Endothelium function in sepsis

被引:87
作者
Volk, T [1 ]
Kox, WJ [1 ]
机构
[1] Humboldt Univ, Univ Hosp Charite, Dept Anaesthesiol & Intens Therapy, D-10117 Berlin, Germany
关键词
endothelium; sepsis; permeability; vasoregulation; coagulation;
D O I
10.1007/s000110050579
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Endothelial cells can be the prime target for an infection and infected endothelial cells may serve as an initiating system for a systemic response as these cells are able to secrete many mediators known to be of paramount importance. Endothelial cell functions in turn are regulated by these circulating mediators. Cellular interactions with leukocytes revealed protective and destructive functions. Single cell and animal studies indicate that endothelial permeability is increased and apart from clinical obvious edema formation in septic patients, the endothelial component remains unknown. Endothelial coagulation activation has been shown in vitro, however human data supporting an endothelial procoagulatory state are lacking. Defects in endothelium dependent vasoregulation in animal models are well known and again human studies are largely missing. An imbalanced production of reactive oxygen species including nitric oxide has been found to be involved in all endothelial functions and may provide a common link which at present can be supported only in animal studies.
引用
收藏
页码:185 / 198
页数:14
相关论文
共 199 条
[1]   Endothelial-dependent mechanisms regulate leukocyte transmigration: A process involving the proteasome and disruption of the vascular endothelial-cadherin complex at endothelial cell-to-cell junctions [J].
Allport, JR ;
Ding, H ;
Collins, T ;
Gerritsen, ME ;
Luscinskas, FW .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 186 (04) :517-527
[2]  
ALTURA BM, 1985, MICROCIRC ENDOTH LYM, V2, P121
[3]  
ALTURA BM, 1985, MICROCIRC ENDOTH LYM, V2, P3
[4]   Ambient but not incremental oxidant generation effects intercellular adhesion molecule 1 induction by tumour necrosis factor α in endothelium [J].
Arai, T ;
Kelly, SA ;
Brengman, ML ;
Takano, M ;
Smith, EH ;
Goldschmidt-Clermont, PJ ;
Bulkley, GB .
BIOCHEMICAL JOURNAL, 1998, 331 :853-861
[5]   Relationship between circulating levels of calcitonin gene-related peptide, nitric oxide metabolites and hemodynamic changes in human septic shock [J].
Arnalich, F ;
Hernanz, A ;
Jimenez, M ;
Lopez, J ;
Tato, E ;
Vazquez, JJ ;
Montiel, C .
REGULATORY PEPTIDES, 1996, 65 (02) :115-121
[6]   MICROVASCULAR FUNCTION AND RHEOLOGICAL CHANGES IN HYPERDYNAMIC SEPSIS [J].
ASTIZ, ME ;
DEGENT, GE ;
LIN, RY ;
RACKOW, EC .
CRITICAL CARE MEDICINE, 1995, 23 (02) :265-271
[7]   PERIPHERAL VASCULAR TONE IN SEPSIS [J].
ASTIZ, ME ;
TILLY, E ;
RACKOW, ED ;
WEIL, MH .
CHEST, 1991, 99 (05) :1072-1075
[8]  
Avirutnan P, 1998, J IMMUNOL, V161, P6338
[9]   Effect of L-NAME, an inhibitor of nitric oxide synthesis, on plasma levels of IL-6, IL-8, TNFα and nitrite/nitrate in human septic shock [J].
Avontuur, JAM ;
Stam, TC ;
Jongen-Lavrencic, M ;
van Amsterdam, JGC ;
Eggermont, AMM ;
Bruining, HA .
INTENSIVE CARE MEDICINE, 1998, 24 (07) :673-679
[10]   Chemokines and leukocyte traffic [J].
Baggiolini, M .
NATURE, 1998, 392 (6676) :565-568