Puré E, Needleman P
J Cardiovasc Pharmacol. 1979 May-Jun;1(3):299-309. doi: 10.1097/00005344-197905000-00003.
Isolated perfused rabbit mesenteric blood vessels selectively metabolized arachidonic acid to prostacyclin (prostaglandin I2). However, the less lipid soluble prostaglandin endoperoxide (PGH2) administered exogenously was not metabolized by vascular prostacyclin synthetase but was partially degraded to prostaglandin E2 (PGE2). Peptide stimulation (e.g., angiotensin II, bradykinin) resulted in formation of both PGI2 and PGE2 from endogenous arachidonic acid. Denuding the blood vessels of their endothelial layer by perfusion with hypotonic fluid did not affect the metabolism of arachidonic acid or the response to peptide stimulation, suggesting that the cyclooxygenase, prostacyclin synthetase, and angiotensin II receptors are present and functional in the subendothelial smooth muscle cells of the vessel walls. In contrast, exogenous PGH2 either escaped completely unmetabolized or was converted to both PGI2 and PGE2 in the presence of vascular injury induced by hypotonic fluid.
离体灌注的兔肠系膜血管可将花生四烯酸选择性地代谢为前列环素（前列腺素I2）。然而，外源性给予的脂溶性较低的前列腺素内过氧化物（PGH2）不会被血管前列环素合成酶代谢，而是部分降解为前列腺素E2（PGE2）。肽刺激（如血管紧张素II、缓激肽）可导致内源性花生四烯酸生成PGI2和PGE2。用低渗液灌注使血管内皮剥脱，并不影响花生四烯酸的代谢或对肽刺激的反应，这表明环氧化酶、前列环素合成酶和血管紧张素II受体存在于血管壁的内皮下平滑肌细胞中且具有功能。相比之下，在低渗液诱导的血管损伤存在的情况下，外源性PGH2要么完全未被代谢而逸出，要么转化为PGI2和PGE2。
