Zhang Z G, Chopp M, Bailey F, Malinski T
Department of Neurology, Henry Ford Health Science System, Detroit, MI 48202-2689, USA.
J Neurol Sci. 1995 Jan;128(1):22-7. doi: 10.1016/0022-510x(94)00216-b.
Using a porphyritic microsensor, we measured the cortical NO concentration within ischemic tissue during 2 h of middle cerebral artery (MCA) occlusion and 1 h of reperfusion in the rat (n = 36). Local cerebral blood flow was simultaneously measured by laser Doppler flowmetry to verify MCA occlusion and reperfusion. Baseline concentration of NO was < 10(-8) M. The maximum concentrations of NO during MCA occlusion and reperfusion were, respectively, 1.47 +/- 0.45 microM and 0.54 +/- 0.24 microM. Administration of N-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthase, prior to ischemia, significantly (p < 0.05) reduced NO release to 0.04 +/- 0.02 microM during MCA occlusion and completely inhibited NO release during 1 h of reperfusion. Administration of L-arginine 30 min after administration of L-NAME restored NO release (3.45 +/- 1.14 microM) during MCA occlusion; however, administration of L-arginine did not overcome the effect of L-NAME on mean arterial blood pressure. Our data indicate that NO is released in the brain after the onset of ischemia and NO levels can be modulated by administration of NO substrate and NO antagonists.
我们使用一种斑状微传感器，在大鼠大脑中动脉（MCA）闭塞2小时及再灌注1小时期间，测量了缺血组织内的皮质一氧化氮（NO）浓度（n = 36）。同时通过激光多普勒血流仪测量局部脑血流量，以验证MCA闭塞和再灌注情况。NO的基线浓度<10^(-8) M。MCA闭塞和再灌注期间NO的最大浓度分别为1.47±0.45微摩尔/升和0.54±0.24微摩尔/升。在缺血前给予NO合酶抑制剂N-硝基-L-精氨酸甲酯（L-NAME），显著（p<0.05）降低了MCA闭塞期间的NO释放至0.04±0.02微摩尔/升，并在再灌注1小时期间完全抑制了NO释放。在给予L-NAME 30分钟后给予L-精氨酸，恢复了MCA闭塞期间的NO释放（3.45±1.14微摩尔/升）；然而，给予L-精氨酸并未克服L-NAME对平均动脉血压的影响。我们的数据表明，缺血发作后大脑中会释放NO，并且可以通过给予NO底物和NO拮抗剂来调节NO水平。
