Characterising the D-Galactosamine Rat Model of Hepatorenal Syndrome

由病毒感染、酒精或日常药物引起的肝功能衰竭患者通常会发展为急性肾功能衰竭(肝肾综合征)。我们不确定这是如何或为什么发生的，但它是由流向肾脏的血液显著减少引起的，这本身是由心脏在全身跳动血液的有效性降低、供应肠道的血管开放以及一系列化合物的产生增加造成的，这些化合物进一步减少了肾脏的血流量。我们似乎有一个很好的这种综合征的动物模型，但它需要进一步的表征，并与发展为肝肾综合征的急性或慢性肝衰竭患者进行直接比较。这项研究的目的是检验这样一种假设，即这种急性肝肾衰竭的动物模型代表了人类疾病。研究的第二部分将确定一些机制，通过这些机制，我们可以改善这种动物模型的肾功能，并有望用于治疗肝肾综合征患者。

Patients with liver failure, caused by virus infection, alcohol or their daily medicines often develop acute kidney failure (hepatorenal syndrome). We are not sure how or why this occurs, but it is caused by a marked decrease of blood flow to the kidneys, itself caused by a reduction in the effectiveness of the heart to beat blood around the body, an opening up of blood vessels that supply the intestines, and increased production of a series of compounds which reduce kidney blood flow further. We appear to have a good animal model of this syndrome, but it needs further characterisation and direct comparison to patients with acute or acute on chronic liver failure who develop the hepatorenal syndrome. The aim of this study is to test the hypothesis that this animal model of acute liver and kidney failure is representative of the human disease. The second part of the study will determine some mechanisms by which we can improve kidney function in this animal model and hopefully use to treat patients with the hepatorenal syndrome.