Sildenafil Postconditioning in a Rat Model of Ventricular Fibrillation/Resuscitation

W. Vanagt, Hesam Amin, A. Brouwers, Chantal C H Pöttgens, T. Wolfs, J. Cleutjens, Q. Swennen, T. Delhaas, F. Prinzen
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Abstract

Objective: To evaluate the multi-organ postconditioning potential of sildenafil during resuscitation. Circulatory arrest/resuscitation induces ischemia/reperfusion (I/R) injury in all organs. I/R injury can be reduced using postconditioning during reperfusion. Sildenafil has proven strong single-organ postconditioning properties.Methods: Ventricular fibrillation (VF) was induced and left untreated for 6 min in anesthetized adult male Wistar rats. During resuscitation, placebo (n=10) or intravenous sildenafil 0.2 mg/kg (n=10) was administered. Troponin-i release, lactate release, blood gases and hemodynamic parameters were assessed. After 3 h of reperfusion, rats were euthanized; brain and heart were removed for infarct staining with triphenyltetrazolium chloride. Urinary kidney injury molecule (KIM-1) was assessed. Data expressed as median (interquartile range), p<0.05 significant.Results: Resuscitation/defibrillation resulted in return of spontaneous circulation in all rats. Compared with the sildenafil group, the control group showed higher overall troponin release (Control 50 (32-60) versus Sildenafil 16 (12-42) h·microg/L, p=0.032) and higher left ventricular infarct percentage (Control 19 (16-24) versus Sildenafil 16 (12-18)%, p=0.039). There was no significant difference between the groups with respect to mortality, hemodynamic recovery, cerebral cortex infarct percentage, lactate release, blood gas values and urinary KIM-1 release. Three rats in the sildenafil group developed pulmonary edema versus none in the control group.Conclusions: Sildenafil postconditioning during resuscitation significantly reduces cardiac injury but does not affect mortality, cerebral and renal injury after resuscitation.
西地那非后处理在大鼠心室颤动/复苏模型中的作用
目的:评价西地那非在复苏过程中的多器官后处理潜力。循环停止/复苏导致各器官缺血/再灌注(I/R)损伤。I/R损伤可以在再灌注过程中使用后处理来减少。西地那非已被证明具有很强的单器官后处理特性。方法:麻醉成年雄性Wistar大鼠诱导心室颤动(VF),静置6 min。复苏期间给予安慰剂(n=10)或静脉注射西地那非0.2 mg/kg (n=10)。评估肌钙蛋白i释放、乳酸释放、血气和血流动力学参数。再灌注3 h后,对大鼠实施安乐死;切除脑和心脏,用三苯基四唑氯染色。检测尿肾损伤分子(KIM-1)。数据以中位数(四分位数间距)表示,p<0.05显著。结果:复苏/除颤均能使大鼠恢复自主循环。与西地那非组相比,对照组总肌钙蛋白释放量更高(对照组50(32-60)比西地那非16 (12-42)h·μ g/L, p=0.032),左室梗死率更高(对照组19(16-24)比西地那非16 (12-18)%,p=0.039)。两组在死亡率、血流动力学恢复、脑皮质梗死率、乳酸释放、血气值和尿KIM-1释放方面无显著差异。西地那非组有3只大鼠出现肺水肿,而对照组没有。结论:复苏时西地那非后处理可显著降低心脏损伤,但不影响复苏后的死亡率和脑、肾损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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