Acute pancreatitis as a model of SIRS

被引:61
作者
Bhatia, Madhav [1 ]
机构
[1] Natl Univ Singapore, Yong Loo Lin Sch Med, Ctr life Sci, Dept Pharmacol, Singapore 117456, Singapore
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2009年 / 14卷
基金
英国医学研究理事会;
关键词
Acute Pancreatitis; Mouse; Rat; Opossum; Substance P; Chemokines; Hydrogen sulfide; Review; PLATELET-ACTIVATING-FACTOR; INDUCED NEUTROPHIL CHEMOATTRACTANT; LUNG INJURY; HYDROGEN-SULFIDE; PROTECTS MICE; SUBSTANCE-P; ACINAR-CELLS; EXPRESSION; CERULEIN; RECEPTOR;
D O I
10.2741/3362
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Acute pancreatitis is a common clinical condition. Excessive systemic inflammatory response syndrome (SIRS) in acute pancreatitis leads to distant organ damage and multiple organ dysfunction syndrome (MODS), which is the primary cause of morbidity and mortality in this condition. Development of in vivo experimental models of acute pancreatitis and associated systemic organ damage has enabled us to study the role played by inflammatory mediators in the pathogenesis of acute pancreatitis and associated systemic organ damage. Using these models, recent studies by us and other investigators have established the critical role played by inflammatory mediators such as TNF-alpha, IL-1 beta, IL-6, PAF, IL-10, CD40L, C5a, ICAM-1, chemokines, substance P and hydrogen sulfide in acute pancreatitis and the resultant MODS. This chapter intends to present an overview of different experimental animal models of acute pancreatitis and associated MODS and the role of inflammatory mediators in the pathogenesis of this condition.
引用
收藏
页码:2042 / 2050
页数:9
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