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）在发育期大鼠纹状体缺氧复氧时局部脑血流量（CBF）的调节中的作用。用一氧化氮（NO）选择性电流型微传感器测定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，并在整个实验过程中连续监测NO反应。在整个实验期间，用激光多普勒血流仪测量纹状体CBF。稳定后，大鼠进行60分钟的缺氧与8%的O2和随后的60分钟再氧与21%的O2。在7日龄大鼠中，我们观察到NO释放逐渐增加，116（]SY. ±-。[)29在缺氧过程中的PA和继发性增加191（]SY ±）。[)31再氧合期间的PA。在14日龄大鼠中，响应于缺氧而释放的NO增加的量和由再氧合诱导的另一增加的量为849（]SY ±-。[）189 关于我们 和847（]SY. [)196 PA，分别。明显通村7日龄大鼠。CBF降至92（± SD）。[)3%，缺氧时增加至124（±）SY。[)3 7日龄大鼠在复氧过程中凡士林的含量为125%，而14日龄大鼠在缺氧和复氧过程中CBF均增加至125%。[)6%和168（±）SY. [)6分别为基线的%。用NO合成酶抑制剂N-硝基-L-精氨酸甲酯预处理可显著抑制两个年龄组大鼠缺氧和复氧时NO的释放。用L-NAME治疗可明显减轻两侧心肌的充血缺氧和/或复氧。也显著减弱了两个年龄组对缺氧和/或复氧的充血反应。我们目前的研究表明，一氧化氮微电极可以检测到纳摩尔水平的一氧化氮释放在发育中的大脑。年轻大鼠缺氧/复氧诱导的NO释放较少，可能表明未成熟脑激活NO合酶的能力低于发育较好的脑。我们的研究结果还表明，在缺氧和复氧过程中的CBF的变化与在体内NO的产生。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