CEREBROVASCULAR EFFECTS OF N(G)-NITRO-L-ARGININE METHYLESTER ARE CONSERVED UNDER HALOTHANE ANESTHESIA

被引:11
作者
DAWSON, DA
MCCULLOCH, J
MACRAE, IM
机构
[1] UNIV GLASGOW,WELLCOME SURG INST,GLASGOW G61 1QH,SCOTLAND
[2] UNIV GLASGOW,HUGH FRASER NEUROSCI LABS,GLASGOW G61 1QH,SCOTLAND
基金
英国惠康基金;
关键词
NITRIC OXIDE (NO); N(G)-NITRO-L-ARGININE METHYLESTER (L-NAME); CEREBRAL BLOOD FLOW; HALOTHANE; ANESTHETICS;
D O I
10.1016/0014-2999(93)90655-2
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The effects of the nitric oxide synthesis inhibitor N(G)-nitro-L-arginine methylester (L-NAME) on mean arterial blood pressure (MABP) and local cerebral blood flow were determined in conscious and halothane-anaesthetised rats. Thirty minutes post-drug administration in conscious rats L-NAME (30 mg kg-1 i.v.) induced significant hypertension (MABP 132 +/- 2 mmHg and 163 +/- 6 mmHg (means +/- S.D.) for saline and L-NAME groups respectively) and significant hypoperfusion throughout the brain (mean +/- S.D. reduction in cerebral blood flow 27.3 +/- 5.9% compared with controls). In contrast, under halothane anaesthesia, L-NAME did not significantly change MABP but significant reductions in cerebral blood flow (43.2 +/- 3.7%) were observed. Thus the cerebrovascular response to L-NAME is conserved under halothane anaesthesia despite attenuation of the peripheral vasoconstrictive action.
引用
收藏
页码:7 / 11
页数:5
相关论文
共 18 条
[1]   DIFFERENCE IN PRESSOR-RESPONSES TO NG-MONOMETHYL-L-ARGININE BETWEEN CONSCIOUS AND ANESTHETIZED RATS [J].
AISAKA, K ;
MITANI, A ;
KITAJIMA, Y ;
OHNO, T ;
ISHIHARA, T .
JAPANESE JOURNAL OF PHARMACOLOGY, 1991, 56 (02) :245-248
[2]   THE NEUROPROTECTIVE EFFECT OF A NITRIC-OXIDE INHIBITOR IN A RAT MODEL OF FOCAL CEREBRAL-ISCHEMIA [J].
BUISSON, A ;
PLOTKINE, M ;
BOULU, RG .
BRITISH JOURNAL OF PHARMACOLOGY, 1992, 106 (04) :766-767
[3]   INHIBITION OF NITRIC-OXIDE SYNTHESIS DOES NOT REDUCE INFARCT VOLUME IN A RAT MODEL OF FOCAL CEREBRAL-ISCHEMIA [J].
DAWSON, DA ;
KUSUMOTO, K ;
GRAHAM, DI ;
MCCULLOCH, J ;
MACRAE, IM .
NEUROSCIENCE LETTERS, 1992, 142 (02) :151-154
[4]   NITRIC-OXIDE MEDIATES GLUTAMATE NEUROTOXICITY IN PRIMARY CORTICAL CULTURES [J].
DAWSON, VL ;
DAWSON, TM ;
LONDON, ED ;
BREDT, DS ;
SNYDER, SH .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (14) :6368-6371
[5]   ROLE OF ENDOTHELIUM-DERIVED RELAXING FACTOR IN CEREBRAL-CIRCULATION - LARGE ARTERIES VS MICROCIRCULATION [J].
FARACI, FM .
AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 261 (04) :H1038-H1042
[6]  
GARDINER SM, 1990, BRIT J PHARMACOL, V101, P62
[7]   GLUTAMATE, NITRIC-OXIDE AND CELL CELL SIGNALING IN THE NERVOUS-SYSTEM [J].
GARTHWAITE, J .
TRENDS IN NEUROSCIENCES, 1991, 14 (02) :60-67
[8]   ENDOTHELIAL NITRIC-OXIDE SYNTHASE - MOLECULAR-CLONING AND CHARACTERIZATION OF A DISTINCT CONSTITUTIVE ENZYME ISOFORM [J].
LAMAS, S ;
MARSDEN, PA ;
LI, GK ;
TEMPST, P ;
MICHEL, T .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (14) :6348-6352
[9]   ENDOTHELIN-1-INDUCED REDUCTIONS IN CEREBRAL BLOOD-FLOW - DOSE DEPENDENCY, TIME COURSE, AND NEUROPATHOLOGICAL CONSEQUENCES [J].
MACRAE, IM ;
ROBINSON, MJ ;
GRAHAM, DI ;
REID, JL ;
MCCULLOCH, J .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1993, 13 (02) :276-284
[10]  
MONCADA C, 1992, NEUROREPORT, V3, P530