高钙,低磷饲料致鸡痛风的病理学研究

用200只21日龄海赛克斯×罗斯杂交商品代鸡,按钙、磷2×2因子设计进行高钙、低磷饲料人工诱发痛风试验。采用病理形态学及血液生化测定方法进行了十三周的试验观察。结果表明,高钙低磷、高钙正磷饲料能引起鸡痛风。尿酸盐沉积形式有内脏性尿酸盐沉积和尿石症。高钙起主导作用,低磷可以促进其发生。痛风发生的原发性损伤部位及病变最严重的器官是肾脏。饲料高钙导致的高钙血症、低磷血症及代谢性碱中毒,通过改变尿液环境而引起尿石症的发生。高钙所致的肾小管原发性损伤和继发于尿石症的损害共同导致鸡肾功能衰竭,而形成高尿酸血症,并出现内脏性尿酸盐沉积。

THE PATHOLOGY OF CHICKEN GOUT INDUCED BY HIGH DIETARY CALCIUM AND LOW DIETARY PHOSPHORUS

Two hundred 21-day-old chicks were divided into four diet treatment groups of 50 each and given a . high calcium and low available phosphorus ( HCLP ) , high calcium and normal available phosphorus ( HCNP ) , normal calcium and low available phosphorus ( NCLP ) ,or normal calcium and normal available phosphorus (NCNP) diets to study the effect of high dietary calcium and low dietary phosphorus on the development of chicken gout and the mechanism of urate deposition, the result shows that HCLP and HCNP diets caused visceral urate deposition and urloithiasis. Kidney was the primarily and worst injured organ in the development of the gout. High dietary calcium caused hypercalciumemia and hypophosphorusemia, and in cooperation with low dietary phosphorus caused metabolism alkalosis, which resulted in urloithiasis by changing urine property. Renal failure was caused by secondary renal tubul injury following urloithiasis and primary injury by high calcium, which resulted in hyperuricemia and visceral urate deposition.