NITRIC-OXIDE AND PROSTANOIDS PARTICIPATE IN CEREBRAL VASODILATION ELICITED BY ELECTRICAL-STIMULATION OF THE ROSTRAL VENTROLATERAL MEDULLA
NITRIC-OXIDE AND PROSTANOIDS PARTICIPATE IN CEREBRAL VASODILATION ELICITED BY ELECTRICAL-STIMULATION OF THE ROSTRAL VENTROLATERAL MEDULLA
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DOI：
10.1038/jcbfm.1994.61
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发表时间：
1994-05-01
影响因子：
6.3
通讯作者：
REIS, DJ
中科院分区：
文献类型：
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作者：
GOLANOV, EV;REIS, DJ
我们调查，使用激光多普勒血流仪，是否一氧化氮（NO）和/或吲哚美辛（IND）敏感的机制介导的局部脑血流量（rCBF）引起的电刺激的头端腹外侧延髓（RVL）在麻醉脊髓大鼠的海拔。刺激RVL 10 s导致额叶皮质rCBF增加31%（n = 46），在22 s达到峰值，持续8 min。静脉注射L-硝基-N-G-精氨酸（NNA）剂量依赖性和可逆性增加动脉压，降低基础和诱发rCBF至对照组的74%和54%（p < 0.05; n = 7）。在皮层上进行超灌注，NNA剂量依赖性地仅降低诱发的rCBF升高，至对照组的39%（p < 0.05; n = 6）。静脉注射IND剂量依赖性地降低基础rCBF，并使RVL引起的升高降低38%（p < 0.05），但IND在灌流时没有影响。静脉注射NNA和IND的效果相加，使rCBF降低70%。然而，当NNA和IND一起灌注时，对诱发的血管舒张的抑制与单独NNA引起的抑制相当。我们的结论是，rCBF的升高引起RVL部分介导的（a）一氧化氮在皮质中合成的本地响应传入神经信号和（B）IND敏感的机制，可能是一个产品的环氧合酶，位于较大的脑动脉，在响应逆行血管信号导致脑内血流增加。
We investigated, using laser-Doppler flowmetry, whether nitric oxide (NO)- and/or indomethacin (IND)-sensitive mechanisms mediate the elevations of regional cerebral blood flow (rCBF) elicited by electrical stimulation of the rostral ventrolateral medulla (RVL) in the anesthetized spinalized rat. Stimulation of the RVL for 10 s caused increased rCBF in the frontal cortex by 31% (n = 46), peaking at 22 s and persisting for up to 8 min. Intravenous L-nitro-N-G-arginine (NNA) dose dependently and reversibly increased arterial pressure and reduced basal and evoked rCBF to 74 and 54% of the control, respectively (p < 0.05; n = 7). Superfused over the cortex, NNA dose dependently reduced only the evoked elevations of rCBF, to 39% of the control (p < 0.05; n = 6). Intravenous IND decreased the basal rCBF dose dependently and decreased the elevations evoked from the RVL by 38% (p < 0.05), but IND was without effect when superfused. Combined, the effects of intravenous NNA and IND summated, reducing rCBF by 70%. However, when NNA and IND were superfused together, the inhibition of the evoked vasodilation was comparable to that elicited by NNA alone. We conclude that the elevation in rCBF elicited from the RVL is partially mediated by (a) NO synthesized locally in the cortex in response to an afferent neural signal and (b) an IND-sensitive mechanism, probably a product of cyclooxygenase, located in larger cerebral arteries, in response to a retrograde vascular signal resulting from increased blood flow within the brain.