Intra- and extrarenal vascular changes in the acute renal failure of the rat caused by mercury chloride.
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.
D058186:Acute Kidney Injury / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology; D000818:Animals; D001158:Arteries / Q000473:pathology*; D001794:Blood Pressure; D002199:Capillary Permeability; D007668:Kidney / Q000098:blood supply*; D007683:Kidney Tubular Necrosis, Acute / Q000473:pathology; D007684:Kidney Tubules / Q000473:pathology; D008297:Male; D008630:Mercury Poisoning / Q000473:pathology* / Q000503:physiopathology; D008854:Microscopy, Electron; D009130:Muscle, Smooth / Q000473:pathology; D051381:Rats; D013997:Time Factors; D014666:Vasomotor System / Q000503:physiopathology