The role of nitric oxide in ethanol postconditioning induced cardioprotection / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate whether the release of nitric oxide (NO) was involved in the cardioprotection of ethanol postconditioning in isolated rat hearts.</p><p><b>METHODS</b>Hearts isolated from male SD rats were subjected to 30 min of regional ischemia (occlusion of left anterior descending artery) followed by 120 min of reperfusion. Ethanol postconditioning was fulfilled through perfusion of 50 mmol/L ethanol for 15 min (at the end of cardiac ischemia for 5 min and at the beginning of reperfusion for 10 min). The rats were divided into five groups: normal, ischemia and reperfusion, ethanol postconditioning, ethanol postconditioning + L-nitro-arginine-methylester (L-NAME) and ethanol postconditioning + atractyloside. The ventricular hemodynamic parameters and lactate dehydrogenase (LDH) release during reperfusion were measured. The infarct size was measured by TTC staining method and NO content was measured by nitric acid reductase method. The expressions of Bcl-2 and Bax mRNA were detected by RT-PCR analysis.</p><p><b>RESULTS</b>In contrast to ischemia and reperfusion, ethanol postconditioning improved left ventricular developed pressure, rate pressure product during reperfusion, reduced LDH release and infarct size. NO content was decreased. The ratio of Bcl-2/Bax was increased. Administration of nitric oxide synthase inhibitor L-NAME or mitochondrial permeability transition pore opener atractyloside both attenuated the role of ethanol postconditioning, which inhibited the recovery of hemodynamic parameters, the decreases of LDH and infarct size. NO content was decreased further. The ratio of Bcl-2/Bax was decreased.</p><p><b>CONCLUSION</b>The cardioprotection of ethanol postconditioning may be associated with reducing nitric oxide release, inhibiting the opening of mitochondrial permeability transition pore and decreasing the happening of apoptosis.</p>

Activation of mitochondrial aldehyde dehydrogenase 2 and inhibition of mitochondrial permeability transition pore involved in cardioprotection of ethanol postconditioning / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate whether activation of mitochondrial aldehyde dehydrogenase 2 (ALDH2) and inhibition of mitochondrial permeability transition pore (mitoPTP) were involved in the cardioprotection of ethanol postconditioning in isolated rat heart.</p><p><b>METHODS</b>Hearts isolated from male Sprague-Dawley rats were perfused on a langendorff apparatus and subjected to 30 min of regional ischemia (occlusion of left anterior descending artery) followed by 120 min of reperfusion. The ventricular hemodynamic parameters and lactate dehydrogenase (LDH) release during reperfusion were measured. Infarct size was measured by TTC staining method and the expression of ALDH2 at mRNA level of left anterior myocardium was detected by RT-PCR.</p><p><b>RESULT</b>In contrast to ischemia and reperfusion, ethanol postconditioning improved the recovery of left ventricular developed pressure, maximal rise/fall rate of left ventricular pressure during reperfusion, reduced LDH release and infarct size. The expression of ALDH2 mRNA level was increased. Administration of mitoPTP activator atractyloside attenuated the effect of ethanol postconditioning, LDH release and infarct size were increased, and the recovery of hemodynamic parameters was inhibited. The expression of ALDH2 mRNA was decreased.</p><p><b>CONCLUSION</b>Ethanol postconditioning has cardioprotection effect, which may be associated with upregulating mitochondrial ALDH2 mRNA expression and inhibiting the opening of mitochondrial permeability transition pore.</p>