Takahashi S, Cook M, Jehle J, Kennedy C, Sokoloff L
Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, MD 20892-4030, USA.
Brain Res. 1995 Apr 24;678(1-2):21-8. doi: 10.1016/0006-8993(95)00129-e.
Effects of inhibition of nitric oxide (NO) synthesis on the cerebrovascular autoregulatory vasodilator response to hypotension were studied in conscious rats. Cerebral blood flow (CBF) was determined with [14C]iodoantipyrine in a saline-treated control group and in three groups following inhibition of NO synthase activity by twice daily intraperitoneal injections of 50 mg/kg of NG-nitro-L-arginine methyl ester (L-NAME) for four days. In the saline-control group (n = 8) and in the L-NAME-treated Group (a) (n = 8) CBF was determined while systemic mean arterial blood pressure (MABP) remained at its resting level (means +/- S.D., 128 +/- 6 and 151 +/- 11 mmHg, respectively). In the other groups CBF was determined after MABP was reduced by blood withdrawal to 118 +/- 9 and 88 +/- 8 mmHg in Groups (b) (n = 8) and (c) (n = 8), respectively. Despite the elevated MABP, global CBF was significantly lower in L-NAME-treated Group (a) than in the saline-controls (P < 0.005), indicating cerebral vasoconstriction resulting from inhibition of NO synthesis. Global CBF was not significantly reduced further in the two groups with hypotension. Local CBF in the hypotensive rats showed no significant reductions below values in L-NAME-treated control rats (Group (a)) in 31 of 32 brain structures; the only exception was in the auditory cortex of the severely hypotensive rats (Group (c)). The autoregulatory mechanism for cerebral vasodilatation to compensate for reduced arterial blood pressure is maintained following inhibition of NO synthesis.
在清醒大鼠中研究了抑制一氧化氮（NO）合成对脑血管自动调节性血管舒张反应的影响。用[14C]碘安替比林测定脑血流量（CBF），实验分为生理盐水处理的对照组以及三组通过每天腹腔注射两次50mg/kg的NG-硝基-L-精氨酸甲酯（L-NAME）抑制一氧化氮合酶活性四天后的实验组。在生理盐水对照组（n = 8）和L-NAME处理组（a）（n = 8）中，当全身平均动脉血压（MABP）保持在静息水平时（平均值±标准差，分别为128±6和151±11mmHg）测定CBF。在其他组中，通过放血使MABP分别降至118±9mmHg（组（b），n = 8）和88±8mmHg（组（c），n = 8）后测定CBF。尽管MABP升高，但L-NAME处理组（a）的全脑CBF显著低于生理盐水对照组（P < 0.005），表明抑制NO合成导致脑血管收缩。低血压的两组中全脑CBF没有进一步显著降低。在32个脑结构中的31个中，低血压大鼠的局部CBF没有比L-NAME处理的对照大鼠（组（a））的值显著降低；唯一的例外是严重低血压大鼠（组（c））的听觉皮层。抑制NO合成后，脑血管舒张以补偿动脉血压降低的自动调节机制得以维持。
