Sameshima H, Ikei S, Mori K, Yamaguchi Y, Egami H, Misumi M, Moriyasu M, Ogawa M
Department of Surgery II, Kumamoto University Medical School, Japan.
Int J Pancreatol. 1993 Oct;14(2):107-15. doi: 10.1007/BF02786116.
Severe acute pancreatitis is often complicated by intraperitoneal infection, resulting in multiple organ failure (MOF). It is known to elevate serum tumor necrosis factor (TNF-alpha) in patients with sepsis and/or MOF. In order to study the role of TNF-alpha in the aggravation of acute pancreatitis, we investigated TNF-alpha production by peritoneal macrophages in acute pancreatitis rat using the cerulein-induced pancreatitis model. TNF-alpha production by isolated peritoneal macrophages following lipopolysaccharide (LPS) stimulation was significantly increased in pancreatitis rats as compared with nonpancreatitis control rats (p < 0.001). Serum TNF-alpha activity was elevated following intraperitoneal administration of LPS as the septic challenge both in pancreatitis rats and in control rats, being significantly higher in the former (p < 0.05). Histological findings and liver function tests revealed that LPS induced more severe liver damage in pancreatitis rats than in control rats within 24 h after LPS administration. These results indicate that increased TNF-alpha production by peritoneal macrophages in acute pancreatitis augmented LPS-induced liver injury and suggest the possibility that TNF-alpha may play a role in the development of MOF during acute pancreatitis complicated by intraabdominal sepsis.
重症急性胰腺炎常并发腹腔内感染，导致多器官功能衰竭（MOF）。已知在脓毒症和/或MOF患者中血清肿瘤坏死因子（TNF-α）会升高。为了研究TNF-α在急性胰腺炎病情加重中的作用，我们使用雨蛙素诱导的胰腺炎模型，对急性胰腺炎大鼠腹腔巨噬细胞产生TNF-α的情况进行了研究。与非胰腺炎对照大鼠相比，胰腺炎大鼠经脂多糖（LPS）刺激后分离出的腹腔巨噬细胞产生TNF-α的量显著增加（p<0.001）。腹腔注射LPS作为脓毒症激发后，胰腺炎大鼠和对照大鼠的血清TNF-α活性均升高，前者显著更高（p<0.05）。组织学检查结果和肝功能测试显示，LPS给药后24小时内，LPS在胰腺炎大鼠中比在对照大鼠中引起更严重的肝损伤。这些结果表明，急性胰腺炎时腹腔巨噬细胞产生TNF-α增加会加重LPS诱导的肝损伤，并提示TNF-α可能在并发腹腔内脓毒症的急性胰腺炎期间MOF的发生中起作用。
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