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正常和动脉粥样硬化猴子肠系膜循环对血清素的反应:对非闭塞性肠缺血发病机制的影响。

Response of the mesenteric circulation to serotonin in normal and atherosclerotic monkeys: implications for the pathogenesis of non-occlusive intestinal ischaemia.

作者信息

Lopez J A, Brown B P, Armstrong M L, Piegors D J, Heistad D D

机构信息

Cardiovascular Division, VA Medical Center, Iowa City.

出版信息

Cardiovasc Res. 1989 Feb;23(2):117-24. doi: 10.1093/cvr/23.2.117.

Abstract

We tested the hypothesis that atherosclerosis potentiates vasoconstrictor responses in the mesenteric circulation to stimulation of serotonergic and alpha-adrenergic receptors. In normal monkeys, infusion of serotonin had little effect on blood flow to the stomach, duodenum, and colon. In contrast, in atherosclerotic monkeys, serotonin produced a modest decrease in blood flow to the stomach and duodenum, and virtually abolished blood flow to the colon. Vasoconstrictor responses to phenylephrine in the stomach and duodenum were not altered by atherosclerosis, but responses were potentiated in the colon of atherosclerotic monkeys. In summary, atherosclerosis greatly potentiates vasoconstrictor responses to serotonin in the mesenteric circulation, particularly in vessels to the colon. We speculate that release of serotonin during adherence and aggregation of platelets at atherosclerotic lesions, coupled with augmented vasoconstrictor responses to serotonin, may play a role in the pathogenesis of non-occlusive mesenteric ischaemia.

摘要

我们验证了这样一个假设

动脉粥样硬化会增强肠系膜循环中血管收缩反应,以应对血清素能和α-肾上腺素能受体的刺激。在正常猴子中,输注血清素对胃、十二指肠和结肠的血流量影响很小。相比之下,在动脉粥样硬化的猴子中,血清素使胃和十二指肠的血流量适度减少,实际上消除了结肠的血流量。动脉粥样硬化并未改变胃和十二指肠对去氧肾上腺素的血管收缩反应,但在动脉粥样硬化猴子的结肠中,这种反应增强了。总之,动脉粥样硬化极大地增强了肠系膜循环中对血清素的血管收缩反应,尤其是在通向结肠的血管中。我们推测,在动脉粥样硬化病变处血小板黏附和聚集过程中血清素的释放,再加上对血清素增强的血管收缩反应,可能在非闭塞性肠系膜缺血的发病机制中起作用。

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