动物模型中败血症引起的急性肾衰竭和肾小管损伤。

A L Linton, J F Walker, R M Lindsay, W J Sibbald
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引用次数: 0

摘要

绵羊盲肠穿孔引起全身性脓毒症。血液动力学参数的连续测量显示,随后的全身性败血症导致心输出量增加和全身抵抗力下降,与已知发生在人类中的情况相当。这些动物的肾小球滤过率在诱导脓毒症48小时后显著下降,在发现低分子量蛋白尿和溶菌酶清除率增加时,有证据表明小管损伤。肾脏病理检查显示肾小球正常,光镜下小管细胞无一致变化,免疫荧光阴性,但EM下近端小管细胞结构改变。在该模型中,非低血压脓毒症可预测地对近端小管细胞造成损害,并伴有GFR降低。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Acute renal failure and tubular damage due to sepsis in an animal model.

Generalised sepsis was induced in sheep by caecal perforation. Serial measurement of haemodynamic parameters revealed that the subsequent generalised sepsis induced increased cardiac output and decreased systemic resistance comparable to that known to occur in man. Glomerular filtration rate in these animals fell significantly 48 hours after induction of sepsis and there was evidence of tubular damage in the finding of low molecular weight proteinuria and increased clearance of lysozyme. Pathological examination of the kidney revealed normal glomeruli, no consistent changes in tubular cells on light microscopy, negative immunofluorescence, but structural changes in proximal tubular cells on EM. In this model, non-hypotensive sepsis predictably produces damage to proximal tubular cells accompanied by reduction in GFR.

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