休克与多器官功能衰竭中的自我消化假说：蛋白酶活性降解
The Autodigestion Hypothesis in Shock and Multi-Organ Failure: Degrading Protease Activity.
作者信息
Schmid-Schönbein Geert W, Penn Alex, Kistler Erik
机构信息
Microcirculation Laboratory, Department of Bioengineering, The Institute of Engineering in Medicine, University of California San Diego, La Jolla, California 92093 - 0412.
出版信息
Bol Soc Port Hemorreol Microcirc. 2011 Jul;26(3):6-15.
Shock and multi-organ failure have one of the highest levels of inflammatory markers, morbidities and mortality. The underlying mechanisms are currently unknown and no effective intervention exists. We present evidence for a previously untested mechanism due to by the digestive enzymes synthesized in the pancreas and transported in the lumen of the intestine as normal part of food digestion. We summarize experimental evidence in support of the autodigestion hypothesis and a new approach for possible intervention against multi-organ failure that is currently entering clinical trials.
休克和多器官功能衰竭的炎症标志物水平、发病率和死亡率都处于最高水平之一。其潜在机制目前尚不清楚，也不存在有效的干预措施。我们提供了证据，证明一种先前未经测试的机制，该机制是由胰腺合成并作为食物消化正常部分在肠腔内运输的消化酶引起的。我们总结了支持自身消化假说的实验证据，以及一种针对多器官功能衰竭可能的干预新方法，该方法目前正在进入临床试验阶段。
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