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Post liver transplantation acute kidney injury in a rat model of syngeneic orthotopic liver transplantation

机译:肝移植后急性肾损伤的同基因异位原位肝移植大鼠模型

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Acute kidney injury (AKI) is a frequent complication after liver transplantation (LT). The mechanism of post-LT AKI remains unclear. We used the rat model of syngeneic orthotopic LT (SOLT) to investigate the mechanism of post-LT AKI. We hypothesized that the condition of the graft, rather than intraoperative hemodynamic instability, has an important role in post-LT AKI in the SOLT model. Rats were randomly assigned into four groups: sham-operated group; vessel-clamped group; full-size LT group; and reduced-size LT group. We identified AKI in both full-size and reduced-size LT groups. In addition to renal tubular necrosis and apoptosis, renal peritubular capillary injury was also present. Pathological changes were more severe in the reduced-size than in the full-size LT group. We found that the systemic inflammatory response induced by LT was the initiating factor in post-LT AKI. This is the first study to investigate the pathological mechanism of AKI in an animal model of SOLT. Our results demonstrate that protection of the liver graft and inhibition of the systemic inflammatory response are vital in reducing the risk of post-LT AKI.
机译:急性肾损伤(AKI)是肝移植(LT)后的常见并发症。 LT后AKI的机制仍不清楚。我们使用同基因原位LT(SOLT)大鼠模型来研究LT后AKI的机制。我们假设移植物的状况,而不是术中血流动力学的不稳定,在SOLT模型中的LT后AKI中具有重要作用。将大鼠随机分为四组:假手术组;假手术组;假手术组。血管钳组大型LT组;和小型LT组。我们在大型和小型LT组中都发现了AKI。除了肾小管坏死和凋亡外,还存在肾小管周围毛细血管损伤。尺寸缩小的病理变化比全尺寸的LT组更为严重。我们发现LT引起的全身性炎症反应是LT AKI后的起始因素。这是第一个研究SOLT动物模型中AKI病理机制的研究。我们的结果表明,保护肝脏移植物和抑制全身炎症反应对于降低LT AKI后的风险至关重要。

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