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Intrarenal Regulating Mechanisms for Renal Hemodynamics during Shock.

机译:肾功能休克时肾脏血流动力学的肾内调节机制。

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Several models of experimental acute renal failure were used to study the leakiness of the tubular epithelium to inulin, the change in intratubular hydrostatic pressure and the operation of the tubulo-glomerular feedback mechanism. The results show that (1) leakage of the acutely damaged tubular epithelium cannot be the causal factor for low inulin clearance, (2) the variability of the intratubular pressure in the acutely damaged kidney precludes the possibility that increased pressure is always associated with acute renal failure and (3) the operation of the tubulo-glomerular feedback mechanism is maintained in acute renal failure and preserves body fluids by glomerular shutdown, with resulting oliguria. (Author)

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