dos Santos Priscila P, Nogueira Bruna F, Rafacho Bruna P M, Azevedo Paula S, Polegato Bertha F, Chiuso-Minicucci Fernanda, Bonomo Camila, Roscani Meliza G, Zorzella-Pezavento Sofia F G, Tanni Suzana E, Pereira Elenize J, Okoshi Marina P, Paiva Sergio A R, Zornoff Leonardo A M, Minicucci Marcos F
Internal Medicine Department, Botucatu Medical School, Univ Estadual Paulista (UNESP), Botucatu, Brazil.
Cell Physiol Biochem. 2012;30(5):1191-201. doi: 10.1159/000343309. Epub 2012 Oct 12.
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.
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.
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)].
Our data do not support the participation of aldosterone in the ventricular remodeling process induced by exposed to cigarette smoke.
背景/目的：在烟草烟雾（TS）模型中，尚未对使用盐皮质激素受体拮抗剂阻断肾素-血管紧张素-醛固酮系统进行研究。因此，本研究调查了螺内酯在烟草烟雾暴露诱导的心脏重塑中的作用。
将雄性Wistar大鼠分为4组：对照组（C组，n = 11）；暴露于香烟烟雾2个月的组（TS-C组，n = 13）；接受20 mg/kg饮食/天螺内酯且未暴露于香烟烟雾的组（TS-S组，n = 13）；以及暴露于香烟烟雾2个月并补充螺内酯的组（S组，n = 12）。对大鼠观察60天，在此期间进行形态学、生化和功能分析。
各组间有创平均动脉压无差异。在形态学和功能分析中，烟草烟雾暴露与螺内酯之间无相互作用。然而，在超声心动图分析中，与非TS组相比，TS组左心室腔扩大、左心室质量指数更高且经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，且不受螺内酯影响。此外，心肌中IFN-γ、TNF-α、IL-10、ICAM-1和GLUT4水平无差异[TS：OR 0.52，95%CI（-0.007；0.11）；螺内酯：OR -0.01，95%CI（-0.07；0.05）]。
我们的数据不支持醛固酮参与香烟烟雾暴露诱导的心室重塑过程。
