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

我们的目标是扩大我们的数据库，以包括一场 体内乙醇暴露对血管反应性的影响 提到前列腺素系统参与了这种影响。 吸入室及监控装置的设计与安装 对于乙醇蒸气暴露范例，我们可以检查 血液乙醇浓度分级(BEC)的心血管后果 在急性和慢性接触期间。为此目的，(1)平滑 建立了肌肉沐浴系统，用于测定分离的 血管系统，使用力位移传感器，以及(2)线束和 为了维持可行走大鼠的插管，建立了系绳系统 同时测量血压(全身动脉压)和 它的反应性，使用压力传感器。我们的体外实验结果是 大鼠主动脉，短期(1天)或长期(14天) 暴露在乙醇蒸气中，表现出关于 对类似血栓素的收缩反应；中度BEC降低 收缩能力，而高水平则没有影响。相似处理的大鼠 显示PGI-2/TXA-2比率显著增加，主要原因是 PGI-2水平升高，这与 伸缩性。大鼠主动脉中PGI-2水平不受影响 具有较高的BEC。长期暴露在乙醇蒸气中会导致类似的 PGI-2/TXA-2比值，但降低这些前列腺素的绝对水平，这 可能是花生四烯酸枯竭所致。 初步研究表明，血压及其反应性 与这些大鼠的BEC有关。急性生理性暴露于 可耐受的BEC可降低血压，并与时间直接相关 暴露在乙醇蒸气中。而高盐大鼠血压升高。 在酒精暴露6天后。血管反应性在正常人中增强 同样暴露在乙醇蒸气中的大鼠；血管加压剂和 血管降压作用明显增强。

The objective was to extend our data base to include the effects of an in vivo ethanol exposure paradigm on vascular reactivity with particular reference to the involvement of the prostaglandin system in such effects. The design and setup of inhalation chambers and a monitor/control apparatus for an ethanol vapor exposure paradigm has allowed us to examine the cardiovascular consequences of graded blood ethanol concentrations (BEC) during acute and chronic exposure periods. For this purpose, (1) a smooth muscle bath system was set up to measure reactivity of isolated vasculature, using force displacement transducers, and (2) a harness and tether system was set up in order to maintain a cannula in ambulatory rats while measuring changes in blood pressure (systemic arterial pressure) and its reactivity, using pressure transducers. Our in vitro results in the rat aorta, following either short-term (1-day) or long-term (14-day) exposure to ethanol vapor, show a biphasic response with regard to the contractile response to a thromboxane-mimic; moderate BEC decreased contractility, whereas high levels had no effect. Similarly treated rats showed a marked increase in the PGI-2/TXA-2 ratio, due primarily to increased PGI-2 levels, which coincided with a depression in contractility. PGI-2 levels were not affected in aorta obtained from rats with high BEC. Chronic exposure to ethanol vapor resulted in a similar PGI-2/TXA-2 ratio but lower absolute levels of these prostaglandins, which may have resulted from arachidonate depletion. Preliminary studies indicate that blood pressure and its reactivity is related to the BEC in these rats. Acute exposure to physiologically tolerable BEC depressed blood pressure and was directly related to the time of exposure of ethanol vapors. However, the BP of high-salt rats increased after 6 days of ethanol exposure. Vasoreactivity was enhanced in normal rats following a similar exposure to ethanol vapors; both vasopressor and vasodepressor effects were markedly potentiated.