期刊
CLINICAL AND APPLIED THROMBOSIS-HEMOSTASIS
卷 15, 期 2, 页码 209-219出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/1076029607309256
关键词
LPS; endotoxin; phospholipase; annexin; phospholipid vesicles; DNA; kallikrein; thrombin; fibrin
Lipopolysaccharides at approximate plasma reactivities >3 ng/mL or beta-glucans at >0.5-1 mu g/mL are toxic for human blood.; lipopolysaccharide interacts with membrane components of susceptible cells (eg, monocytes) activating phospholipase A, that destroys the cell membrane. Cell fragments (microparticles or DNA) possess poly-negative niches that activate intrinsic hemostasis. Pathologic disseminated intravascular coagulation arises. Blood vessels are Obstructed by disseminated thrombi., and vital organ areas become ischemic. MUltiorgan failure tbreatens life of the patient. Diagnosis and therapy of pathologic disseminated intravascular coagulation is of extreme clinical importance. For early diagnosis of pathologic disseminated intravascular coagulation, specific activation markers of coagulation (eg, plasmatic amidolytic thrombin activity) or the plasmatic lipopolysaccharide or glucan reactivity can be measured. A new treatment target might be kallikrein or factor XIIa; 10 to 20 mM arginine is the approximate 50% inhibitory concentration against the contact phase of coagulation. The complex interaction between cell fragments and hemostasis causes pathologic disseminated intravascular coagulation in sepsis.
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