离体灌注大鼠小肠对血小板活化因子的反应中白三烯C4的释放
Release of leukotriene C4 by isolated, perfused rat small intestine in response to platelet-activating factor.
作者信息
Hsueh W, Gonzalez-Crussi F, Arroyave J L
出版信息
J Clin Invest. 1986 Jul;78(1):108-14. doi: 10.1172/JCI112538.
Abstract
We reported a rat model of necrotizing enterocolitis by injecting platelet-activating factor (PAF) into the mesenteric vascular bed, and suggested that leukotrienes (LT) are secondary mediators. The present study, using isolated, buffer-perfused rat small intestine, shows: Isolated, perfused small intestine synthesizes LTs in response to PAF. Leukotriene C4 (LTC4) was the predominant LT released. The initial vasoconstriction after PAF injection was due to a transient release of LTC4 since FPL 55712 pretreatment abolished the vasoconstriction. The sustained rise in perfusion pressure was also blocked by FPL 55712, which suggests that other vasoconstrictors released are regulated by LTs. The vasoconstrictor(s) responsible for sustained rise in perfusion pressure is unknown, but is not thromboxane. Most of the LT was released from intestinal tissue rather than mesenteric arteries. Vasodilating prostaglandins (PGs) were also released, probably secondary to LTs. The complex interaction of these lipid mediators (PAF, LTs, and PGs) and their subtle balance may affect the course of the disease.
摘要
我们报道了一种通过向肠系膜血管床注射血小板活化因子（PAF）建立的坏死性小肠结肠炎大鼠模型，并提出白三烯（LT）是继发性介质。本研究使用离体、缓冲液灌注的大鼠小肠，结果显示：离体灌注的小肠在PAF作用下合成LT。白三烯C4（LTC4）是释放的主要LT。注射PAF后的初始血管收缩是由于LTC4的短暂释放，因为FPL 55712预处理可消除血管收缩。FPL 55712也可阻断灌注压的持续升高，这表明释放的其他血管收缩剂受LT调节。导致灌注压持续升高的血管收缩剂尚不清楚，但不是血栓素。大多数LT是从肠道组织而非肠系膜动脉释放的。血管舒张性前列腺素（PGs）也会释放，可能继发于LT。这些脂质介质（PAF、LT和PGs）的复杂相互作用及其微妙平衡可能会影响疾病的进程。
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