Modulation of endothelium-dependent responses by chronic alterations of blood flow.
Modulation of endothelium-dependent responses by chronic alterations of blood flow.
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通过血流的慢性改变调节内皮依赖性反应。
DOI：
10.1152/ajpheart.1986.251.3.h520
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Vanhoutte,PM
中科院分区：
文献类型：
--
作者：
Miller,VM;Aarhus,LL;Vanhoutte,PM
为了确定血管长期暴露的血流量和O2张力是否可以调节内皮依赖性反应，通过引起股动脉部分闭塞或在股动脉和静脉之间形成瘘来改变犬的这些参数。血流减少了75%，在夹紧的动脉;平均动脉压不变。在瘘近端的血管中，血流量升高，静脉和动脉中的O2张力相似。6周后，切除股动脉和静脉，并在体外研究其内皮依赖性反应。与假手术动脉相比，瘘管手术动脉对乙酰胆碱、二磷酸腺苷和α 2-肾上腺素能刺激的内皮依赖性舒张作用增强。钳夹血管对这些药物的反应与假手术血管没有差异。动脉中花生四烯酸的舒张与血流量呈反比关系。在瘘近端的静脉中，乙酰胆碱的内皮依赖性舒张增强，并且存在对α 2-肾上腺素能刺激的内皮依赖性舒张;仅在假手术肢体的静脉中观察到对后者的收缩反应。这些研究表明，在暴露于慢性血流量升高的血管中，内皮依赖性舒张增加。
To determine whether the blood flow and O2 tension to which a blood vessel is chronically exposed could modulate endothelium-dependent responses, these parameters were altered in the dog either by causing partial occlusion of the femoral artery or by creating a fistula between the femoral artery and vein. Blood flow was reduced by 75% in the clamped artery; mean arterial pressure was unchanged. In the vessels proximal to the fistula, blood flow was elevated and O2 tensions were similar in the vein and artery. After 6 wk the femoral arteries and veins were excised, and their endothelium-dependent responses were studied in vitro. The endothelium-dependent relaxations to acetylcholine, adenosine diphosphate, and alpha 2-adrenergic stimulation were augmented in fistula-operated compared with sham-operated arteries. The responses to these agents in the clamp-operated vessels were not different from those of the sham-operated ones. Relaxation to arachidonic acid in the arteries showed an inverse relationship to blood flow. In the veins proximal to the fistula, the endothelium-dependent relaxations to acetylcholine were augmented and an endothelium-dependent relaxation to alpha 2-adrenergic stimulation was present; only a contractile response was observed in veins from the sham-operated limb in response to the latter. These studies suggest a pattern of increased endothelium-dependent relaxation in vessels exposed to chronically elevated blood flow.