Effect of Endotoxin on Acute Renal Failure Induced by High-Dose Cisplatin in Rats

[Objective] To study the relationship between plasma endotoxin and renal function in acute renal failure induced by high dose cisplatin (DDP) in rats. [Method] 36 SD rats were divided randomly into 6 groups: DDP 6 h, DDP 48 h, DDP control, normal saline (NS) 6 h, 48 h and NS control group ( n = 6 in each group). 10 mg/kg DDP was injected intraperitoneally while same volume of natural saline was given as the control. Toxic effects of DDP were observed subsequently. Heparinized blood samples were obtained by heart punctures 6 h and 48 h after DDP and NS administration and plasma endotoxin was measured by using the BET-16 bacterium endotoxin cryoscope. At the same time blood samples were obtained from orbital venous sinus and blood urea nitrogen (BUN) and creatinine (Cre) were measured by automatic biochemistry analyzer. [Result] Body weight of the rats decreased significantly at 6 h after DDP administration; diarrhea increased progressively at 48 h after DDP administration and the rats died in 3 d. There were no significant differences in blood BUN and creatinine between cisplatin group and control group 6 hours after administrations (P >;0.05); Blood BUN and Cre increased to (18.71 ±9.9) mmol/L and (49.6±14.1) μmol/L respectively in rats 48 h after DDP administrations, significantly higher than the (7.48 ±0.6) mmol/L and (27.17±1.7) μmol/L in control group (P<;0.05). Plasma endotoxin decreased below the detection limit of 0.0218 Eu/ml 6 h after DDP administration, significantly lower than the (0.3141±0.1477) Eu/ml in control group (P<;0.01), while it increased above the detection limit of 0.70 Eu/ml 48 h after DDP administration, obviously higher than the (0.1661 ±0.1198) Eu/ml in control group ( P<;0.01). [Conclusion] Although there was no positive correlation between plasma endotoxin and renal injure in 6 h after DDP administration, the increase of plasma endotoxin may be an important p- - athophysiological factor of cisplatin-induced nephrotoxicity.