Effect of russell's viper venom on the renal handling of inorganic phosphorus in dogs

Abstract

The investigation was performed to study the effects of Russell’s viper venom on general circulation and renal function on the relation to renal handling of inorganic phosphorus. Experiment was done on sixteen anesthetized male mongrel dogs. Two groups of eight animals were devided into intact animals as control group and thyroparathyroidectomized (TPTX) group. Each animal recived 0.02 mg/kg.bw of Russell’s viper venom by intrarenal arterial infusion at the rate of 0.32 ml/min. During initial post infusion period, a transient fall in mean arterial blood pressure (MAP), narrow pulse pressure (PP) and a decrease in heart rate (HR) were observed in intact and TPTX animals. A rising in mean arterial blood pressure, narrowing in pulse pressure and heart rate were significant throughout the experiment following a transient decrease. The magnitude of the rising in mean arterial blood pressure, heart rate and narrowing in pulse pressure was apparent in intact animals whereas, the TPTX animals was returned to the control level within a short time. The packed cell volume increased slightly at the initial postinfusion period, then it gradually declined to control level in both groups. Plasma sodium, chloride and calcium concentrations did not alter throughout the experiment in both groups. The plasma calcium concentration of TPTX group showed significant less than the intact group throughout the study period. The plasma potassium concentration increased significantly throughout the experiment in intact and TPTX groups. Plasma inorganic phosphorus concentration of TPTX animals increased significantly during 1 ½ - 3 hours after envenomation and it returned to the control level within 4 hours period. The renal plasma flow, renal blood flow, glomerular filtration rate, urine flow rate and filtered load of electrolysters decreased significantly in accordance with the increase in renal vascular resistance throughout the postinfusion period of both groups. The magnitude of those responses of TPTX animals were alleviated and returned to control level within a short time as compared to the intact animals. Free water clearance of intact animals increased slightly during the initial postinfusion period, while it decreased gradually throughout the experiment in the TPTX animals. The initial changes in free water clearance of both groups were not statistically significant, but at 4-5 hours after envenomation a significant differences between groups were apparent. The filtration fraction increased slightly at the initial postinfusion period and then it declined to the control level till the end of experiment. There was no significant difference in filtration fraction between intact and TPTX groups. The urinary excretion of sodium, potassium, chloride, calcium, inorganic phosphorus and titratable acid of both groups decreased significantly along with to a decrease in the rate of urine flow. The decrease of those variables of TPTX group were alleviated and returned to control condition within a short time when compared with the intact group. The fractional excretion of potassium increased significantly in both groups after envenomation. The fractional excretion of sodium, calcium and inorganic phosphorus of TPTX group increased significantly at the last portion of postinfusion period, while it showed a tendency to increase in intact group. The fractional excretion of chloride showed the same respond as fractional excretion of sodium of each group. These date indicate that TPTX alleviated the effect of Russell’s viper venom on general circulation, renal hemodynamics and tubular function as compared to the intact animals. It is possible that, extracellular calcium concentration contributed to the sequence of intracellular events which culminate in those response. It could be concluded that the phosphaturic effect of Russell’s viper venom in independent on parathyroid hormone, hypocalcemia and extracellular volume expansion. The hyperphosphaturia is most likely mediated by aninhibition on sodium-inorganic phosphate cotransport system in the renal tubule. Possible disturbance in acid-base balance could not be rules out during envenomation.