Saruc M, Yuceyar H, Turkel N, Ozutemiz O, Tuzcuoglu I, Yuce G, Huseyinov A
Department of Gastroenterology, Celal Bayar University, Manisa, Turkey.
Braz J Med Biol Res. 2003 Jul;36(7):879-86. doi: 10.1590/s0100-879x2003000700008. Epub 2003 Jun 26.
The literature indicates that acute pancreatitis is a complication of massive hemolysis with a prevalence of about 20%. We describe an experimental model of hemolysis-induced acute pancreatitis. Hemolytic anemia was induced in rats by a single ip injection of 60 mg/kg of 20 mg/ml acetylphenylhydrazine (APH) in 20% (v/v) ethanol on the first experimental day (day 0). One hundred and fifty Wistar albino rats weighing 180-200 g were divided into three groups of 50 animals each: groups 1, 2 and 3 were injected ip with APH, 20% ethanol, and physiological saline, respectively. Ten rats from each group were sacrificed on study days 1, 2, 3, 4 and 5. Serum amylase, lipase levels and pancreatic tissue tumor necrosis factor-alpha (TNF-alpha) and platelet-activating factor (PAF) contents were determined and a histological examination of the pancreas was performed. No hemolysis or pancreatitis was observed in any of the rats in groups 2 and 3. In group 1, massive hemolysis was observed in 35 (70%) of 50 rats, moderate hemolysis in seven (14%), and no hemolysis in eight (16%). Thirty-three of 35 (94.2%) rats with massive hemolysis had hyperamylasemia, and 29 of these rats (82.8%) had histologically proven pancreatitis. The most severe pancreatitis occurred on day 3, as demonstrated by histology. Tissue TNF-alpha and PAF levels were statistically higher in group 1 than in groups 2 and 3. Acute massive hemolysis induced acute pancreatitis, as indicated by histology, in almost 80% of cases. Hemolysis may induce acute pancreatitis by triggering the release of proinflammatory and immunoregulatory cytokines.
文献表明，急性胰腺炎是大量溶血的一种并发症，其患病率约为20%。我们描述了一种溶血诱导的急性胰腺炎实验模型。在第一个实验日（第0天），通过腹腔注射60 mg/kg的20 mg/ml乙酰苯肼（APH）于20%（v/v）乙醇中，在大鼠中诱导溶血性贫血。150只体重180 - 200 g的Wistar白化大鼠被分为三组，每组50只动物：第1、2和3组分别腹腔注射APH、20%乙醇和生理盐水。在研究的第1、2、3、4和5天，每组处死10只大鼠。测定血清淀粉酶、脂肪酶水平以及胰腺组织肿瘤坏死因子-α（TNF-α）和血小板活化因子（PAF）含量，并对胰腺进行组织学检查。第2组和第3组的任何大鼠均未观察到溶血或胰腺炎。在第1组中，50只大鼠中有35只（70%）出现大量溶血，7只（14%）出现中度溶血，8只（16%）未出现溶血。35只出现大量溶血的大鼠中有33只（94.2%）出现高淀粉酶血症，其中29只（82.8%）经组织学证实患有胰腺炎。组织学显示，最严重的胰腺炎发生在第3天。第1组的组织TNF-α和PAF水平在统计学上高于第2组和第3组。组织学表明，急性大量溶血在几乎80% 的病例中诱发了急性胰腺炎。溶血可能通过触发促炎和免疫调节细胞因子的释放来诱发急性胰腺炎。
