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一种诱导全肝缺血同时防止继发于内脏血管充血的循环衰竭的新模型。

A new model for inducing total hepatic ischemia while preventing circulatory collapse secondary to splanchnic vascular congestion.

作者信息

Gonce M E, Brackett D J, Squires R A, Gibson D D, Kajdacsy-Balla A, Lerner M R, McCay P B, Pennington L R

机构信息

Department of Surgery, University of Oklahoma Health Sciences Center, Oklahoma City 73190, USA.

出版信息

Shock. 1995 Jun;3(6):440-6.

PMID:7656069
Abstract

Animal models used to study liver ischemia are limited by the lethal effect of splanchnic venous engorgement from portal triad occlusion (PTO). We compared a passive porto-systemic shunt (PSS) to a pump-driven PSS. The passive and pumped PSS groups (n = 6) received 60 min of PTO followed by 2 h of reperfusion. A control group received all interventions, but no PTO, and remained stable throughout. During PTO, severe circulatory shock with intestinal ischemia occurred in the passive group, while the pumped group remained stable. During reperfusion, both shunted groups experienced varying degrees of metabolic acidosis with decreases in cardiac index, stroke volume, superior mesenteric artery flow, and increases in systemic and intestinal vascular resistance. The mortality rate for the passive group was 83% vs. 0% for the pumped group. These results suggest that pumped PSS prevents splanchnic engorgement and allows for reproducible, isolated total hepatic ischemia in vivo.

摘要

用于研究肝脏缺血的动物模型受到门静脉三联体闭塞(PTO)导致的内脏静脉充血致死效应的限制。我们比较了被动门体分流术(PSS)和泵驱动的PSS。被动和泵驱动PSS组(n = 6)接受60分钟的PTO,然后再灌注2小时。对照组接受所有干预措施,但不进行PTO,并且在整个过程中保持稳定。在PTO期间,被动组出现严重的循环性休克并伴有肠道缺血,而泵驱动组则保持稳定。在再灌注期间,两个分流组均出现不同程度的代谢性酸中毒,心脏指数、每搏输出量、肠系膜上动脉血流量降低,全身和肠道血管阻力增加。被动组的死亡率为83%,而泵驱动组为0%。这些结果表明,泵驱动的PSS可防止内脏充血,并允许在体内进行可重复的、孤立的全肝缺血。

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