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首页> 外文期刊>Shock: Molecular, cellular, and systemic pathobiological aspects and therapeutic approaches = The official journal of the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies >Local attenuation of systemically mediated splanchnic vasoconstriction during shock due to cholera.
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Local attenuation of systemically mediated splanchnic vasoconstriction during shock due to cholera.

机译：本地系统介导的衰减在冲击由于内脏血管收缩霍乱。

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Hypovolemic shock, most often due to hemorrhage, is typically associated with intense splanchnic vasoconstriction. This can be severe enough to impair the functional and structural integrity of the gastrointestinal tract. Paradoxically, with cholera the structure of the gastrointestinal tract is preserved, and the intestine continues to secrete fluid delivered to it in the circulating blood in spite of severe hypovolemic shock. This suggests that splanchnic blood flow is maintained at higher levels in hypovolemic shock due to cholera than in hypovolemic shock due to hemorrhage. Our hypothesis is that cholera toxin in the intestinal lumen activates local mechanisms that attenuate systemically mediated splanchnic vasoconstriction. Blood flow to an isolated ileal segment in situ in the anesthetized rabbit was measured continuously (ultrasound transit-time volume flow probe) for 5 to 6 h after instillation of cholera toxin into the isolated intestinal lumen. Norepinephrine was infused selectively into the mesenteric artery supplying the segment to elicit local responses uncomplicated by compensatory changes secondary to systemic effects of norepinephrine. Baseline vascular conductance increased gradually and became significantly greater in cholera toxin experiments than in vehicle experiments 5 h after treatment (P < 0.035). Animals treated with cholera toxin were less responsive to norepinephrine than vehicle treated animals were (P < 0.05) and became more so over time (P < 0.001). Our conclusion is that cholera toxin activates local mechanisms that attenuate systemically mediated splanchnic vasoconstriction, at least in part by reducing vascular responsiveness to a systemic vasoconstrictor, norepinephrine.
机译：低血容量性休克,通常由于出血,通常是与强烈的内脏吗血管收缩。影响的功能和结构完整性胃肠道。霍乱胃肠道的结构道是保存,肠道仍在继续分泌液体送到的血液循环尽管严重低血容量性冲击。维持在较高水平低血容量性休克由于霍乱比低血容量性休克由于出血。毒素在肠内腔激活当地减弱系统介导的机制内脏血管收缩。孤立的原位回肠段麻醉兔连续测量(超声波渡越时间体积流量探头)5滴剂后6 h的霍乱毒素孤立的肠道流明。注入选择性肠系膜动脉提供部分诱发局部反应简单的二次补偿变化去甲肾上腺素的系统性影响。血管和电导也逐渐增加成为了霍乱毒素明显更大实验比车辆实验5 h后治疗(P < 0.035)。霍乱毒素不响应去甲肾上腺素比车辆对待动物(P < 0.05),随着时间的推移变得如此(P <0.001)。激活本地机制减弱系统介导的内脏通过减少血管收缩,至少在部分血管系统响应能力血管收缩剂,去甲肾上腺素。

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