一氧化氮合酶对早期内毒素休克猕猴肾脏的影响

目的 探讨早期内毒素休克肾脏损伤的发病机制。方法 猕猴11只，随机分成两组：对照组5只静脉注射生理盐水；实验组6只，静脉注射脂多糖（LPS）2．8mg／kg。LPS攻击后120min，处死动物，取肾脏标本，用免疫组化方法卵白素一生物素一过氧化物酶法（ABc法）]进行内皮型一氧化氮合酶（eNOs）和诱导型一氧化氮合酶（iNOS）染色。观察eNOS和iN0s在早期猕猴内毒素休克肾脏中的表达，同时观察肾脏超微结构的改变、酸性磷酸酶（ACP）活性变化。结果LPS攻击后120min，可见肾脏组织超微结构明显破坏和细胞内溶酶体数量增加。实验组iN0s在肾小球血管内皮、肾小管上皮、肾小球血管内和肾小管周围均有表达，对照组无表达。eNOS在实验组和对照组的肾小球血管内皮及周围血管内皮细胞均有表达。结论 一氧化氮在猕猴内毒素休克早期肾脏损伤中发挥了重要作用。

Effects of nitric oxide synthases on kidney in early phase of endotoxic shock in macaque

Objective To study the pathogenesis of kidney injury in early-phase of endotoxic shock. Methods Eleven macaques were anesthetized and randomly divided into two groups: an experimental group (n=6), receiving a dose of 2.8 mg/kg lipopolysaccharides (LPS) by intravenous injection, and a control group (n=5), injected with normal saline of 1 ml/kg. The animals were sacrificed 120 minutes following endotoxin injection. With immunohistochemical technique endothelium nitric oxide synthases (eNOS) and inducible nitric oxide synthases (iNOS) protein of the renal tissue were determined. The ultrastructure was studied with electron microscope. Acid phosphatase (ACP) was also assayed. Results One hundred and twenty minutes after LPS challenge, damages to the glomerulus and renal tubules were found, and lysosomes were increased in the renal cells. iNOS was positively expressed in vascular endothelium of glomerulus and epithelium of renal tubules in the experimental group, but not in the control group. eNOS was positively expressed in vascular endothelium of glomerul; and peri-vascular region in both groups. Conclusion The present findings indicate that NO contributed to the pathogenesis of renal injury in the early phase of endotoxic shock in primates.