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首页> 外文期刊>Parasitology Research >Acute Trypanosoma cruzi experimental infection induced renal ischemic/reperfusion lesion in mice
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Acute Trypanosoma cruzi experimental infection induced renal ischemic/reperfusion lesion in mice

机译:急性克鲁氏锥虫实验性感染诱发小鼠肾脏缺血/再灌注损伤

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Experimental acute infection with Trypanosoma cruzi in mice promotes an intense myocarditis and other systemic changes. However, the network of pathophysiological disorders and renal injury caused by the infection has not been elucidated. Our previous results with a murine model observed a discrete acute myocarditis and high mortahty with significant inflammatory kidney injury with T. cruzi infection. The aim of this study was to investigate the mechanisms of kidney injury caused by the parasite in mice during the experimental acute phase. Results employing BALB/c mice infected with T. cruzi of Y strain showed renal injury on the 6th day postinfection (dpi) caused by a transitory decrease of renal blood flow. Acute kidney injury (AKI) was also observed similar to the model of ischemia/ reperfusion lesion in these infected mice. The injury was not related to the presence (or multiplication) of parasites. Only rare nests were microscopically detected, and the presence of scattered parasites in renal parenchyma was seen on the 15th dpi. Thus, it was observed that during the acute phase of the disease, AKI in infected mice is linked to early cardiovascular effects, including heart failure, caused by striking inflammatory lesions in the myocardium, which lead to the high mortality rate of animals.
机译:实验性克氏锥虫的急性感染会引起强烈的心肌炎和其他全身性变化。然而,尚未阐明由感染引起的病理生理疾病和肾损伤的网络。我们先前在鼠模型中得到的结果观察到离散型急性心肌炎和高死亡率,并伴有克鲁氏锥虫感染,引起严重的炎症性肾损伤。这项研究的目的是研究在实验急性期小鼠体内由寄生虫引起的肾脏损伤机制。使用感染了Y株克鲁氏酵母的BALB / c小鼠的结果显示,感染后第6天(dpi)肾损伤是由于肾血流量的短暂减少引起的。在这些感染的小鼠中,还观察到急性肾损伤(AKI),类似于缺血/再灌注损伤模型。伤害与寄生虫的存在(或繁殖)无关。在显微镜下仅检测到稀有的巢,并且在第15 dpi观察到肾实质中存在散在的寄生虫。因此,据观察,在疾病的急性期,被感染的小鼠中的AKI与早期的心血管作用有关,包括心力衰竭,这是由于心肌中的炎性病变引起的,从而导致动物高死亡率。

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