Study on the effects of nitric oxide on cerebral blood flow in developmental brain.

本研究旨在探讨一氧化氮（NO）在发育大鼠纹状体缺氧和复氧过程中对脑血流（CBF）的调节作用。采用一氧化氮选择性安培微传感器测量了大鼠纹状体一氧化氮（NO）的产生。我们将工作电极插入右侧纹状体，在整个实验过程中连续监测NO的反应。在整个实验期间，用激光多普勒血流仪测量纹状体脑血流。稳定后，大鼠接受8% O2缺氧60分钟，随后用21% O2复氧60分钟。在7日龄大鼠中，我们观察到NO释放逐渐增加116(]SY.+-。[]缺氧过程中29pa，继发性增加191（[SY.+-]）。[] 31 pA。在14日龄大鼠中，缺氧引起的NO释放量增加和再氧化引起的NO释放量增加分别为849（]SY.+-）。[][参考译文](分别)196 pA。它们明显高于7天大的大鼠。CBF降至92（]SY.+-）。[)低氧时为基线的3%，增加到124(]SY.+-。[) 7日龄大鼠再充氧时服用3%凡士林，而14日龄大鼠缺氧和再充氧时CBF均增加至125（[SY.+-]）。[)6%和168(]SY.+-。[)分别为基线的6%。n -硝基- l -精氨酸甲酯（n -硝基- l -精氨酸甲酯）加NO合成酶抑制剂的L-NAME预处理能显著减弱两组小鼠缺氧和复氧过程中NO的释放。L-NAME治疗显著将双眼充血转为缺氧和/或再氧合。在两个年龄段中，对缺氧和/或再氧合的充血反应也显著减弱。我们的研究表明，一氧化氮微电极可以检测发育中的大脑中释放的纳米摩尔水平的一氧化氮。缺氧和再氧作用导致幼龄大鼠一氧化氮释放量减少，这可能表明未成熟的大脑激活一氧化氮合酶的能力低于较发达的大脑。我们的研究结果还表明，缺氧和再氧化过程中CBF的改变与体内NO的产生有关。少

The present study was performed to investigate the role of nitric oxide (NO) in regulation of regional cerebral blood flow (CBF) during hypoxia and reoxygenation in developing rats striatum. The production of nitric oxide (NO) production in rat striatum was measured by using a NO-selective amperometric microsensor. We inserted the working electrode into the right striatum and monitored NO response continuously throughout the experiment. CBF in striatum was measured by laser Doppler flowmetry throughout the experimental period. Following stabilization, rats were subjected to 60-min hypoxia with 8% O2 and the subsequent 60-min reaxygenation with 21% O2. In 7-day-old rets, we observed a gradual increase in NO release by 116(]SY.+-。[)29 pA in the course of hypoxia and a secondary increase by 191(]SY.+-。[)31 pA during reoxygenation. In 14-day-old rats, the amount of an increase of NO released in response to hypoxia and that of another increase induced by reoxygenation were 849(]SY.+-。[)189 … More and 847(]SY.+-。[)196 pA,respectively. They were singificantly greater thon those in 7-day-old rats. CBF decreased to 92(]SY.+-。[)3% of baseline during hypoxia and increased to124(]SY.+-。[)3% of vaseline during reoxygenation in 7-day-old rats, whereas CBF increased by both hypoxia and reoxygenation in 14-day-old rats to 125(]SY.+-。[)6% and 168(]SY.+-。[)6% of baseline, respectively. Pretreatment with L-NAME pretreatment with a NO synthase inhibitor, N-nitro-L-arginine methyl ester remarkably attenuated NO release during hypoxia and reoxygenation at both ages. Treatrment with L-NAME signifcantly attencated the hyperemic to hypoxia and/or reoxyg enation in both eges. also significantly attenuated the hyperemic responses to hypoxia and/or reoxygenation in both ages. Our present study demonstrates that the NO microelectrode can detect nanomolar levels of NO released in developing brain. Smaller NO release induced by hypoxia and reoxygenation in younger rats may indicate that immature brain has less abitity to aciivate NO synthase than more developed brain. Our results also indicated that the alteration of CBF during hypoxia and reoxygenation are associated with in vivo NO production. Less