 min of crystalloid cardioplegia and 60 min of reperfusion. Control hearts were perfused with Krebs-Henseleit buffer. Acidic buffer post-conditioning hearts were perfused with acidic K-H buffer (pH 6.8) for the first 3 min of reperfusion. Acidic buffer plus cyclosporine A hearts were perfused with K-H acidic buffer (pH 6.8) containing cyclosporine A (0.2 μmol/L) for the first 3 min of reperfusion.
Results:
Compared with the control group, acidic buffer or plus cyclosporine A post-conditioning significantly improved myocardial performance, decreased cytochrome C release into the cytosol, increased Bcl-2 expression and decreased Bax expression, decreased sensitivity of mPTP-opening to [Ca2+] and the rate of apoptosis after reperfusion.
Conclusion:
These findings suggested that acidic buffer or plus cyclosporine A post-conditioning prevented apoptosis-related mitochondrial permeabilization and provided the myocardial protection after cardioplegic arrest.
