Bagby G J, Spitzer J A
Am J Physiol. 1980 Mar;238(3):H325-30. doi: 10.1152/ajpheart.1980.238.3.H325.
The present studies were designed to delineate changes in heart and adipose tissue lipoprotein lipase (LPL) activity following the administration of E. coli endotoxin. Plasma triglyceride levels were elevated in animals given endotoxin compared to saline-injected controls. Heart LPL activity decreased from 126.4 mumol fatty acid released per gram wet wt per hour in control rats to less than 22.5 mumol . g-1 . h-1 by 7 h following the injection of endotoxin. Although endotoxin was administered in doses producing 0-100% mortalities in a 24-h period, myocardial LPL activity was depressed to the same extent (75-80%) regardless of dose. The response of adipose tissue was less pronounced. Epididymal fat pad LPL activity fell significantly over the 24-h observation period in control and endotoxin-treated rats with the latter group somewhat more depressed 7 h after treatment. The findings are consistent with the suggestion that hypertriglyceridemia often observed during endotoxic shock may be related to depressed LPL activity; the degree of depression is probably tissue dependent.
本研究旨在描述大肠杆菌内毒素给药后心脏和脂肪组织脂蛋白脂肪酶（LPL）活性的变化。与注射生理盐水的对照组相比，给予内毒素的动物血浆甘油三酯水平升高。心脏LPL活性从对照大鼠每克湿重每小时释放126.4微摩尔脂肪酸降至注射内毒素后7小时的每克湿重每小时低于22.5微摩尔。尽管内毒素的给药剂量在24小时内产生了0 - 100%的死亡率，但无论剂量如何，心肌LPL活性均下降至相同程度（75 - 80%）。脂肪组织的反应不太明显。在对照大鼠和内毒素处理的大鼠中，附睾脂肪垫LPL活性在24小时观察期内显著下降，后一组在处理后7小时下降得更明显。这些发现与以下观点一致，即内毒素休克期间经常观察到的高甘油三酯血症可能与LPL活性降低有关；降低程度可能取决于组织。
