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一氧化碳对兔脑动脉的影响。

Effect of carbon monoxide on rabbit cerebral arteries.

作者信息

Brian J E, Heistad D D, Faraci F M

机构信息

Department of Anesthesia, University of Iowa College of Medicine, Iowa City.

出版信息

Stroke. 1994 Mar;25(3):639-43; discussion 643-4. doi: 10.1161/01.str.25.3.639.

DOI:10.1161/01.str.25.3.639
PMID:8128519
Abstract

BACKGROUND AND PURPOSE

Carbon monoxide produces relaxation in some peripheral arteries. Recently it has been suggested that carbon monoxide may be generated in brain tissue. In the present study we examined the hypothesis that carbon monoxide directly relaxes cerebral blood vessels.

METHODS

The aorta and basilar and middle cerebral arteries were removed from New Zealand White rabbits and mounted for tension recording in vitro. Canine basilar arteries were also studied. After precontraction, cumulative relaxation concentration-response curves to carbon monoxide, nitric oxide, sodium nitroprusside, acetylcholine (rabbit arteries), and ATP (dog basilar artery) were obtained. Maximum relaxation and the concentration of agonists that induced half-maximal relaxation (ED50) were determined.

RESULTS

Carbon monoxide (10(-6) to 3 x 10(-4) mol/L) did not affect tension in rabbit or dog cerebral arteries. In rabbit aorta, carbon monoxide induced 29 +/- 4% (mean +/- SEM) relaxation at the highest concentration used (3 x 10(-4) mol/L). In contrast, nitric oxide produced 80% to 100% relaxation of all arteries, with ED50 values ranging from 7.1 to 7.4 -log mol/L. Nitroprusside, acetylcholine, and ATP also produced 80% to 100% relaxation of the arteries.

CONCLUSIONS

Carbon monoxide does not appear to have significant effect on tone in cerebral arteries. In contrast, at high concentrations carbon monoxide produces concentration-dependent relaxation in rabbit aorta. Factors that account for this regional heterogeneity are not clear. Although neurons may produce both nitric oxide and carbon monoxide, our findings suggest that only nitric oxide has direct effects on cerebral vascular tone.

摘要

背景与目的

一氧化碳可使一些外周动脉舒张。最近有研究表明,脑组织中可能会生成一氧化碳。在本研究中,我们检验了一氧化碳直接舒张脑血管这一假说。

方法

从新西兰白兔体内取出主动脉、基底动脉和大脑中动脉,置于体外进行张力记录。同时也对犬基底动脉进行了研究。预收缩后,分别获得一氧化碳、一氧化氮、硝普钠、乙酰胆碱(兔动脉)和三磷酸腺苷(犬基底动脉)的累积舒张浓度-反应曲线。测定最大舒张率和诱导半数最大舒张率(ED50)的激动剂浓度。

结果

一氧化碳(10⁻⁶至3×10⁻⁴mol/L)对兔或犬的脑动脉张力无影响。在兔主动脉中,一氧化碳在最高使用浓度(3×10⁻⁴mol/L)时可诱导29±4%(平均值±标准误)的舒张。相比之下,一氧化氮可使所有动脉舒张80%至100%,ED50值在7.1至7.4 -log mol/L之间。硝普钠、乙酰胆碱和三磷酸腺苷也可使动脉舒张80%至100%。

结论

一氧化碳似乎对脑动脉张力无显著影响。相比之下,高浓度一氧化碳可使兔主动脉产生浓度依赖性舒张。造成这种区域异质性的因素尚不清楚。虽然神经元可能同时产生一氧化氮和一氧化碳,但我们的研究结果表明,只有一氧化氮对脑血管张力有直接影响。

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