TUMOR-NECROSIS-FACTOR-ALPHA INCREASES MYOCARDIAL MICROVASCULAR TRANSPORT IN-VIVO

被引:19
作者
HANSEN, PR
SVENDSEN, JH
HOYER, S
KHARAZMI, A
BENDTZEN, K
HAUNSO, S
机构
[1] UNIV COPENHAGEN, DEPT MED B, DIV CARDIOL, DK-2100 COPENHAGEN, DENMARK
[2] UNIV COPENHAGEN, DEPT PATHOL, DK-2100 COPENHAGEN, DENMARK
[3] UNIV COPENHAGEN, DEPT CLIN MICROBIOL, DK-2100 COPENHAGEN, DENMARK
[4] UNIV COPENHAGEN, DEPT MED TTA, DK-2100 COPENHAGEN, DENMARK
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1994年 / 266卷 / 01期
关键词
HEART; MICROCIRCULATION; CAPILLARY; NEUTROPHILS; DOGS;
D O I
10.1152/ajpheart.1994.266.1.H60
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Tumor necrosis factor-oc (TNF-a) is a primary mediator in the pathogenesis of tissue injury, and high circulating levels of TNF-a are found in a variety of pathological conditions. In open-chest anesthetized dogs, the effects of intracoronary recombinant human TNF-alpha (rTNF-alpha; 100 ng/kg for 60 min) on myocardial microvascular transport of a small hydrophilic indicator was examined by the single-injection, residue-detection method. Intracoronary infusion of rTNF-alpha increased myocardial microvascular transport after 120 min. This increase was preceeded by a sustained decline in cardiac output and was associated with the appearance of areas with myocardial necrosis in the regional left ventricular wall. The myocardial plasma flow rate and maximum plasma flow rate in response to a 30-s coronary occlusion were not influenced by rTNF-alpha, although a decrease in the myocardial plasma flow rate was observed after 180 min. Circulating neutrophil counts were increased by rTNF-alpha, but the increase in myocardial capillary permeability could not be ascribed to regional neutrophil infiltration. We conclude that picomolar levels of rTNF-alpha, can influence the movement of small hydrophillic molecules across the myocardial microvascular barrier in vivo and induce a prolonged decrease in cardiac performance. These effects may be important elements in myocardial pathophysiology.
引用
收藏
页码:H60 / H67
页数:8
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