Siren A L, Letts G, Feuerstein G
Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814-4799.
Eur J Pharmacol. 1988 Feb 9;146(2-3):331-5. doi: 10.1016/0014-2999(88)90311-1.
N-Acetyl-leukotriene E4 administered to conscious freely moving rats produced a dose-dependent vasoconstriction in the mesenteric vessels which led to profound reduction of blood flow to the gut. Renal and hindquarter blood flow and vascular resistance were not affected even by high doses of N-Acetyl-leukotriene E4. N-Acetyl-leukotriene E4 was 10-fold more potent than the thromboxane analog U-46619 and 1000-fold more potent than prostaglandin F2 alpha but 2-5-fold less potent than leukotriene D4/E4 to induce mesenteric vasoconstriction. These data indicate that N-acetyl-leukotriene E4 is a biologically active metabolite of peptide leukotrienes, and might play a role in cardiovascular derangements mediated by leukotrienes.
给清醒自由活动的大鼠注射N-乙酰白三烯E4后,肠系膜血管会出现剂量依赖性血管收缩,导致肠道血流显著减少。即使使用高剂量的N-乙酰白三烯E4,肾和后肢的血流及血管阻力也不受影响。在诱导肠系膜血管收缩方面,N-乙酰白三烯E4的效力比血栓素类似物U-46619强10倍,比前列腺素F2α强1000倍,但比白三烯D4/E4弱2至5倍。这些数据表明,N-乙酰白三烯E4是肽白三烯的一种生物活性代谢产物,可能在白三烯介导的心血管紊乱中起作用。