EFFECTS OF CROTALUS-DURISSUS CASCAVELLA VENOM IN THE ISOLATED RAT-KIDNEY

Citation
Amc. Martins et al., EFFECTS OF CROTALUS-DURISSUS CASCAVELLA VENOM IN THE ISOLATED RAT-KIDNEY, Toxicon (Oxford), 36(10), 1998, pp. 1441-1450
Citations number
45
Categorie Soggetti
Toxicology,"Pharmacology & Pharmacy
Journal title
ISSN journal
00410101
Volume
36
Issue
10
Year of publication
1998
Pages
1441 - 1450
Database
ISI
SICI code
0041-0101(1998)36:10<1441:EOCCVI>2.0.ZU;2-Y
Abstract
Crotalus durissus cascavella (C.d.c) is a snake usually found in scrub land of Brazilian Northeast and its bite constitutes an important publ ic health problem. Isolated kidneys from wistar rats, weighing 240 to 280 g, were perfused with Krebs-Henseleit solution containing 6 g% of previously dialysed bovine serum albumin. The effects of C.d.c venom w ere studied on the perfusion pressure (PP), urinary flow (UF), glomeru lar filtration rate (GFR), percent of sodium tubular transport (%TNa+) and percent of proximal tubule sodium transport (%pTNa(+)). All exper iments were preceded jy a 30 min internal control period and an extern al control group. The infusion of C.d.c (10 mu g ml(-1)) increased the PP, UF at 60 and 90 min of perfusion, and decreased the GFR, %TNa+ an d %pTNa(+) at 120 min of perfusion. The proximal renal tubule was the major site for this toxic effect. In the group treated with the venom we found hyalin cylinders inside ail tubules and proteinaceous materia l, alternating from moderate to intense presence in urinary space. Dex amethasone (Dexa 20 mu g ml(-1)) protected against the increase in PP, UF, and against the decrease in GFR, it produced the reversion of the effect also in %TNa+ and %pTNa(+). Indomethacin (Indo 10 mu g ml(-1)) antagonized the effect observed in PP and UF, but was not able to rev erse the changes in GFR, %TNa+ and %pTNa(+). Nifedipine (Nif 10 mu g m l(-1)) promoted a reversion of almost all functional changes, except t he %pTNa(+) was not reversed. We conclude that these alterations may b e caused by a direct action of the venom on the kidneys and indirectly by the release of mediators from endothelial cells. Dexa protected ag ainst renal lesions caused by the venom, perhaps by inhibiting phospho lipase A, a toxic component of the venom. The reversion partially indu ced by indo may be due to cyclooxygenase inhibition that will inhibit the formation of prostaglandins. Nif blocked the renal alterations tha t may involve cell calcium influx that resulted from the venom aggress ion. (C) 1998 Elsevier Science Ltd. All rights reserved.