Direct coronary and cerebral vascular responses to dexmedetomidine. Significance of endogenous nitric oxide synthesis.
Direct coronary and cerebral vascular responses to dexmedetomidine. Significance of endogenous nitric oxide synthesis.
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对右美托咪定的直接冠状动脉和脑血管反应。
DOI：
10.1097/00000542-199211000-00024
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发表时间：
1992
期刊：
影响因子：
8.8
通讯作者：
Warltier,DC
中科院分区：
文献类型：
--
作者：
Coughlan,MG;Lee,JG;Bosnjak,ZJ;Schmeling,WT;Kampine,JP;Warltier,DC
右美托咪定可激活中枢神经系统和外周血管系统中的α 2-肾上腺素能受体。已发现体内右美托咪定通过刺激血管平滑肌α 2受体引起冠状动脉和脑血流以及动脉压的改变。α 2-肾上腺素能激动剂的直接血管收缩作用可能被认为是一氧化氮的内皮源性舒张因子的释放所对抗。最近在犬冠状动脉侧支血管中发现了功能性内皮细胞。本研究旨在评估右美托咪定对离体犬近端和远端冠状动脉、冠状侧支血管和大脑中动脉的直接影响。在存在吲哚美辛10（-5）M以及存在和不存在NG硝基-L-精氨酸甲酯（L-NAME）（一种血管一氧化氮合成抑制剂）的情况下，在组织浴中测量反应。右美托咪定（3 x 10（-8）至3 x 10（-3.9）M）引起所有血管收缩（近端和远端冠状动脉、大脑中动脉和冠状侧支血管分别为3.9、5.5、72.8和2.3%，表示为KCl诱导收缩的百分比）。这种收缩增强的L-NAME的存在下，除脑动脉的所有血管。选择性α 2-肾上腺素能拮抗剂阿替美唑（10（-4）M）可消除大脑中动脉、近端冠状动脉和冠状侧支血管对低浓度（但非高浓度）右美托咪定的反应。（250字处删节）
Dexmedetomidine activates alpha 2-adrenergic receptors in the central nervous system and in the peripheral vasculature. In vivo dexmedetomidine has been found to cause alterations in coronary and cerebral blood flows and arterial pressure by stimulation of vascular smooth muscle alpha 2 receptors. The direct vasoconstrictor effects of alpha 2-adrenergic agonists may be opposed by release of endothelium-derived relaxing factor believed to be nitric oxide. A functional endothelium was demonstrated recently in canine coronary collateral vessels. The objective of the current study was to assess the direct effect of dexmedetomidine on isolated canine proximal and distal coronary arteries, coronary collateral vessels, and middle cerebral arteries. Responses were measured in tissue baths in the presence of indomethacin 10(-5) M and in the absence and presence of NG nitro-l-arginine methyl ester (L-NAME), an inhibitor of vascular nitric oxide synthesis. Dexmedetomidine (3 x 10(-8) to 3 x 10(-3.9) M) caused constriction (3.9, 5.5, 72.8, and 2.3% for proximal and distal coronary arteries, middle cerebral arteries, and coronary collateral vessels, respectively, expressed as a percentage of KCl-induced contraction) in all vessels. This constriction was enhanced by the presence of L-NAME in all vessels except cerebral arteries. The selective alpha 2-adrenergic antagonist atipamezole (10(-4) M) abolished the response to low but not high concentrations of dexmedetomidine in middle cerebral arteries, proximal coronary arteries, and coronary collateral vessels.(ABSTRACT TRUNCATED AT 250 WORDS)