Christman C W, Wei E P, Kontos H A, Povlishock J T, Ellis E F
Am J Physiol. 1984 Oct;247(4 Pt 2):H631-7. doi: 10.1152/ajpheart.1984.247.4.H631.
The effects of topical application of 15-hydroperoxy-eicosatetraenoic acid (15-HPETE, 200 micrograms/ml) on cerebral arterioles were studied in anesthetized cats equipped with cranial windows. 15-HPETE induced arteriolar dilation during application, sustained dilation 1 h after washout, and reduced responsiveness to the vasoconstrictive effects of hypocapnia. Electron microscopy of cerebral arterioles disclosed discrete endothelial lesions and focal morphological abnormalities of the vascular smooth muscle. Topical application of superoxide dismutase or catalase or the combination of the two inhibited the functional and morphological abnormalities induced by 15-HPETE. The results show that the vascular effects of 15-HPETE are mediated by superoxide anion radical and hydrogen peroxide or by other radicals derived from them, such as the hydroxyl radical. The results, together with earlier findings, support the view that the oxygen radicals responsible for these cerebral vascular effects are generated via the prostaglandin hydroperoxidase reaction.
在装有颅骨视窗的麻醉猫身上,研究了局部应用15-氢过氧二十碳四烯酸(15-HPETE,200微克/毫升)对脑微动脉的影响。应用15-HPETE期间可诱导微动脉扩张,冲洗后1小时仍持续扩张,并降低了对低碳酸血症血管收缩作用的反应性。脑微动脉的电子显微镜检查显示有离散的内皮损伤和血管平滑肌的局灶性形态异常。局部应用超氧化物歧化酶或过氧化氢酶或两者联合应用可抑制15-HPETE诱导的功能和形态异常。结果表明,15-HPETE的血管效应是由超氧阴离子自由基和过氧化氢或由它们衍生的其他自由基(如羟自由基)介导的。这些结果与早期发现一起支持了这样一种观点,即负责这些脑血管效应的氧自由基是通过前列腺素氢过氧化物酶反应产生的。