THE ROLE OF PROSTAGLANDINS IN MEDIATING THE EFFECTS OF ALCOHOL ON SMOOTH MUSCLE

乙醇引起的血压、血管反应性和血压的变化 血小板聚集可能有常见的病因，包括 前列腺素代谢紊乱与儿茶酚胺 分泌物。乙醇已被证明能显著改变omega-6 脂肪酸水平、前列腺素代谢和儿茶酚胺 心血管系统中的水平。前列腺素，如 前列环素(PGI2)和血栓素A2(TXA2)，还有 儿茶酚胺，如肾上腺素(E)和去甲肾上腺素(NE) 在心血管系统中很活跃，并可能在 与酒精消费相关的病理生理学。使用我们的 吸入室精确控制的自动化装置 乙醇蒸气和血液乙醇浓度的影响 乙醇剂量范围对血管张力和反应性、血小板的影响 聚集、脂肪酸含量、前列腺素产量和 测定大鼠血浆儿茶酚胺水平。急性 暴露于中等血液乙醇浓度(BEC)的人 与血管生成PGI2和血浆增加有关 儿茶酚胺减少，而TXA2的血小板生成减少。 然而，这些动物的血压会升高，而血小板 去甲肾上腺素(NE)的聚集和升压作用 略有下降。长期接触高BEC与 随着血管和血小板前列腺素的急剧减少 (PG)产量和血浆儿茶酚胺略有增加 级别。PGs的脂肪酸前体浓度为 在这些脂肪提取物中减少了高达50% 准备工作。这些动物的血压通常是降低的。 而血小板聚集率显著下降，然而， 血栓素A2和去甲肾上腺素的升压作用明显增强。 长期接触酒精并不能减少脂肪含量 PGS的酸前体或生产2系列PG的能力 饲喂富含伽马亚麻酸的饲料的动物(20：3)。

Ethanol-induced changes in blood pressure, vasoreactivity and platelet aggregation may have common etiologies which include the disruption of prostaglandin metabolism and catecholamine secretion. Ethanol has been shown to markedly alter omega-6 fatty acid levels, prostaglandin metabolism, and catecholamine levels in the cardiovascular system. Prostaglandins such as prostacyclin (PGI2) and thromboxane (TXA2), and also catecholamines such as epinephrine (E) and norepinephrine (NE) are active in the cardiovascular system and may play a role in the pathophysiology associated with ethanol consumption. Using our automated apparatus for precise control of inhalation chamber ethanol vapor and blood ethanol concentrations, the effects of a range of ethanol doses on vascular tone and reactivity, platelet aggregation, fatty acid content, prostaglandin production and plasma catecholamine levels were determined in the rat. Acute exposure to moderate blood ethanol concentrations (BEC) was associated with increased vascular production of PGI2 and plasma catecholamines, whereas platelet production of TXA2 decreased. Blood pressure is elevated in these animals, however, platelet aggregation and the pressor effect of norepinephrine (NE) were mildly decreased. Chronic exposure to high BEC is associated with a dramatic reduction in vascular and platelet prostaglandin (PG) production and a slight increase in plasma catecholamine levels. Concentrations of fatty acid precursors to PGs were reduced by as much as 50% in the lipid extracts of these preparations. Blood pressure is generally reduced in these animals and platelet aggregation decreases dramatically, however, the pressor effects of TXA2 and NE were significantly increased. Long-term ethanol exposure did not induce a reduction in fatty acid precursors of PGs or the capacity to produce 2-series PG in animals fed a diet rich in gamma-linolenic acid (20:3).