HYPOTHEMIA REVERSIBLY INHIBITS ENDOTHELIAL-CELL EXPRESSION OF E-SELECTIN AND TISSUE FACTOR

被引：42

作者：

JOHNSON, M ^{[1
]}

HADDIX, T ^{[1
]}

POHLMAN, T ^{[1
]}

VERRIER, ED ^{[1
]}

机构：

[1] UNIV WASHINGTON,DEPT SURG,DIV CARDIOTHORAC SURG,SEATTLE,WA 98155

来源：

JOURNAL OF CARDIAC SURGERY | 1995年 / 10卷 / 04期

关键词：

D O I：

10.1111/j.1540-8191.1995.tb00673.x

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Hypothermia frequently accompanies cardiopulmonary bypass (CPB) and myocardial protection strategies during cardiac surgery, With CPB, the blood/artificial surface interface activates components of the humoral and cellular inflammatory cascades and may contribute to postoperative end organ dysfunction including the heart or multiple other organ systems. The endothelial cell (EC) monolayer normally mediates components of solute transport, vasomotor function, coagulation, cell differentiation/growth, and immune/inflammatory processes, E-selectin is a vascular adhesion molecule that mediates neutrophil adherence and that is inducible in ECs by inflammatory mediators such as cytokines, Tissue factor (TF) is similarly an inducible procoagulant factor in ECs that contributes to thrombosis, The induction, transcription, and expression of both molecules were studied in cultured human umbilical vein cells at normothermic (37 degrees), hypothermic (25 degrees), and rewarmed (37 degrees) conditions after stimulation with the cytokines tumor necrosis factor alpha and interleukin-1, Hypothermia reversibly inhibits the transcription and expression but not the induction of both E-selectin and TF.

引用

页码：428 / 435

页数：8

共 47 条

[1]

Hearse D, Braimbridge M, Jynge P, Protection of the ischemic myocardium: Cardioplegia

[2]

Cave A, Hearse D, Ischaemic preconditioning and contractile function: Studies with normothermic and hypothermic global ischaemia, J Mol Cell Cardiol, 24, pp. 1113-1123, (1992)

[3]

Lichtenstein S, Ashe K, Dalati H, Et al., Warm heart surgery, J Thorac Cardiovasc Surg, 101, pp. 269-274, (1991)

[4]

Tonz M, Mihaljevic T, Pasic M, Et al., The warm versus cold perfusion controversy: A clinical comparative study, European Journal of Cardio-Thoracic Surgery, 7, pp. 623-627, (1993)

[5]

Amrani M, Mankad P, Yacoub M, Improved preservation of endothelial function at 4°C, Eur J Cardiothorac Surg, 6, pp. 72-78, (1992)

[6]

Hansen T, Dawson P, Brockbank K, Effects of hypothermia upon endothelial cells: Mechanisms and clinical importance, Cryobiology, 31, pp. 101-106, (1994)

[7]

Hashimoto K, Pearson P, Schaff H, Et al., Endothelial cell dysfunction after ischemic arrest and reperfusion: A possible mechanism of myocardial injury during reflow, J Thorac Surg, 102, pp. 688-694, (1991)

[8]

Kurose I, Anderson D, Miyasaka M, Et al., Molecular determinants of reperfusion‐induced leukocyte adhesion and vascular protein leakage, Circ Res, 74, pp. 336-343, (1994)

[9]

Lefer A, Lefer D, Pharmacology of the endothelium in ischemia‐reperfusion and circulatory shock, Annu Rev Pharmacol Toxocol, 33, pp. 71-90

[10]

Verrier E, The vascular endothelium: Friend or foe, Ann Thorac Surg, 55, pp. 818-819, (1993)

← 1 2 3 4 5 →