This study aimed to assess the role of oxygen free radicals in acute pancreatitis. Acute pancreatitis was induced in rats by infusion of the CCK-analogue cerulein (5 micrograms/kg per hour) for 30 minutes, 3.5 hours, and 12 hours. After the infusion, serum enzymes and conjugated tissue dienes and malondialdehyde were measured and tissue samples were subjected to electron and light microscopy. Electron microscopy after 30 minutes showed moderate intracellular alterations. After 3.5 hours of cerulein infusion interstitial oedema and intravascular margination of granulocytes in the pancreatic gland were seen. After 12 hours histological evaluation showed pronounced zymogen degranulation, extensive tissue necrosis, and migration of granulocytes into the tissue. Amylase and lipase activities increased 15 and 35-fold respectively during this time. After 30 minutes of cerulein infusion conjugated dienes and malondialdehyde increased, they reached their peak after 3.5 hours and decreased to normal values after 12 hours. Treatment with superoxide dismutase (100,000 U/kg/hour) and catalase (400,000 U/kg/hour) either before or after the start of the cerulein infusion prevented lipid peroxidation and reduced zymogen degranulation and tissue necrosis. Tissue oedema and inflammatory response, however, were not affected in any of the treated rats. Oxygen free radicals are instrumental in the development of acute pancreatitis. Even after its onset, scavenger treatment reduced the tissue damage normally observed.
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机译:这项研究旨在评估氧自由基在急性胰腺炎中的作用。通过在30分钟,3.5小时和12小时内注入CCK-类似物cerulein(每小时5微克/千克)来诱发大鼠急性胰腺炎。输注后,测量血清酶,结合的组织二烯和丙二醛,并对组织样品进行电子和光学显微镜检查。 30分钟后的电子显微镜检查显示中等的细胞内改变。注射青霉素3.5小时后,可见胰腺中的间质性水肿和粒细胞的血管内边缘化。 12小时后,组织学评估显示明显的酶原脱颗粒,广泛的组织坏死和粒细胞向组织内的迁移。在此期间,淀粉酶和脂肪酶的活性分别增加了15倍和35倍。在30分钟的铜绿素注入后,共轭二烯和丙二醛含量增加,在3.5小时后达到峰值,在12小时后降至正常值。在开始注射铜蓝蛋白之前或之后,用超氧化物歧化酶(100,000 U / kg /小时)和过氧化氢酶(400,000 U / kg /小时)进行处理可防止脂质过氧化并减少酶原脱粒和组织坏死。然而,在任何治疗的大鼠中组织水肿和炎症反应均未受到影响。氧自由基有助于急性胰腺炎的发展。甚至在其发作后,清除剂治疗也减少了通常观察到的组织损伤。
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