ENDOTHELIAL AND VASCULAR SMOOTH-MUSCLE FUNCTION IN SEPSIS

被引：41
作者：
HOLLENBERG, SM [1 ]
CUNNION, RE [1 ]
机构：
[1] RUSH PRESBYTERIAN ST LUKES MED CTR,DIV CARDIOL,CHICAGO,IL 60612
来源：
JOURNAL OF CRITICAL CARE | 1994年 / 9卷 / 04期
关键词：
D O I：
10.1016/0883-9441(94)90006-X
中图分类号：
R4 [临床医学];
学科分类号：
1002 ; 100602 ;
摘要：
The vascular abnormalities that arise during sepsis imply disturbances in the delicately tuned homeostatic mechanisms of vascular endothelium and smooth muscle. In the microvasculature, smooth muscle tone represents a complex equilibrium among metabolic stimuli, hemodynamic forces, and neurohumoral influences. Local tissue perfusion also is modulated by vasoactive mediators that can be produced locally, through endothelium-dependent adhesion and activation of inflammatory cells, or at a distance. In sepsis, derangement of normal autoregulation of perfusion, together with toxic effects of mediators, may be severe enough to result in organ dysfunction. Recent advances in vascular biology have illuminated a variety of targets, such as adhesion molecules, platelet activating factor, and inducible nitric oxide synthase for potential therapeutic intervention in sepsis. Copyright (C) 1994 by W.B. Saunders Company
引用
收藏
页码：262 / 280
页数：19
相关论文
共 123 条
[51]  
Katusic, Shepherd, Endothelium-derived vasoactive factors: II. Endothelium-dependent contraction, Hypertension, 18, (1991)
[52]  
Kilbourn, Gross, Jubran, Et al., NG-methylL-arginine inhibits tumor necrosis factor-induced hypotension: Implications for the involvement of nitric oxide, Proc Natl Acad Sci USA, 87, pp. 3629-3632, (1990)
[53]  
Kiowski, Luscher, Linder, Et al., Endothelin1-induced vasoconstriction in humans. Reversal by calcium channel blockade but not by nitrovasodilators or endothelium-derived relaxing factor, Circulation, 83, pp. 469-475, (1991)
[54]  
Koller, Kaley, Endothelial regulation of wall shear stress and blood flow in skeletal muscle microcirculation, Am J Physiol, 260, pp. H862-H868, (1991)
[55]  
Koltai, Hosford, Braquet, Role of PAF and cytokines in microvascular tissue injury, J Lab Clin Med, 119, pp. 461-466, (1992)
[56]  
Korthuis, Anderson, Granger, Role of neutrophil-endothelial cell adhesion in inflammatory disorders, J Crit Care, 9, pp. 47-71, (1994)
[57]  
Kubes, Granger, Nitric oxide modulates vascular permeability, Am J Physiol, 262, pp. H611-H615, (1992)
[58]  
Kubes, Grisham, Barrowman, Et al., Leukocyte-induced vascular protein leakage in cat mesentery, Am J Physiol, 261, pp. H1872-H1879, (1991)
[59]  
Kubes, Suzuki, Granger, Nitric oxide: An endogenous modulator of leukocyte adhesion, Proc Natl Acad Sci USA, 88, pp. 4651-4655, (1991)
[60]  
Kurose, Anderson, Miyasaka, Et al., Molecular determinants of reperfusion-induced leukocyte adhesion and vascular protein leakage, Circ Res, 74, pp. 336-343, (1994)
12345678910