Inhibition of vasoconstrictor responses by prostacyclin (PGI2) in the feline mesenteric vascular bed.
Inhibition of vasoconstrictor responses by prostacyclin (PGI2) in the feline mesenteric vascular bed.
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猫肠系膜血管床中前列环素 (PGI2) 抑制血管收缩反应。
DOI：
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发表时间：
1979
影响因子：
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通讯作者：
P. Kadowitz
中科院分区：
文献类型：
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作者：
H. Lippton;B. Chapnick;A. Hyman;P. Kadowitz
在猫的肠系膜血管床中研究了输注前列环素、PGI2 对交感神经刺激、去甲肾上腺素和血管紧张素 II 的血管收缩反应的影响。刺激交感神经和动脉内注射去甲肾上腺素和血管紧张素以频率和剂量依赖性方式增加肠系膜灌注压。对神经刺激和升压激素的反应是可重复的，并且不会因输注 PGI2 的 Tris 载体或 PGI2 分解产物 6-酮-PGF1 α 而改变。输注 PGI2（1 微克/分钟和 0.3 微克/分钟）可降低肠系膜动脉灌注压，并且在较高输注速率下，显着降低对神经刺激、去甲肾上腺素和血管紧张素的反应。在较低的输注速率下，PGI2 引起对去甲肾上腺素和神经刺激的反应小幅但显着的降低，但不改变对血管紧张素的反应。这些研究的结果表明，PGI2 具有抑制猫肠道血管床中血管收缩反应的能力，并表明这种作用是连接后的。
The effects of infusion of prostacyclin, PGI2, on vasoconstrictor responses to sympathetic nerve stimulation, norepinephrine and angiotensin II were investigated in the mesenteric vascular bed of the cat. Stimulation of the sympathetic nerves and intra-arterial injections of norepinephrine and angiotensin increased mesenteric perfusion pressure in a frequency and dose-dependent manner. Responses to nerve stimulation and pressor hormones were reproducible and not altered by infusions of the Tris vehicle for PGI2 or the PGI2 breakdown product, 6-keto-PGF1 alpha. Infusions of PGI2, 1 and 0.3 micrograms/min, decreased mesenteric arterial perfusion pressure and, at the higher infusion rate, markedly reduced responses to nerve stimulation, norepinephrine and angiotensin. At the lower infusion rate PGI2 caused small but significant reductions in responses to norepinephrine and nerve stimulation but did not alter responses to angiotensin. Results of these studies demonstrate that PGI2 possesses the ability to inhibit vasoconstrictor responses in the feline intestinal vascular bed and suggest that this effect is postjunctional.