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免疫复合物对兔血浆甘油三酯的影响。

Effects of immune complexes on plasma triglycerides in rabbits.

作者信息

Kerttula Y, Weber T H, Wager O

出版信息

Atherosclerosis. 1980 Apr;35(4):451-9. doi: 10.1016/0021-9150(80)90186-0.

Abstract

The effect of immune complexes on plasma lipids, especially triglycerides (TG) was studied in rabbits. After a single intravenous dose of bovine serum albumin (BSA), serological aberrations suggestive of immune complexes appeared around the 14th day. Changes in the plasma TG or cholesterol values were not observed within a follow-up period of 4 weeks. However, reimmunization with a second dose of BSA 2 months later led to a significant decrease in plasma TG (P less than 0.01). In fat tolerance tests TG emulsion was given intravenously to rabbits immunized 14 days earlier with BSA. The elimination curve of exogenous TG (followed for 100 men) was in its first phase exponential and in it second phase linear in all experimental groups. The significance of the second phase, however, has to be interpreted with some caution because of the possible recirculation of TG into the blood stream. In the rabbits immunized with one dose of BSA the fractional removal rate of TG did not differ from that of the controls. However, in the rabbits reimmunized with a second dose of BSA 2 months later the fractional removal rate of TG was greater than in the controls (P less than 0.01). It was concluded that immune complex lesions under certain circumstances may affect the TG metabolism. The mechanism concerned may be increased permeability of the injured vascular endothelial cells, possibly through the increased release of lipoprotein lipase (LPL).

摘要

在兔子身上研究了免疫复合物对血浆脂质,尤其是甘油三酯(TG)的影响。单次静脉注射牛血清白蛋白(BSA)后,在第14天左右出现了提示免疫复合物的血清学异常。在4周的随访期内未观察到血浆TG或胆固醇值的变化。然而,2个月后再次注射第二剂BSA导致血浆TG显著降低(P<0.01)。在脂肪耐量试验中,给14天前用BSA免疫的兔子静脉注射TG乳剂。在所有实验组中,外源性TG的消除曲线(观察100分钟)在第一阶段呈指数形式,在第二阶段呈线性。然而,由于TG可能再循环进入血流,对第二阶段的意义必须谨慎解释。在用一剂BSA免疫的兔子中,TG的分数清除率与对照组无差异。然而,在2个月后再次注射第二剂BSA的兔子中,TG的分数清除率高于对照组(P<0.01)。得出的结论是,在某些情况下,免疫复合物损伤可能会影响TG代谢。相关机制可能是受损血管内皮细胞的通透性增加,可能是通过脂蛋白脂肪酶(LPL)释放增加所致。

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