【Abstract】Objective To investigate therapeutic effect and mechanism of hyperbaric oxygen and ulinastatin respectively or combinatively used to treat acute necrotizing pancreatitis (ANP).
Methods One hundred and twenty SD rats were divided into 6 groups randomly: group of normal control, group receiving sham operation, group of untreated acute necrotizing pancreatitis (ANP group), group of acute necrotizing pancreatitis treated with hyperbaric oxygen (HBO group), group of acute necrotizing pancreatitis treated with ulinastatin (ULT group), and group of acute necrotizing pancreatitis treated with combined hyperbaric oxygen and ulinastatin (HBO+ULT group). The rat model of acute necrotizing pancreatitis was established according to Aho HJ et al. Concentrations of amylase, TNFα, TXB2 and 6ketoPGF1α in blood were measured through ELISA or radioimmunoassay. Changes of pancreatic histopathology were investigated. SPSS 10.0 was used in statistical analysis.
Results The concentrations of amylase, TNFα, TXB2 in the ANPtreated groups were significantly lower than those of ANP group (P＜0.01) except for 6ketoPGF1α and the levels of amylase and TNFα of HBO group were strikingly higher than those in HBO+ULT group. Only the level of AMS was significantly different between ULT group and HBO+ULT group (P＜0.01). Pancreas histopathological scores(HS) and CD8 counts of ANP group were significantly higher than those the other three group, but CD4 counts and CD4/CD8 ratio were on the contrary (P＜0.05). HS of HBO and ULT were strikingly higher than those of HBO+ULT (P＜0.05).
Conclusion ①Hyperbaric oxygen or ulinastatin can effectively decrease the blood levels of enzymes and cytokines and improve the pancreatic immunity. ②Hyperbaric oxygen in combination with ulinastatin are more effective than either of them in the treatment of ANP.
Citation：
TIAN Bingzhang,LI Yongguo,YANG Zhulin,WU J inshu.. Experimental Study on the Combined Hyperbaric Oxygen and Ulinastatin of Acute Necrotizing Pancreatitis. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2005, 12(5): 438-442. doi:
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- 1. Zhou ZG, Chen YD, Sun W, et al. Pancreatic microcirculatory impairment in experimental acute pancreatitis in rats [Ｊ]. World J Gastroenterol, 2002; 8(5)∶933.
- 2. Menger MD, Plasczy KT. Microcirculatory derangements in acute pancreatitis [Ｊ]. J Hepatobiliary Pancreat Surg, 2001； 8(3)∶187.
- 3. Mager M, Rau B. Inflammatory mediators in human acute pancreatitis: Clinical and pathophysiological implications [Ｊ]. Gut, 2000; 47(4)∶546.
- 4. Aho HJ, Nevalainen TJ, Lindbgrg RL, et al. Experimental pancreatitis in the rat, the role of phospholipase A in sodium taurocholateinduced acute haemorrhagic pancreatitis [Ｊ]. Scand J Gastroenterol, 1980; 15（8）∶1027.
- 5. 秦仁义，王春友，邹声泉.乌司他丁治疗急性胰腺炎的实验及临床研究 [Ｊ]. 中国普通外科杂志， 2001; 10（4）∶292.
- 6. Spormann H, Sokolowski A, Letko G. Effect of temporary ischemia upon development and histological patterns of acute pancreatitis in the rat [Ｊ]. Pathol Res Pract, 1989； 184（5）∶507.
- 7. 刘军昌主编. 高压氧医学新理论与新技术 [M]. 第1版. 北京：军事医学科学出版社，1998∶50~52.
- 8. Menger MD, Plasczy KT. Microcirculatory derangements in acute pancreatitis [Ｊ]. J Hepatobiliary Pancreat Surg, 2001; 8(3)∶187.
- 9. 康骅，孙家邦, 朱斌，等. 高压氧对急性胰腺炎大鼠 TXA2 与PGI2 的影响 [Ｊ]. 肝胆胰外科杂志, 1997; 9（2）∶77.
- 10. Tschiya R. Experimental study of hyperbaric oxygen therapy for severe acute pancreatitis [C]. Colloquia of the research committee of intractable disease of the pancreas. Tokyo; Japanese Ministry of health and welfare, 1989∶246-247.
- 11. Bhatnagar A, Wigj D, Iajumdar H. Immunological findings in acute and chronic pancreatitis [Ｊ]. ANZ J Surg, 2003; 73(1-2)∶59.
- 12. Toma H, Winston JH, Iicci IA, et al.Characterization of the neurotrophic response to acute pancreatitis [Ｊ]. Pancreas, 2002; 25(1)∶31.
