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[猪大肠杆菌肠毒血症发病机制的实验研究。4. 经肠胃外给药脂多糖内毒素对断奶仔猪的影响]

[Experimental studies on the pathogenesis of Coli-enterotoxemia in swine. 4. Effect of lipopolysaccharide endotoxin on weaned piglets following parenteral administration].

作者信息

Johannsen U

出版信息

Arch Exp Veterinarmed. 1977;31(2):191-202.

PMID:332109
Abstract

Ten clinically intact weaned piglets were experimentally intoxicated by intravenous injection of lipoproteide-free lipopolysaccharide endotoxin according to Westphal of E. coli O 127:B8. Severe endotoxin shock with all clinical manifestations of experimental coli-enterotoxaemia was induced in all animals and included circulatory disorder with tachycardia, intermittent pallor and/or cyanosis, symptoms of severe systemic intoxication, neurological symptoms, such as lack of coordination, hindleg staggering, spasm, paresis, paralysis, changes in respiration, such as rise in respiratory frequency and deepened breathing premortal deceleration of respiration and gasping for breath, temperature, variation, including hyperthermia and aggravating hypothermia, gastro-intestinal symptoms, such as temporary vomiting and persistent diarrhoea, leucopenia, eosinopenia, variation of haematocrit, edematisation, increased transudation, congestion, and gastro-intestinal shock lesions. Eight animals died. These experiments quite obviously have confirmed that endotoxin shock is the common pathogenetic principle behind all forms of coli-entertoxaemia (i.e, the forms of edematisation, cardiovascular failure, and gastro-intestinal processes.) Lipopolysaccharide endotoxin alone may be responsible for the development of both edemas and neurotoxic symptoms (edema disease) and diarrhoea (gastro-intestinal form of coli-enterotoxaemia). The pathogenetic relevance of additional toxins (neurotoxin and enterotoxin) is discussed under this aspect.

摘要

根据大肠杆菌O 127:B8的韦斯特法尔法,对10只临床健康的断奶仔猪进行静脉注射无脂蛋白脂多糖内毒素实验性中毒。所有动物均诱发了伴有实验性大肠杆菌肠毒血症所有临床表现的严重内毒素休克,包括伴有心动过速、间歇性苍白和/或发绀的循环障碍、严重全身中毒症状、神经症状,如协调能力缺乏、后肢蹒跚、痉挛、轻瘫、瘫痪、呼吸变化,如呼吸频率增加和呼吸加深、死前呼吸减速和喘息、体温变化,包括体温过高和体温过低加重、胃肠道症状,如暂时呕吐和持续腹泻、白细胞减少、嗜酸性粒细胞减少、血细胞比容变化、水肿、渗出增加、充血以及胃肠道休克病变。8只动物死亡。这些实验很明显证实了内毒素休克是所有形式的大肠杆菌肠毒血症(即水肿、心血管衰竭和胃肠道病变形式)背后的共同发病机制。单独的脂多糖内毒素可能是水肿和神经毒性症状(水肿病)以及腹泻(胃肠道形式的大肠杆菌肠毒血症)发展的原因。在这方面讨论了其他毒素(神经毒素和肠毒素)的发病机制相关性。

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