Abstract
Objective To investigate the effect of hydrogen-rich saline postconditioning on the expression of vascular endothelial growth factor receptor-1 (VEGFR1) during myocardial ischemia-reperfusion (I/R) injury in rats. Methods Thirty-six adult male Sprague-Dawley rats, weighing 250-280 g, were randomly divided into 3 groups (n=12 each) using a random number table: sham operation group (group S), group I/R and hydrogen-rich saline group (group H2). Myocardial I/R was induced by 30 min ligation of anterior descending branch of the left coronary artery followed by 2 h reperfusion.In group H2, hydrogen-rich saline 5 ml/kg was injected intravenously at 5 min before reperfusion, while the equal volume of normal saline was given in group I/R.Left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP) and ± dp/dtmax were measured and recorded during reperfusion and at 120 min of reperfusion.The rats were sacrificed at 120 min of reperfusion, and myocardial specimens were obtained for determination of myocardial infarct size, contents of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) (using ELISA), and expression of VEGFR1 (by Western blot). At 120 min of reperfusion, blood samples were collected from the common carotid artery to measure cardiac troponin I (cTnI) concentrations in serum. Results Compared with group S, LVSP and ± dp/dtmax were significantly decreased, LVEDP was increased, the myocardial infarct size was enlarged, cTnI concentrations in serum and contents of IL-6 and TNF-α were increased, and the expression of VEGFR1 was down-regulated at 120 min of reperfusion in H2 and I/R groups.Compared with group I/R, LVSP and ± dp/dtmax were significantly increased, LVEDP and myocardial infarct size were decreased, cTnI concentrations in serum and contents of IL-6 and TNF-α were decreased, and the expression of VEGFR1 was up-regulated at 120 min of reperfusion in group H2. Conclusion Hydrogen-rich saline postconditioning can reduce myocardial I/R injury possibly by up-regulating myocardial VEGFR1 expression and inhibiting inflammatory responses in the myocardium of rats. Key words: Hydrogen; Myocardial Reperfusion injury; Vascular endothelial growth factorreceptor-1; Ischemic postconditioning
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