Dirnagl U, Lindauer U, Villringer A
Department of Neurology, Klinikum Grosshadern, Munich, FRG.
Neurosci Lett. 1993 Jan 4;149(1):43-6. doi: 10.1016/0304-3940(93)90343-j.
We tested the hypothesis that nitric oxide (NO) is a mediator in the coupling of cerebral blood flow to neuronal activation. The production of NO was blocked in anesthetized rats with the NO-synthase inhibitor N omega-nitro-L-arginine (L-NA). In controls, vibrissae stimulation for 60 s led to a fast (< or = 2 s), 17% increase in regional cerebral blood flow (rCBF) in the contralateral somatosensory cortex. Systemical (10 mg/kg) as well as topical (10(-3) M) application of L-NA reduced the response to stimulation by approximately 50%. Systemical application primarily attenuated the early component of the response, whereas topical application led to an attenuation throughout the whole 60-s stimulation interval. We conclude that NO is involved in rCBF coupling to neuronal activation.
我们验证了一氧化氮（NO）是脑血流与神经元激活之间耦合作用的介质这一假设。使用一氧化氮合酶抑制剂Nω-硝基-L-精氨酸（L-NA）阻断麻醉大鼠体内NO的生成。在对照组中，刺激触须60秒会导致对侧体感皮层的局部脑血流（rCBF）快速（≤2秒）增加17%。全身性（10毫克/千克）以及局部（10⁻³摩尔/升）应用L-NA可使刺激反应降低约50%。全身性应用主要减弱反应的早期成分，而局部应用则导致在整个60秒刺激间隔内反应均减弱。我们得出结论，NO参与了rCBF与神经元激活的耦合。
