[Pharmacological studies on experimental nephritic rats (13). The development and aggravation of nephritis due to the repeated administration of liquoid (author's transl)].
In order to elucidate the role of blood coagulation system in the development and aggravation of glomerulonephritis, liquoid (Liq) was repeatedly administered to normal or nephritic rats. When Liq 10 mg/kg was given i.v. daily X 22 to normal rats (group I), the urinary excretions of protein and N-acetyl-beta-glucosaminidase and urea nitrogen content did not significantly change as compared with those in the normal control group. In rats given Liq 10 mg/kg i.v. either every 3 days X 8 (group III) or every day X 22 (group IV) from the 15th day after the i.v. administration of anti-rat glomerular basement membrane rabbit serum (AGS) [0.5 ml/150g body weight], these biochemical parameters were not significantly different from those of nephritic control rats given AGS only (group II). The deposits of fibrin or fibrinoids in glomeruli of groups I, II, III and IV, examined by a fluorescence antibody technique were evident in 2, 2, 8 and 10, respectively, out of 10 rats in each group, although the degree of deposition was slight. Under light microscopy, the adhesion between the glomerular capillary wall and Bowman's capsule, hypercellularity, crescent formation and hyalinization were demonstrated in a part of glomeruli, even in group I. concerning the influence of Liq in nephritic rats, the most prominent glomerular change was hyalinization. While in group II the hyalinization was evident in only 17% of glomeruli, in groups III and IV the hyalinization was 41 and 55%, respectively. Although no significant difference was seen between groups II and III regarding other glomerular changes except for hypercellularity, these changes in group IV increased as compared with those in group II. However, hypercellularity was less in groups III and IV than in group II. A slight occlusion of the glomerular capillary lumen was observed, even in group I. In nephritic groups, the degree of the capillary lumen occlusion in group IV was greater than that in group II. From these results, the acceleration of intraglomerular blood coagulation is considered to be a major factor in the development and aggravation of glomerulonephritis.
D000818:Animals; D001557:Benzenesulfonates / Q000008:administration & dosage*; D001835:Body Weight / Q000187:drug effects; D003029:Coagulants / Q000008:administration & dosage*; D005921:Glomerulonephritis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D007106:Immune Sera; D007668:Kidney / Q000473:pathology; D008297:Male; D011074:Polyanetholesulfonate / Q000008:administration & dosage*; D051381:Rats; D011919:Rats, Inbred Strains
D001557:Benzenesulfonates; D003029:Coagulants; D007106:Immune Sera; D011074:Polyanetholesulfonate