Busse R, Pohl U, Kellner C, Klemm U
Pflugers Arch. 1983 Apr;397(1):78-80. doi: 10.1007/BF00585175.
The role of endothelial cells in the dilatory response of arteries to hypoxia was studied in vitro using perfused arterial segments of rat and dog. The pO2 of the intra- and extraluminal perfusate could be varied separately. Intraluminal hypoxia (pO2 of 40 mmHg) induced a dilation irrespective of extraluminal pO2 level. On the contrary extraluminal hypoxia could not elicit a dilation during intraluminal normoxic perfusion. Dilation during extraluminal hypoxia could only be induced if the segment was not intraluminally perfused. The dilatory response to intraluminal hypoxia was abolished after enzymatical or mechanical removal of the endothelium. While theophylline and lipoxygenase inhibitors did not influence this endothelium-induced dilation, a significant reduction of the response could be observed after incubation with indomethacin. These results support the concept that prostacyclin (PGI2) might be involved in the hypoxic endothelium-induced dilation.
利用大鼠和犬的灌注动脉段在体外研究了内皮细胞在动脉对缺氧的舒张反应中的作用。管腔内和管腔外灌注液的氧分压（pO2）可以分别改变。管腔内缺氧（pO2为40 mmHg）可引起血管舒张，而与管腔外pO2水平无关。相反，在管腔内常氧灌注期间，管腔外缺氧不能引起血管舒张。仅当动脉段未进行管腔内灌注时，管腔外缺氧才能诱导血管舒张。在酶促或机械去除内皮后，对管腔内缺氧的舒张反应消失。虽然茶碱和脂氧合酶抑制剂不影响这种内皮诱导的舒张，但与吲哚美辛孵育后可观察到反应显著降低。这些结果支持前列环素（PGI2）可能参与缺氧内皮诱导的舒张这一概念。
