一氧化氮介导兔对静脉注射腺苷的血流反应。

Circulatory shock Pub Date : 1994-07-01
L D McKie, B L Bass, B J Dunkin, J W Harmon
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引用次数: 0

摘要

本研究的目的是确定一氧化氮是否介导外源性给药腺苷对外周血流量的影响。在雄性新西兰大白兔体内静脉注射腺苷(1.0 μ mol/kg/min),通过放射性标记微球测量整个胃肠道、心脏和肾脏的血流量,结果显示血流量增加。先前给予硝基- l -精氨酸甲酯(L-NAME) 10mg /kg静脉注射完全阻断腺苷对所有器官的充血作用。l -精氨酸(300mg /kg, 50mg /kg/min)联合L-NAME可恢复腺苷的充血作用。这种现象被指定为l -精氨酸/一氧化氮途径,因为苯肾上腺素(1.5微克/千克/分钟)诱导的类似升压反应并没有阻断腺苷的作用。我们得出结论,外周血管扩张剂对静脉滴注腺苷的反应是由一氧化氮介导的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Nitric oxide mediates the blood flow response to intravenous adenosine in the rabbit.

The objective of this study was to determine if nitric oxide mediates the effects of exogenously administered adenosine on peripheral blood flow. An intravenous infusion of adenosine (1.0 mumol/kg/min) into male New Zealand white rabbits caused an increase in blood flow, measured using radiolabeled microspheres, throughout the gastrointestinal tract, as well as in the heart and kidneys. Prior administration of nitro-L-arginine methyl ester (L-NAME) 10 mg/kg i.v. completely blocked the hyperemic effect of adenosine on all organs studied. Administration of L-arginine (300 mg/kg bolus and 50 mg/kg/min infusion) together with L-NAME restored the hyperemic effect of adenosine. This phenomenon was specified to the L-arginine/nitric oxide pathway in that a similar pressor response induced by phenylephrine (1.5 micrograms/kg/min) did not block the effects of adenosine. We conclude that the peripheral vasodilator response to intravenously administered adenosine in the rabbit is mediated by nitric oxide.

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