ROLE OF NITRIC-OXIDE IN THE COUPLING OF CEREBRAL BLOOD-FLOW TO NEURONAL ACTIVATION IN RATS

ROLE OF NITRIC-OXIDE IN THE COUPLING OF CEREBRAL BLOOD-FLOW TO NEURONAL ACTIVATION IN RATS
复制标题

DOI:
10.1016/0304-3940(93)90343-j
复制
发表时间:
1993-01-04
影响因子:
2.5
通讯作者:
VILLRINGER, A
VILLRINGER, A
中科院分区:
医学4区
文献类型:
--
作者:
DIRNAGL, U;LINDAUER, U;VILLRINGER, A

文献摘要

被引文献

相似文献

我们测试的假设,一氧化氮(NO)是一个介导的耦合脑血流神经元激活。用NO合成酶抑制剂N(ω)-L-精氨酸(L-NA)阻断麻醉大鼠NO的产生。在对照组中,60 s的触须刺激导致对侧体感皮层的局部脑血流量(rCBF)快速(小于或等于2 s)增加17%。全身(10 mg/kg)和局部(10(-3)M)应用L-NA可使对刺激的反应降低约50%。全身应用主要衰减的早期组件的反应,而局部应用导致整个60秒的刺激间隔衰减。我们的结论是NO参与rCBF耦合神经元激活。
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)-L-arginine (L-NA). In controls, vibrissae stimulation for 60 s led to a fast (less-than-or-equal-to 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.