Benyó Z, Görlach C, Wahl M
Department of Physiology, Ludwig-Maximilians University, Munich, Germany.
J Cereb Blood Flow Metab. 1998 Jun;18(6):616-8. doi: 10.1097/00004647-199806000-00003.
Inhibition of nitric oxide (NO) synthesis induces vasoconstriction and reduction of the blood flow in the brain, indicating that basal release of NO provides a resting vasorelaxant tone in the cerebral circulation. In the present study, the contractile effect of the NO synthase blocker NG-nitro-L-arginine (100 mumol/L) in isolated rat middle cerebral arteries was attenuated markedly in the presence of the cyclooxygenase inhibitor indomethacin (5 mumol/L), the thromboxane A2 synthase inhibitor ridogrel (10 mumol/L), or the thromboxane receptor antagonist ICI 192605 (100 mumol/L). These results indicate that removal of the endogenous NO stimulates the release of thromboxane A2 in cerebral vessels and basal NO production regulates the resting cerebrovascular tone, at least in part, by suppressing thromboxane A2.
一氧化氮（NO）合成的抑制会导致血管收缩以及脑血流量减少，这表明基础状态下NO的释放为脑循环提供了静息性血管舒张张力。在本研究中，在环氧化酶抑制剂吲哚美辛（5 μmol/L）、血栓素A2合酶抑制剂利托格雷（10 μmol/L）或血栓素受体拮抗剂ICI 192605（100 μmol/L）存在的情况下，NO合酶阻滞剂NG-硝基-L-精氨酸（100 μmol/L）对离体大鼠大脑中动脉的收缩作用明显减弱。这些结果表明，内源性NO的去除会刺激脑血管中血栓素A2的释放，并且基础状态下NO的产生至少部分地通过抑制血栓素A2来调节静息脑血管张力。
