Pathophysiology of the burn wound and pharmacological treatment. The Rudi Hermans lecture, 1995

被引:145
作者
Arturson, G
机构
[1] Burn Center, University Hospital, Uppsala
关键词
TUMOR-NECROSIS-FACTOR; THERMALLY INJURED PATIENTS; EPIDERMAL GROWTH-FACTOR; ALTERNATIVE COMPLEMENT PATHWAY; NEUTROPHIL-ACTIVATING PEPTIDE; BLOOD MONONUCLEAR-CELLS; LIPID PROTEIN COMPLEX; OXYGEN-FREE-RADICALS; GUINEA-PIG MODEL; POLYMORPHONUCLEAR LEUKOCYTES;
D O I
10.1016/0305-4179(95)00153-0
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
The body's reaction to thermal injury is much more than an initial, local inflammatory response. The burn wound is a continuous, severe threat against the rest of the body due to invasion of infectious agents, antigen challenge and repeated additional trauma caused by wound cleaning and excision. The inflammatory mediators which control blood supply and microvascular permeability in the wound have been extensively studied and are largely understood. Attempts to suppress the inflammatory reaction by different drugs have, however, been less successful. Extensive thermal injury and sepsis also results in immunosuppression. The defects causing immunosuppression are still very much under consideration. An understanding of thee defects is essential for the development of therapies. The increasing interest in the control of the inflammatory reactions by cytokines may, in the near future, be of great importance. (C) 1996 Elsevier Science Ltd for ISBI.
引用
收藏
页码:255 / 274
页数:20
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