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两种不同程度腹腔内高压对猪模型细菌易位的影响。

Influence of two different levels of intra-abdominal hypertension on bacterial translocation in a porcine model.

机构信息

Department of Pediatric Cardiology and Intensive Care, University Children's Hospital, Hannover Medical School (MHH), Carl-Neuberg-Str, 1, 30625 Hannover, Germany.

出版信息

Ann Intensive Care. 2012 Jul 5;2 Suppl 1(Suppl 1):S17. doi: 10.1186/2110-5820-2-S1-S17.

DOI:10.1186/2110-5820-2-S1-S17
PMID:22873417
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3390291/
Abstract

BACKGROUND

The purpose of the present study was to quantify bacterial translocation to mesenteric lymph nodes due to different levels of intra-abdominal hypertension (IAH; 15 vs. 30 mmHg) lasting for 24 h in a porcine model.

METHODS

We examined 18 anesthetized and intubated pigs (52.3 ± 4.7 kg) which were randomly allocated to three experimental groups (each n = 6) and studied over a period of 24 h. After preparation and establishing a steady state, the intra-abdominal pressure (IAP) was increased stepwise to 30 mmHg in six animals using a carbon dioxide (CO2) insufflator (IAP-30 group). In the second group, IAP was increased to 15 mmHg (IAP-15 group), while IAP remained unchanged in another six pigs (control group). Using a pulse contour cardiac output (PiCCO®) monitoring system, hemodynamic parameters as well as blood gases were recorded periodically. Moreover, peripheral and portal vein blood samples were taken for microbiological examinations. Lymph nodes from the ileocecal junction were sampled during an intra-vital laparotomy at the end of the observational period. After sacrificing the animals, bowel tissue samples and corresponding mesenteric lymph nodes (MLN) were extracted for histopathological and microbiological analyses.

RESULTS

Cardiac output decreased in all groups. In IAP-30 animals, volumetric preload indices significantly decreased, while those of IAP-15 pigs did not differ from those of controls. Under IAH, the mean arterial pressure (MAP) in the IAP-30 group declined, while MAP in the IAP-15 group was significantly elevated (controls unchanged). PO2 and PCO2 remained unchanged. The grade of ischemic damage of the intestines (histopathologically quantified using the Park score) increased significantly with different IAH levels. Accordingly, the amount of translocated bacteria in intestinal wall specimens as well as in MLN significantly increased with the level of IAH. Lymph node cultures confirmed the relation between bacterial translocation (BT) and IAP. The most often cultivated species were Escherichia coli, Staphylococcus, Clostridium, Pasteurella, and Streptococcus. Bacteremia was detected only occasionally in all three groups (not significantly different) showing gut-derived bacteria such as Proteus, Klebsiella, and E. coli spp.

CONCLUSION

In this porcine model, a higher level of ischemic damage and more BT were observed in animals subjected to an IAP of 30 mmHg when compared to animals subjected to an IAP of 15 mmHg or controls.

摘要

背景

本研究的目的是量化由于不同水平的腹腔内高压(IAH;15 与 30mmHg)持续 24 小时导致的细菌向肠系膜淋巴结转移的情况,该研究使用猪模型进行。

方法

我们检查了 18 头麻醉和插管的猪(52.3±4.7kg),这些猪被随机分配到三个实验组(每组 n=6),并在 24 小时内进行研究。在准备和建立稳定状态后,使用二氧化碳(CO2)吹入器将 6 只动物的腹腔内压(IAP)逐步升高至 30mmHg(IAP-30 组)。在第二组中,将 IAP 升高至 15mmHg(IAP-15 组),而另外 6 只猪的 IAP 保持不变(对照组)。使用脉搏轮廓心输出量(PiCCO®)监测系统,定期记录血流动力学参数和血气。此外,采集外周和门静脉血样进行微生物学检查。在观察期结束时进行活体剖腹术,从回盲肠交界处采集淋巴结样本。在处死动物后,提取肠组织样本和相应的肠系膜淋巴结(MLN)进行组织病理学和微生物学分析。

结果

所有组的心输出量均下降。在 IAP-30 动物中,容量前负荷指数显著降低,而 IAP-15 猪的这些指数与对照组无差异。在 IAH 下,IAP-30 组的平均动脉压(MAP)下降,而 IAP-15 组的 MAP 显著升高(对照组不变)。PO2 和 PCO2 保持不变。肠缺血损伤的程度(通过 Park 评分进行组织病理学量化)随着 IAH 水平的不同而显著增加。相应地,肠壁标本和 MLN 中转移细菌的数量随着 IAH 水平的增加而显著增加。淋巴结培养证实了细菌易位(BT)与 IAP 之间的关系。最常培养的物种是大肠杆菌、葡萄球菌、梭菌、巴氏杆菌和链球菌。所有三组均偶尔检测到菌血症(无显著差异),显示出源自肠道的细菌,如变形杆菌、克雷伯菌和大肠杆菌属。

结论

在该猪模型中,与 IAP 为 15mmHg 或对照组的动物相比,IAP 为 30mmHg 的动物观察到更高水平的缺血损伤和更多的 BT。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80e2/3390291/bcdc53ba93c4/2110-5820-2-S1-S17-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80e2/3390291/166a639afeda/2110-5820-2-S1-S17-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80e2/3390291/2c1be1fab2da/2110-5820-2-S1-S17-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80e2/3390291/19ce063baae0/2110-5820-2-S1-S17-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80e2/3390291/bcdc53ba93c4/2110-5820-2-S1-S17-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80e2/3390291/166a639afeda/2110-5820-2-S1-S17-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80e2/3390291/2c1be1fab2da/2110-5820-2-S1-S17-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80e2/3390291/19ce063baae0/2110-5820-2-S1-S17-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80e2/3390291/bcdc53ba93c4/2110-5820-2-S1-S17-4.jpg

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