Effect of renal hemodynamics of intrarenal arterial infusion of Russell's viper venom in dogs

Abstract

The effect of an intrarenal arterial infusion of Russell’s viper venom (RVV) on renal hemodynamic and histopathological changes were investigated in 18 adult male dogs. Dogs were divided into three groups: group I was the control group and infused with 5 ml of an isotonic saline solution, group II and III were experimental groups and infused with RVV 0.05 and 0.1 mg/kg bw., respectively. The renal functions of both kidneys were determined throughout the experimental period of 5 hour postinfusion. The histopathological studies were performed in all groups. In comparison between pre and post experimental periods, either RVV 0.05 or 0.1 mg/kg bw. Was able to produce a sharp decrease in mean arterial pressure and renal blood pressure over fifteen minutes period and then recurred to the control level. An effective renal plasma flow, renal blood flow and also glomerular filtration rate were decreased significantly whereas renal vascular resistance was increased persistently throughout the experimental period. Urine flow rate was diminished consequently, accompanied with a decrease in glomerular filtration rate. It was also noted that oliguria was seen in the first hour, following by polyuria in the second and third hour and then returned to the oliguria again. Hemoglobinuria as well as intravascular hemolysis was usually found which confirmed by an increase in plasma potassium concentration. In all kidneys, filtered loads of electrolytes were reduced significantly. Obviously, an increase in fractional excretion of sodium following venom administration was exhibited. Plasma creatinine was elevated slightly while blood urea nitrogen increased significantly. In comparison between both kidneys, the renal hemodynamic alterations were more prominent in the infused kidney than the contralateral one. The morphological changes of both kidneys were compared, RVV 0.05 mg/kg bw. Produced glomerular congestion with degeneration of proximal tubular cells diffusely. Tubular necrosis was infrequently noted scattering in the renal parenchyma and diffuse congestion of the interstitium was seen. Additionally, renal tubular cells following RVV 0.1 mg/kg bw. Infusion were undergoing variable degree of degeneration and frequent tubular necrosis. There were occationally clumps of red blood cell in tubular lumen and glomeruli as well. Small number of segmented neutrophils was seen infrequently infiltrating the interstitium. Scattered foci of interstitial hemorrhage and wedge-shaped area of hemorrhagic necrosis were noted. However, the direct infused kidney of both groups was more damaged and seen seriously. In conclusion, the RVV produced an initial hypotension associated with a decline in glomerular filtration and tubular reabsorption. Hence, the pathophysiological changes of oliguric renal failure may affected from two components. Firstly, is an initial hypotension which primarily responsible for decrease in renal function. Secondly, a direct nephrotoxicity may play a role and leading to a decrease in glomerular filtration and tubular reabsorption. Therefore, the alterations of renal functions might be potentiated by hypotension, intravascular hemolysis and coagulation abnormality.