Jakupi M, Dreshaj I A, Mandura I, Haxhiu M A
Institut za klinicku fiziologiju, Medicinski fakultet, Pristina.
Plucne Bolesti. 1991 Jan-Jun;43(1-2):16-20.
The response of the pulmonary artery smooth muscle tone to ethanol, and the effects of haloperidol (a dopaminergic receptor blocker), propranolol (a beta-adrenergic receptor blocker) and verapamil (a calcium channel blocker) on the response to ethanol were studied using the dog pulmonary artery smooth muscle. The results have shown that ethanol consistently induces a dose-dependent contraction of pulmonary artery smooth muscle which is not substantially modulated by the prior administration of haloperidol, but is partially blocked by propranolol, suggesting that catecholaminergic receptors are partly involved in the mediation of the ethanol induced pulmonary artery smooth muscle contraction. However, the results of this study have shown that ethanol induced contraction of pulmonary smooth muscle is not altered by verapamil in doses which blocked the contractil response of airway smooth muscle to ethanol. Due to these studies it can be concluded that ethanol, acting directly on pulmonary vasculature, might contribute to development of pulmonary hypertension and cor pulmonate chronicum.
利用犬肺动脉平滑肌研究了肺动脉平滑肌张力对乙醇的反应，以及氟哌啶醇（一种多巴胺能受体阻滞剂）、普萘洛尔（一种β-肾上腺素能受体阻滞剂）和维拉帕米（一种钙通道阻滞剂）对乙醇反应的影响。结果表明，乙醇始终诱导肺动脉平滑肌产生剂量依赖性收缩，预先给予氟哌啶醇对此收缩作用基本无调节作用，但部分被普萘洛尔阻断，提示儿茶酚胺能受体部分参与乙醇诱导的肺动脉平滑肌收缩的介导过程。然而，本研究结果表明，在能阻断气道平滑肌对乙醇收缩反应的剂量下，维拉帕米并未改变乙醇诱导的肺平滑肌收缩。基于这些研究可以得出结论，乙醇直接作用于肺血管系统，可能促成肺动脉高压和慢性肺源性心脏病的发生。
