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

被引:196
|
作者
DIRNAGL, U
LINDAUER, U
VILLRINGER, A
机构
[1] Department of Neurology, Klinikum Grosshadern, Munich
关键词
ENDOTHELIUM; CEREBRAL CIRCULATION; LASER-DOPPLER; SOMATOSENSORY STIMULATION; RAT;
D O I
10.1016/0304-3940(93)90343-J
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
引用
收藏
页码:43 / 46
页数:4
相关论文
共 50 条
  • [1] NITRIC-OXIDE SYNTHESIS COUPLES CEREBRAL BLOOD-FLOW AND METABOLISM
    GOADSBY, PJ
    KAUBE, H
    HOSKIN, KL
    BRAIN RESEARCH, 1992, 595 (01) : 167 - 170
  • [2] DOES NITRIC-OXIDE MEDIATE THE INCREASES IN CEREBRAL BLOOD-FLOW ELICITED BY HYPERCAPNIA
    IADECOLA, C
    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (09) : 3913 - 3916
  • [3] INHIBITION OF NITRIC-OXIDE SYNTHESIS INDUCES A SIGNIFICANT REDUCTION IN LOCAL CEREBRAL BLOOD-FLOW IN THE RAT
    TANAKA, K
    GOTOH, F
    GOMI, S
    TAKASHIMA, S
    MIHARA, B
    SHIRAI, T
    NOGAWA, S
    NAGATA, E
    NEUROSCIENCE LETTERS, 1991, 127 (01) : 129 - 132
  • [4] NITRIC-OXIDE MEDIATES THE INCREASE IN LOCAL CEREBRAL BLOOD-FLOW DURING FOCAL SEIZURES
    DEVASCONCELOS, AP
    BALDWIN, RA
    WASTERLAIN, CG
    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (08) : 3175 - 3179
  • [5] NITRIC-OXIDE (NO) IS INVOLVED IN INCREASED CEREBRAL CORTICAL BLOOD-FLOW FOLLOWING STIMULATION OF THE NUCLEUS BASALIS OF MEYNERT IN ANESTHETIZED RATS
    ADACHI, T
    INANAMI, O
    SATO, A
    NEUROSCIENCE LETTERS, 1992, 139 (02) : 201 - 204
  • [6] CONTROL OF CORONARY BLOOD-FLOW BY ENDOTHELIAL RELEASE OF NITRIC-OXIDE
    LOSANO, G
    PAGLIARO, P
    GATTULLO, D
    MARSH, NA
    CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, 1994, 21 (10) : 783 - 789
  • [7] CEREBRAL BLOOD-FLOW AND CEREBROVASCULAR REACTIVITY AFTER INHIBITION OF NITRIC-OXIDE SYNTHESIS IN CONSCIOUS GOATS
    FERNANDEZ, N
    GARCIA, JL
    GARCIAVILLALON, AL
    MONGE, L
    GOMEZ, B
    DIEGUEZ, G
    BRITISH JOURNAL OF PHARMACOLOGY, 1993, 110 (01) : 428 - 434
  • [8] HYPOTHALAMIC BLOOD-FLOW REMAINS UNALTERED FOLLOWING CHRONIC NITRIC-OXIDE SYNTHASE BLOCKADE IN RATS
    BENYO, Z
    SZABO, C
    STUIVER, BT
    BOHUS, B
    SANDOR, P
    NEUROSCIENCE LETTERS, 1995, 198 (02) : 127 - 130
  • [9] CONTROL OF REGIONAL BLOOD-FLOW BY ENDOTHELIUM-DERIVED NITRIC-OXIDE
    GARDINER, SM
    COMPTON, AM
    BENNETT, T
    PALMER, RMJ
    MONCADA, S
    HYPERTENSION, 1990, 15 (05) : 486 - 492
  • [10] ANGIOTENSIN-II - NITRIC-OXIDE INTERACTION AND THE DISTRIBUTION OF BLOOD-FLOW
    SIGMON, DH
    BEIERWALTES, WH
    AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 265 (06): : R1276 - R1283