Xin Duan1, Bingyang Ji, Kun Yu, Feilong Hei, Jinping Liu, Cun Long. 1. Fuwai 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.
Abstract
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.
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.
Authors: Emilie Farine; Petra Niederberger; Rahel K Wyss; Natalia Méndez-Carmona; Brigitta Gahl; Georg M Fiedler; Thierry P Carrel; Hendrik T Tevaearai Stahel; Sarah L Longnus Journal: Front Physiol Date: 2016-11-22 Impact factor: 4.566
Authors: Antonio Carlos Cerqueira Oliveira; Norma Sueli Pinheiro Módolo; Maria Aparecida Custódio Domingues; Paulo Adriano Schwingel Journal: Acta Cir Bras Date: 2019-10-14 Impact factor: 1.388