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首页> 外文期刊>American Journal of Physiology >Mechanisms of polymicrobial sepsis-induced ileus.
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Mechanisms of polymicrobial sepsis-induced ileus.

机译：微生物败血症诱发肠梗阻的机制。

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Sepsis frequently occurs after hemorrhage, trauma, burn, or abdominal surgery and is a leading cause of morbidity and mortality in severely ill patients. We performed experiments to delineate intestinal molecular and functional motility consequences of polymicrobial sepsis in the clinically relevant cecal ligation and puncture (CLP) sepsis model. CLP was performed on male Sprague-Dawley rats. Gastrointestinal transit, colonic in vivo pressure recordings, and in vitro muscle contractions were recorded. Histochemistry was performed for macrophages, monocytes, and neutrophils. Inflammatory gene expressions were quantified by real-time RT-PCR. CLP delayed gastrointestinal transit, decreased colonic pressures, and suppressed in vivo circular muscle contractility of the jejunum and colon over a 4-day period. A leukocytic infiltrate of monocytes and neutrophils developed over 24 h. Real-time RT-PCR demonstrated a significant temporal elevation in IL-6, IL-1beta, monocyte chemoattractant protein-1, and inducible nitric oxide synthase, with higher expression levels of IL-6 and inducible nitric oxide synthase in colonic extracts compared with small intestine. Polymicrobial CLP sepsis induces a complex inflammatory response within the intestinal muscularis with the recruitment of leukocytes and elaboration of mediators that inhibit intestinal muscle function. Differences were elucidated between endotoxin and CLP models of sepsis, as well as a heterogeneous regional response of the gastrointestinal tract to CLP. Thus the intestine is not only a source of bacteremia but also an important target of bacterial products with major functional consequences to intestinal motility and the generation of cytokines, which participate in the development of multiple organ failure.
机译：败血症经常在出血，外伤，烧伤或腹部手术后发生，并且是重症患者发病和死亡的主要原因。我们进行了实验，以在临床相关的盲肠结扎和穿刺（CLP）脓毒症模型中描述多菌性脓毒症在肠道分子和功能运动方面的后果。在雄性Sprague-Dawley大鼠上进行CLP。记录胃肠道运输，结肠体内压力记录和体外肌肉收缩。对巨噬细胞，单核细胞和嗜中性白细胞进行组织化学。通过实时RT-PCR定量炎性基因表达。 CLP在4天的时间内延缓了胃肠道的运输，降低了结肠的压力，并抑制了空肠和结肠的体内环形肌肉收缩力。单核细胞和中性粒细胞的白细胞浸润在24小时内发展。实时RT-PCR显示IL-6，IL-1beta，单核细胞趋化蛋白1和诱导型一氧化氮合酶的时间明显升高，与结肠提取物中IL-6和诱导型一氧化氮合酶的表达水平相比，小肠。微生物CLP脓毒症会引起白细胞募集和抑制肠道肌肉功能的介体合成，从而引起肠道肌层内复杂的炎症反应。阐明了内毒素和脓毒症的CLP模型之间的差异，以及胃肠道对CLP的异质区域反应。因此，肠不仅是菌血症的来源，而且还是细菌产物的重要靶标，其对肠道运动和细胞因子的产生具有重要的功能后果，参与了多器官功能衰竭的发展。

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