Effect of bilateral sympathectomy in a rat model of dilated cardiomyopathy induced by doxorubicin.

Coutinho E Silva, Raphael Dos Santos; Zanoni, Fernando Luiz; Simas, Rafael; Martins da Silva, Mateus Henrique Fernandes; Armstrong Junior, Roberto; Correia, Cristiano de Jesus; Breithaupt Faloppa, Ana Cristina; Moreira, Luiz Felipe Pinho · J Thorac Cardiovasc Surg · 2020

basic_science · Level V

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Abstract

The study objective was to evaluate the effect of bilateral sympathectomy on ventricular remodeling and function in a rat model of dilated cardiomyopathy induced by doxorubicin. Dilated cardiomyopathy was induced in male Wistar rats by weekly intraperitoneal injection of doxorubicin (2 mg/kg) for 9 weeks. Animals were divided into 4 groups: dilated cardiomyopathy; bilateral sympathectomy, submitted on day 15 of the protocol to bilateral sympathectomy; angiotensin-converting enzyme inhibitor, treated with enalapril through day 15 until the end of the experimental protocol; and sham, nonsubmitted through doxorubicin protocol, with weekly intraperitoneal injections of saline solution (0.9%). The left ventricular function was assessed, and the heart was collected for posterior analyses. The dilated cardiomyopathy group presented a significant decrease in the myocardial efficiency when compared with the sham group (33.4% vs 71.2%). Only the bilateral sympathectomy group was able to preserve it (57.5%; P = .0001). A significant dilatation in the left ventricular chamber was observed in the dilated cardiomyopathy group (15.9 μm<sup>2</sup>) compared with the sham group (10.2 μm<sup>2</sup>; P = .0053). Sympathectomy and enalapril prevented ventricular remodeling (9.5 and 9.6 μm<sup>2</sup>, respectively; P = .0034). There was a significant increase in interstitial myocardial fibrosis in the dilated cardiomyopathy group (14.8%) when compared with the sham group (2.4%; P = .0001). This process was significantly reduced with sympathectomy and enalapril (8.7 and 3.9%, respectively; P = .0001). Bilateral sympathectomy was effective in preventing remodeling and left ventricular dysfunction in a rat model of dilated cardiomyopathy induced by doxorubicin.

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