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幼犬中缺氧诱导的细菌易位。

Hypoxia-induced bacterial translocation in the puppy.

作者信息

Lelli J L, Drongowski R A, Coran A G, Abrams G D

机构信息

Section of Pediatric Surgery, C.S. Mott Children's Hospital, Ann Arbor, MI.

出版信息

J Pediatr Surg. 1992 Aug;27(8):974-81; discussion 981-2. doi: 10.1016/0022-3468(92)90543-g.

DOI:10.1016/0022-3468(92)90543-g
PMID:1403561
Abstract

Because hypoxia is one of the most common major stresses to which a neonate is exposed, we postulated that it alone might be the cause of intestinal bacterial translocation, which could be the underlying etiology of neonatal sepsis. An animal model, in which hypoxia is the sole stress, was developed in our laboratory and tested in 18 puppies to determine the effect of hypoxia and reoxygenation on intestinal bacterial translocation. In group I (n = 8), following laparotomy and cannulation of the superior mesenteric vein (SMV), the FIO2 was decreased from 21% to 9% for 90 minutes followed by reoxygenation at 21% for 120 minutes. The abdomen was closed and the animals were allowed to recover. After 24 hours the mesenteric lymph nodes (MLNs), spleen, and liver were harvested for bacterial determination and the ileum and jejunum for histological evaluation. Group II (n = 7) was treated the same as group I with the FIO2 maintained at 21%. Group III (n = 3) animals were killed, without intervention, for bacterial analysis. In group I, the systemic PO2 decreased by 75%, SMV PO2 decreased by 64%, and oxygen delivery to the small bowel decreased by 80% in comparison with group II. The mean arterial pressure and cardiac output were not significantly different between group I and group II; however, the mucosal blood flow was decreased by 60% (P less than .001) in group I. Arterial and SMV blood lactic acid levels were unchanged in group I in comparison with group II, suggesting that anaerobic metabolism was not initiated in the splanchnic circulation during hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

由于缺氧是新生儿所面临的最常见的主要应激之一,我们推测仅缺氧这一因素可能就是肠道细菌易位的原因,而肠道细菌易位可能是新生儿败血症的潜在病因。我们实验室建立了一种仅以缺氧作为应激因素的动物模型,并在18只幼犬身上进行了测试,以确定缺氧和复氧对肠道细菌易位的影响。在第一组(n = 8)中,剖腹并对上肠系膜静脉(SMV)进行插管后,将吸入氧分数(FIO2)从21%降至9%,持续90分钟,随后再将FIO2恢复到21%,持续120分钟。关闭腹腔,让动物恢复。24小时后,采集肠系膜淋巴结(MLN)、脾脏和肝脏进行细菌检测,并采集回肠和空肠进行组织学评估。第二组(n = 7)的处理方式与第一组相同,但FIO2维持在21%。第三组(n = 3)的动物未经干预即处死,用于细菌分析。与第二组相比,第一组的全身动脉血氧分压(PO2)下降了75%,SMV的PO2下降了64%,小肠的氧输送量下降了80%。第一组和第二组之间的平均动脉压和心输出量无显著差异;然而,第一组的黏膜血流量下降了60%(P <.001)。与第二组相比,第一组的动脉血和SMV血乳酸水平未发生变化,这表明在缺氧期间内脏循环未启动无氧代谢。(摘要截断于250字)

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