Andraus Wellington, Jukemura José, Dutra Fernando, Bechara Etelvino, Cunha José E M, Leite Katia R M, Machado Marcel Cerqueira César
Department of Surgery, São Paulo University, Medical College, São Paul, SP, Brazil.
Clinics (Sao Paulo). 2007 Aug;62(4):483-90. doi: 10.1590/s1807-59322007000400016.
Hypothermia is a frequent event in severe acute pancreatitis (AP) and its real effects on the normal pancreas have not been well demonstrated. Moreover, neither have its effects on the outcome of acute pancreatitis been fully investigated. One hypothesis is that oxidative stress may be implicated in lesions caused or treated by hypothermia.
To investigate the effect of hypothermia in cerulein-induced acute pancreatitis (CIAP) in rats and the role played by oxidative stress in this process.
Male Wistar rats were divided into hypothermic and normothermic groups. Hypothermia was induced with a cold mattress and rectal temperature was kept at 30 masculineC for one hour. Acute pancreatitis was induced with 2 doses of cerulein (20 ìg/kg) administered at a one-hour interval. Serum amylase, pancreas vascular permeability by Evan's blue method, pancreas wet-to-dry weight ratio and histopathology were analyzed in each group.
When compared with normothermic rats, hypothermic animals, with cerulein-induced acute pancreatitis, showed higher levels of pancreatic vascular permeability (p < 0.05), pancreas wet-to-dry weight ratio (p = 0.03), and histologically verified edema (p < 0.05), but similar serum amylase levels. The hypothermic group showed a higher oxidized-reduced glutathione ratio than the normothermic group.
Moderate hypothermia produced a greater inflammatory response in established acute pancreatitis induced by cerulein in rats. Moreover, this study suggests that oxidative stress may be one of the mechanisms responsible for the worse outcome in hypothermic rats with cerulein-induced acute pancreatitis.
体温过低在重症急性胰腺炎(AP)中较为常见,其对正常胰腺的实际影响尚未得到充分证实。此外,其对急性胰腺炎预后的影响也未得到全面研究。一种假说认为,氧化应激可能与体温过低所导致或治疗的损伤有关。
探讨体温过低对大鼠雨蛙肽诱导的急性胰腺炎(CIAP)的影响以及氧化应激在此过程中所起的作用。
将雄性Wistar大鼠分为体温过低组和正常体温组。使用冷床垫诱导体温过低,直肠温度维持在30℃ 1小时。间隔1小时注射2剂雨蛙肽(20μg/kg)诱导急性胰腺炎。分析每组的血清淀粉酶、用伊文思蓝法检测的胰腺血管通透性、胰腺湿重与干重之比以及组织病理学。
与正常体温大鼠相比,体温过低且患有雨蛙肽诱导的急性胰腺炎的动物,其胰腺血管通透性水平更高(p < 0.05)、胰腺湿重与干重之比更高(p = 0.03)、组织学证实的水肿更严重(p < 0.05),但血清淀粉酶水平相似。体温过低组的氧化型谷胱甘肽与还原型谷胱甘肽之比高于正常体温组。
中度体温过低在大鼠雨蛙肽诱导的既定急性胰腺炎中产生了更大的炎症反应。此外,本研究表明氧化应激可能是体温过低且患有雨蛙肽诱导的急性胰腺炎的大鼠预后较差的机制之一。