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[大肠杆菌内毒素诱导的猪休克导致血浆胆囊收缩素增加]

[Increase of plasma cholecystokinin by Escherichia coli endotoxin-induced shock in swine].

作者信息

Riepl R, Jenssen T G, Revhaug A, Burhol P G, Gierchksky K E, Lehnert P

出版信息

Z Gastroenterol. 1986 Nov;24(11):691-9.

PMID:3544541
Abstract

The gastrointestinal tract is the source of numerous peptide hormones. Since the gut will be altered severely during prolonged general circulatory low flow states, the reactions of the gut hormones are of great interest. In this study 18 anesthetized pigs were put into shock states to get first informations about the changes of the plasma levels of cholecystokinin (CCK). 12 pigs (group I and II) were exposed to a general circulatory shock state by a 2-hr intravenous infusion of a sublethal dose of Escherichia coli endotoxin. 6 of them (gr. II) first received a gastroenterectomy apart from a small duodenal remnant proximal and distal to the papilla of Vater. The remaining 6 pigs (gr. III) suffered a severe hemorrhagic-hypovolemic shock over a 150-min period by arterial bleeding. Plasma CCK increased significantly (p less than 0.05) in the aorta (gr. I, II), the portal vein (gr. I, II), the superior caval vein (gr. I), and the internal jugular vein (gr. I) at the end of the 2-hr endotoxin infusion. In group II, the rise of CCK levels in the superior caval vein was also marked, but insignificant. The CCK-concentrations in the internal jugular vein were measured only in group I. By contrast, no changes in plasma CCK were seen in hemorrhagic shock (gr. III). Within each group plasma samples taken from the various blood vessels at identical time points showed no significant differences. Since the plasma concentrations of CCK remained unchanged during hemorrhagic shock, the release of CCK by E. coli endotoxin is not due to the general circulatory low flow state.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

胃肠道是众多肽类激素的来源。由于在长时间的全身循环低流量状态下肠道会发生严重改变,因此肠道激素的反应备受关注。在本研究中,18头麻醉猪被置于休克状态,以获取有关胆囊收缩素(CCK)血浆水平变化的初步信息。12头猪(I组和II组)通过静脉输注亚致死剂量的大肠杆菌内毒素2小时,使其处于全身循环休克状态。其中6头猪(II组)除了在 Vater 乳头近端和远端保留一小段十二指肠残余外,首先接受了胃肠切除术。其余6头猪(III组)通过动脉出血在150分钟内遭受严重的失血性低血容量休克。在2小时内毒素输注结束时,主动脉(I组、II组)、门静脉(I组、II组)、上腔静脉(I组)和颈内静脉(I组)中的血浆CCK显著升高(p < 0.05)。在II组中,上腔静脉中CCK水平的升高也很明显,但不显著。仅在I组中测量了颈内静脉中的CCK浓度。相比之下,在失血性休克(III组)中未观察到血浆CCK的变化。在每组中,在相同时间点从不同血管采集的血浆样本没有显著差异。由于在失血性休克期间CCK的血浆浓度保持不变,大肠杆菌内毒素引起的CCK释放并非由于全身循环低流量状态。(摘要截短至250字)

相似文献

1
[Increase of plasma cholecystokinin by Escherichia coli endotoxin-induced shock in swine].[大肠杆菌内毒素诱导的猪休克导致血浆胆囊收缩素增加]
Z Gastroenterol. 1986 Nov;24(11):691-9.
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The origin and fall of plasma motilin during Escherichia coli endotoxin shock in pigs.猪大肠杆菌内毒素休克期间血浆胃动素的变化及其机制
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Cholecystokinin octapeptide improves cardiac function by activating cholecystokinin octapeptide receptor in endotoxic shock rats.八肽胆囊收缩素通过激活内毒素休克大鼠的八肽胆囊收缩素受体改善心脏功能。
World J Gastroenterol. 2005 Jun 14;11(22):3405-10. doi: 10.3748/wjg.v11.i22.3405.