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首页> 外文期刊>Cellular Physiology and Biochemistry >Aldosterone is not Involved in the Ventricular Remodeling Process Induced by Tobacco Smoke Exposure
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Aldosterone is not Involved in the Ventricular Remodeling Process Induced by Tobacco Smoke Exposure

机译:醛固酮不参与烟草烟雾暴露引起的心室重塑过程

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摘要

Background/Aims: Renin-angiotensin-aldosterone system blockade with a mineralocorticoid-receptor antagonist has not yet been studied in exposure to tobacco smoke (TS) models. Thus, this study investigated the role of spironolactone on cardiac remodeling induced by exposure to tobacco smoke. Methods: Male Wistar rats were divided into 4 groups: a control group (group C, n=11); a group with 2 months of cigarette smoke exposure (group TS-C, n=13); a group that received spironolactone 20 mg/kg of diet/day and no cigarette smoke exposure (group TS-S, n=13); and a group with 2 months of cigarette smoke exposure and spironolactone supplementation (group S, n=12). The rats were observed for a period of 60 days, during which morphological, biochemical and functional analyses were performed. Results: There was no difference in invasive mean arterial pressure among the groups. There were no interactions between tobacco smoke exposure and spironolactone in the morphological and functional analysis. However, in the echocardiographic analysis, the TS groups had left chamber enlargement, higher left ventricular mass index and higher isovolumetric relaxation time corrected by heart rate compared with the non-TS groups. In vitro left ventricular diastolic function also worsened in the TS groups and was not influenced by spironolactone. In addition, there were no differences in myocardial levels of IFN-γ, TNF-α, IL-10, ICAM-1 and GLUT4 [TS: OR 0.52, 95%CI (-0.007; 0.11); Spironolactone: OR -0.01, 95%CI (-0.07;0.05)]. Conclusion: Our data do not support the participation of aldosterone in the ventricular remodeling process induced by exposed to cigarette smoke.
机译:背景/目的:在暴露于烟草烟雾(TS)模型中,尚未研究用盐皮质激素受体拮抗剂阻断肾素-血管紧张素-醛固酮系统。因此,本研究调查了螺内酯对暴露于烟草烟雾引起的心脏重塑的作用。方法:雄性Wistar大鼠分为4组:对照组(C组,n = 11);对照组(C组,n = 11)。接触香烟烟雾2个月的组(TS-C组,n = 13);每天接受20 mg / kg的螺内酯饮食且无烟的人群(TS-S组,n = 13);以及有2个月的香烟烟雾暴露和补充螺内酯的组(S组,n = 12)。观察大鼠60天,在此期间进行形态,生化和功能分析。结果:各组间的侵入性平均动脉压无差异。在形态和功能分析中,烟草烟雾暴露与螺内酯之间没有相互作用。然而,在超声心动图分析中,与非TS组相比,TS组左室增大,左心室质量指数更高和通过心率校正的等容舒张时间更长。 TS组的体外左心室舒张功能也恶化,并且不受螺内酯的影响。此外,IFN-γ,TNF-α,IL-10,ICAM-1和GLUT4的心肌水平无差异[TS:OR 0.52,95%CI(-0.007; 0.11);螺内酯:或-0.01,95%CI(-0.07; 0.05)]。结论:我们的数据不支持醛固酮参与暴露于香烟烟雾引起的心室重塑过程。

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