Methylene blue and ETYA block flow-dependent dilation in canine femoral artery.
Methylene blue and ETYA block flow-dependent dilation in canine femoral artery.
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亚甲蓝和 ETYA 可阻断犬股动脉的血流依赖性扩张。
DOI：
10.1152/ajpheart.1986.250.6.h974
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
SparksJr,HV
中科院分区：
文献类型：
--
作者：
Kaiser,L;HullJr,SS;SparksJr,HV
犬股动脉的流量依赖性扩张是内皮细胞依赖性的，不受肾上腺素、肾上腺素能或胆碱能受体、微循环的上行信息或肌原性机制介导。我们在38只戊巴比妥麻醉的狗上研究了血流扩张的机制。构建股动脉-颈静脉分流，并在控制和最大流量（1 l/min）期间连续测量股动脉直径（sonomicometer晶体）。吲哚美辛对前列腺素形成的抑制并没有改变对流量增加的扩张反应，但脂氧合酶-环氧合酶抑制剂5，8，11，14二十碳四炔酸（ETYA）不可逆地抑制了对流量增加的扩张反应。鸟苷酸环化酶抑制剂，亚甲蓝，引起了剂量依赖性减少的扩张反应增加流量。预处理与H1受体拮抗剂tripelennamine敏化血管的抑制作用的亚甲蓝。亚甲蓝和ETYA都使乙酰胆碱舒张的ED 50向右移动两个数量级，但没有改变血管对其他刺激的扩张或收缩能力。这些数据表明，环鸟苷酸和花生四烯酸的非前列腺素代谢产物参与血流扩张。我们认为内皮细胞释放一种花生四烯酸的代谢产物，刺激血管平滑肌鸟苷酸环化酶，导致血管舒张。组胺在该系统中的作用尚不清楚。
Flow-dependent dilation of the canine femoral artery is endothelial cell dependent and is not mediated by prostaglandins, adrenergic or cholinergic receptors, an ascending message from the microcirculation, or by myogenic mechanisms. We investigated the mechanism of flow dilation in 38 pentobarbital anesthetized dogs. A femoral artery-jugular vein shunt was constructed, and femoral artery diameter was continuously measured (sonomicrometer crystals) during control and maximum flow (1 l/min). Inhibition of prostaglandin formation by indomethacin did not alter the dilation response to increased flow, but the lipoxygenase-cyclooxygenase inhibitor 5, 8, 11, 14 eicosatetraynoic acid (ETYA) irreversibly inhibited the dilation response to increased flow. The guanylate cyclase inhibitor, methylene blue, caused a dose-dependent decrease in the dilation response to increased flow. Pretreatment with the H1 receptor antagonist tripelennamine sensitized the vessel to the inhibitory effects of methylene blue. Both methylene blue and ETYA shifted the ED50 for acetylcholine relaxation two orders of magnitude to the right, but did not alter the ability of the vessel to dilate or constrict to other stimuli. These data suggest that both cyclic GMP and a non-prostaglandin metabolite of arachidonic acid are involved in flow dilation. We propose that endothelial cells release a metabolite of arachidonic acid that stimulates vascular smooth muscle guanylate cyclase leading to relaxation. The role of histamine in this system is unknown.