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肝素给药后脂蛋白脂肪酶的消耗。

Depletion of lipoprotein lipase after heparin administration.

作者信息

Chevreuil O, Hultin M, Ostergaard P, Olivecrona T

机构信息

Department of Medical Biochemistry and Biophysics, University of Umeå, Sweden.

出版信息

Arterioscler Thromb. 1993 Oct;13(10):1391-6. doi: 10.1161/01.atv.13.10.1391.

Abstract

Some or most of the turnover of lipoprotein lipase (LPL) occurs by dissociation from vascular endothelial sites in extrahepatic tissues and further degradation in the liver. Heparin greatly enhances this dissociation and delays but does not abolish uptake in the liver, raising the possibility that heparin could lead to accelerated catabolism of functional LPL. To investigate this, we determined time curves for heparin (anti-factor Xa activity) and for LPL and hepatic lipase after injection in rats of two doses of conventional unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH). The high dose (250 U/kg) of both heparins resulted in similar initial levels of LPL activity in plasma, but at 30 minutes the activity with LMWH had declined by more than 80%, whereas with UFH it remained essentially unchanged during this time. In contrast, time curves for heparin activity in blood were similar for the two heparins. The low dose (50 U/kg) led to lower initial levels of LPL activity with LMWH in spite of slower elimination of heparin activity from the blood. These results agree with previous studies that indicate that LMWH has a similar ability as UFH to release LPL, but a lesser ability to delay its removal by the liver. Only slight differences were noted in the time curves for hepatic lipase with the two heparins. To assess the possible depletion of the lipases, we administered a second large dose of conventional heparin. One hour after the first injection, the second injection resulted in lower plasma LPL activities in all four groups.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

脂蛋白脂肪酶(LPL)的部分或大部分更新是通过从肝外组织的血管内皮部位解离,并在肝脏中进一步降解来实现的。肝素可极大地增强这种解离作用,并延迟但不会消除其在肝脏中的摄取,这增加了肝素可能导致功能性LPL分解代谢加速的可能性。为了对此进行研究,我们测定了在大鼠中注射两剂常规普通肝素(UFH)或低分子量肝素(LMWH)后,肝素(抗Xa因子活性)、LPL和肝脂肪酶的时间曲线。两种肝素的高剂量(250 U/kg)导致血浆中LPL活性的初始水平相似,但在30分钟时,LMWH组的活性下降了80%以上,而UFH组在此期间基本保持不变。相比之下,两种肝素在血液中的肝素活性时间曲线相似。低剂量(50 U/kg)导致LMWH组LPL活性的初始水平较低,尽管肝素活性从血液中的消除较慢。这些结果与之前的研究一致,即LMWH与UFH释放LPL的能力相似,但延迟肝脏对其清除的能力较弱。两种肝素在肝脂肪酶的时间曲线上仅观察到细微差异。为了评估脂肪酶可能的耗竭情况,我们给予了第二剂大剂量的常规肝素。在第一次注射后1小时,第二次注射导致所有四组的血浆LPL活性降低。(摘要截断于250字)

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