Pancreatic enzymes and microvascular cell activation in multiorgan failure

被引:18
|
作者
Schmid-Schönbein, GW
Hugli, TE
Kistler, EB
Sofianos, A
Mitsuoka, H
机构
[1] Univ Calif San Diego, Dept Bioengn, La Jolla, CA 92093 USA
[2] Scripps Res Inst, Res Inst, Dept Immunol, La Jolla, CA 92037 USA
关键词
endothelium; flee radicals; neutrophil; protease; pseudopod formation; shock;
D O I
10.1038/sj.mn.7300146
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Cell activation in the microcirculation leads to an inflammatory cascade and is accompanied by many cardiovascular complications. There is a need to identify the trigger mechanisms that lead to the production of in vivo activating factors. We review here mechanisms for cell activation in the microcirculation and specifically the production of humoral cell activators in physiological shock. The elevated levels of activating factors in plasma could be traced to the action of pancreatic enzymes in the ischemic intestine. New interventions against the production of the activators are proposed. The evidence suggests that pancreatic enzymes in the ischemic intestine may attack several tissue components and generate cellular activators that are associated with multiorgan dysfunction in physiological shock.
引用
收藏
页码:5 / 14
页数:10
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