Karanian J W, Salem N
Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892.
Adv Alcohol Subst Abuse. 1988;7(3-4):221-5. doi: 10.1300/J251v07n03_28.
Rats were exposed to alcohol vapors by an inhalation technique and blood pressure and its reactivity and platelet aggregation were measured. Acute exposure to alcohol levels which produced moderate blood alcohol concentration (BAC) was associated with increased vascular production of prostacyclin (PGI2) and plasma catecholamines, whereas platelet production of thromboxane (TXA2) decreased. Blood pressure is elevated in these animals, however, the platelet aggregating and pressor effects of noradrenaline (NE) were decreased. Chronic exposure to high BAC is associated with a dramatic reduction in vascular and platelet prostaglandin (PG) production and a marked increase in plasma catecholamine levels. Platelet aggregation decreased in these animals, however, the pressor effect of TXA2 and NE was significantly increased. The fatty acid precursors to PG were reduced by 50% in the lipid extracts of these preparations. These findings suggest that alterations in fatty acid metabolism may lead to a functional deficiency in PG production from dependent rats. Qualitative differences may exist between acute and chronic exposure with respect to the cardiovascular state. Locally produced PG and circulating catecholamines may mediate alcohol-induced alterations in vascular smooth muscle tone and platelet aggregation.
通过吸入技术使大鼠暴露于酒精蒸汽中,并测量其血压、血压反应性和血小板聚集情况。急性暴露于产生中度血液酒精浓度(BAC)的酒精水平与血管前列环素(PGI2)生成增加及血浆儿茶酚胺增多有关,而血小板血栓素(TXA2)生成减少。这些动物的血压升高,然而,去甲肾上腺素(NE)的血小板聚集和升压作用减弱。长期暴露于高BAC与血管和血小板前列腺素(PG)生成显著减少及血浆儿茶酚胺水平显著升高有关。这些动物的血小板聚集减少,然而,TXA2和NE的升压作用显著增强。这些制剂的脂质提取物中PG的脂肪酸前体减少了50%。这些发现表明,脂肪酸代谢改变可能导致依赖大鼠PG生成功能缺陷。急性和慢性暴露在心血管状态方面可能存在质的差异。局部产生的PG和循环儿茶酚胺可能介导酒精诱导的血管平滑肌张力和血小板聚集改变。