Zimmermann H D, Schmidt E, Weller E, Becker C, Dieker P
Virchows Arch A Pathol Anat Histol. 1977 Jan 20;372(4):259-85. doi: 10.1007/BF00432403.
Histologic evidence of intrarenal vasomotor changes were observed in the rat in the course of acute renal failure caused by the injection of HgCl2. Male Wistar rats injected s.c. with 2.5 or 4.7 mg HgCl2 per kg b. wt. developed fibrinoid damage in the media segments of preglomerular renal vessels, mostly in the arcuate and interlobular arteries. The lesions were patchy and irregularly scattered throughout the kidneys. 24 h post-injection the lesions were very rare and of only mild degree, whereas they were fully developed and regularly seen 48 h post-injection. A high percentage of similar changes was found in certain extrarenal vascular areas especially in the mesentery and pancreas. The damaged vascular segments were usually dilated. The results of various thichrome stains and histochemical reactions suggested edema of vascular smooth muscle cells and imbibition of the media by blood plasma substances, sometimes reaching the degree of fibrinoid necrosis. These findings were confirmed by electron microscopy. The imbibition of the smooth muscle cells by blood plasma material was clearly evidenced by the demonstration of intracellular fibrin precipitations. In connection with the degeneration of smooth muscle cells, accumulations of crystal-like fibrin formations could often be shown. Subendothelial fibrin formations were not observed. 96 h after the 2.5 mg injection the changes were already regressing, but edema of the vascular wall and signs of disturbed vasotonia persisted for several days. The maximum of the vascular changes usually coincided with the maximum of azotemia and the formation of debris cylinders in the renal tubules. However, no clear relationship was recognizable in individual cases between vascular damage, extent of tubular necrosis and renal function. The pathogenesis of the vascular changes is obscure, but neurogenic factors, increased release of catecholamines and/or vasoactive agents of renal origin in connection with other factors might play a decisive role. Arterial hypertension was absent. It is assumed that the structural damage of the vascular media is mainly brought about by prolonged or recurring vasospasms, or by alternating spasm and vasodilatation with local ischemia and increased tension of the vascular wall in the dilated segments. The altered function and structure of the vascular wall might, to a certain extent, contribute to renal insufficiency.
在注射氯化汞所致急性肾衰竭过程中，在大鼠体内观察到肾内血管运动变化的组织学证据。给雄性Wistar大鼠皮下注射每千克体重2.5或4.7毫克氯化汞后，肾小体前血管的中膜段出现纤维蛋白样损伤，主要见于弓形动脉和小叶间动脉。病变呈斑片状，不规则地散布于整个肾脏。注射后24小时，病变非常罕见且程度较轻，而在注射后48小时则充分发展且经常可见。在某些肾外血管区域，尤其是肠系膜和胰腺中，发现了高比例的类似变化。受损的血管段通常扩张。各种硫堇染色和组织化学反应的结果提示血管平滑肌细胞水肿以及血浆物质浸润中膜，有时达到纤维蛋白样坏死程度。这些发现通过电子显微镜得到证实。血浆物质对平滑肌细胞的浸润通过细胞内纤维蛋白沉淀得以清晰证明。与平滑肌细胞变性相关，经常可见结晶样纤维蛋白形成的积聚。未观察到内皮下纤维蛋白形成。注射2.5毫克氯化汞96小时后，变化已开始消退，但血管壁水肿和血管张力紊乱的迹象持续了数天。血管变化的高峰期通常与氮质血症的高峰期以及肾小管中碎屑管型的形成相一致。然而，在个别病例中，血管损伤、肾小管坏死程度与肾功能之间未发现明确关系。血管变化的发病机制尚不清楚，但神经源性因素、儿茶酚胺释放增加和/或肾脏来源的血管活性物质与其他因素可能起决定性作用。未出现动脉高血压。据推测，血管中膜的结构损伤主要是由长期或反复的血管痉挛，或由痉挛与血管扩张交替出现伴局部缺血以及扩张段血管壁张力增加所致。血管壁功能和结构的改变可能在一定程度上导致肾功能不全。
