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[肝硬化大鼠实验模型中自发性细菌性腹膜炎的发生。与肠道细菌移位的关系]

[Development of spontaneous bacterial peritonitis in an experimental model in cirrhotic rats. Relationship with intestinal bacterial translocation].

作者信息

Martín L, Sánchez E, Casafont F, Agüero J, Ledesma P, Nevado N, Pons Romero F

机构信息

Servicio de Aparato Digestivo, Hospital Universitario Marqués de Valdecilla, Santander.

出版信息

Rev Esp Enferm Dig. 1995 Sep;87(9):632-6.

PMID:7577121
Abstract

Spontaneous bacterial peritonitis (SBP) is one of the most important complication in cirrhotic patients with ascites, but is pathogenesis is not well known. It is thought that the impaired host defences and the passage of enteric bacteria into the mesenteric lymph nodes, named bacterial translocation, may be two important mechanisms in the pathogenesis of SBP. We have studied this phenomenon in an experimental model with oral CC14 induced cirrhotic rats. SBP occurred in 36% of ascitic rats, all cases being produced by enteric Gram (-) bacteria. Bacterial translocation was observed in 100% of rats with SBP but in 53% of rats without SBP (p < 0.05). In all cases the same organism was isolated in ascitic fluid and in mesenteric lymph nodes. These results suggest that bacterial translocation could play an important role in the pathogenesis of SBP.

摘要

自发性细菌性腹膜炎(SBP)是肝硬化腹水患者最重要的并发症之一,但其发病机制尚不清楚。人们认为宿主防御功能受损以及肠道细菌进入肠系膜淋巴结(即细菌移位)可能是SBP发病机制中的两个重要机制。我们在口服四氯化碳诱导的肝硬化大鼠实验模型中研究了这一现象。36%的腹水大鼠发生了SBP,所有病例均由肠道革兰氏阴性菌引起。100%的SBP大鼠出现了细菌移位,但无SBP的大鼠中这一比例为53%(p<0.05)。在所有病例中,腹水中和肠系膜淋巴结中分离出的是同一种微生物。这些结果表明,细菌移位可能在SBP的发病机制中起重要作用。

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