Why the study?
Does ET-monoclonal antibody improve renal function and protect against tissue damage in a rat model of ischemic acute renal failure?
Does ET-monoclonal antibody improve renal function and protect against tissue damage in a rat model of ischemic acute renal failure?
Endogenously increased endothelin may be an important deleterious mediator in the pathogenesis of ischemic acute renal failure, and its blockade with a monoclonal antibody offers renoprotection in a rat model.
ET-monoclonal antibody may attenuate ischemic renal injury in rats; leaves open clinical translation of ET blockade in human AKI.
In conscious rats, the i.v. injection of endothelin (ET) caused an increase in blood urea nitrogen (BUN), an index of renal dysfunction. In the model of acute renal failure which was induced by occlusion of the bilateral renal arteries of rats followed by reperfusion, ET-monoclonal antibody improved the renal function. In this model, ET-antibody also protected the kidneys from renal proximal tubular necrosis and suppressed Ca++-accumulation in necrotic tissues. Plasma ET level increased 5 min and 5 hr and renal ET content did 5 and 20 hr after reperfusion. BUN level increased 5 and 20 hr after reperfusion. These results strongly suggest that the endogenously increased ET may be one of the important deleterious mediators in the pathogenesis of ischemic acute renal failure.
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Shibouta et al. (1990) studied this question.
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