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动态观察了大鼠静注内皮素（ＥＴ－１）后肾脏组织学及超微结构变化，同时检测了肾功能（ＢＵＮ、Ｃｒ）及肾组织ＭＤＡ、前列腺素的含量，对ＥＴ作用下肾脏病变发生的机理进行了初步探讨。结果发现：ＥＴ可引起肾脏损伤，光镜下见肾小球毛细血管发生收缩（０．５ｈ）、舒张甚至扩张的变化，肾小管上皮出现局灶性水样变性、坏死，以３、２４ｈ明显。电镜下肾小球的变化更为突出，早期可见内皮细胞肿胀、窗孔减少；脏层上皮细胞足突局部融合。后期可见细胞（内皮、系膜细胞）肥大，４８ｈ出现系膜细胞明显增生。肾功能的变化与肾脏病理变化相平行，且肾功能的变化与肾组织ＭＤＡ的变化明显相关。表明：本试验条件下ＥＴ可引起肾脏损伤发生，其所致的肾脏病变尤其是肾小球的变化是肾功能降低的形态学基础，提示ＥＴ在ＡＲＦ的发生发展中具有重要作用。此外本研究尚提示脂质过氧化增强是ＥＴ作用下肾损伤的重要因素之一。
The renal histological and ultrastructural changes were observed dynamically after ET-1 in rats, meanwhile, the renal function (BUN, Cr) and the contents of MDA and prostaglandin in renal tissue were detected. The renal lesions The mechanism of the occurrence of a preliminary discussion. The results showed that: ET can cause renal damage, under the light microscope see glomerular capillaries contraction (0.5h), diastolic or even expansion of the expansion of the tubular epithelial cells showed focal watery degeneration and necrosis, to 3,24h significantly . Electron microscopic glomerular changes are more prominent early visible endothelial cell swelling, window reduction; visceral epithelial cells foot process local fusion. Late visible cells (endothelial, mesangial cells) hypertrophy, mesangial cells 48h obvious proliferation. Changes in renal function and pathological changes in parallel with the kidney, and changes in renal function and changes in renal tissue MDA was significantly correlated. It is indicated that ET can cause renal injury under the conditions of this experiment. The changes of renal lesions, especially glomeruli, are the morphological basis of renal function decline, suggesting that ET plays an important role in the occurrence and development of ARF. In addition, this study still suggests that lipid peroxidation is one of the important factors of renal injury under ET.