Dhein S, Salameh A, Klaus W
Pharmacological Institute, University of Cologne, F.R.G.
Eur Heart J. 1989 Nov;10 Suppl F:82-5. doi: 10.1093/eurheartj/10.suppl_f.82.
In order to investigate the influence of the endothelium on hypoxia-induced vasospasms we examined vascular tone after reduction of the oxygen supply, dependent on endothelial function. Therefore, after ligation of all side branches, vessel segments of porcine or human right coronary arteries or of rabbit abdominal aorta, prepared either with or without endothelium, were cannulated, perfused with Tyrode's solution and arranged in a serial manner (system I: endothelium-denuded vessel followed by a normal segment; system II: normal vessel followed by an endothelium-denuded segment). The pressure gradient over each segment was continuously measured as a function of vessel radius. After 2 h equilibration the oxygen concentration in the perfusion and superfusion solutions was lowered (reduction from 'control' = 95% O2/5% CO2 to 'hypoxia' = 95% N2/5% CO2) leading to a marked long-lasting vasoconstriction in those endothelium-denuded vessel segments which were mounted distal to a normal vessel with an intact endothelium, whereas the other vessels did not change their tone. This hypoxic contraction could be inhibited by pretreatment with either 1 mumol l-1 dexamethasone or quinacrine or indomethacine. From these results it is concluded that endothelium releases a vasoconstricting factor (EDCF) under hypoxic conditions probably dependent on phospholipase A2 and cyclooxygenase. This EDCF may be of pathophysiological importance by inducing or aggravating hypoxic vasospasms.
为了研究内皮对缺氧诱导的血管痉挛的影响，我们根据内皮功能，在减少氧气供应后检测了血管张力。因此，在结扎所有侧支后，将猪或人右冠状动脉或兔腹主动脉的血管段（有或无内皮）插管，用台氏液灌注，并串联排列（系统I：去内皮血管段后接正常血管段；系统II：正常血管段后接去内皮血管段）。连续测量每个血管段上的压力梯度作为血管半径的函数。平衡2小时后，降低灌注液和超灌注液中的氧浓度（从“对照”=95%O₂/5%CO₂降至“缺氧”=95%N₂/5%CO₂），导致那些安装在具有完整内皮的正常血管远端的去内皮血管段出现明显的持久血管收缩，而其他血管的张力未改变。这种缺氧收缩可被1μmol/L地塞米松或奎纳克林或吲哚美辛预处理所抑制。从这些结果可以得出结论，内皮在缺氧条件下可能依赖磷脂酶A₂和环氧化酶释放一种血管收缩因子（EDCF）。这种EDCF可能通过诱导或加重缺氧性血管痉挛而具有病理生理学重要性。
