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蛙皮素诱导的急性胰腺炎会导致轻度肺部炎症和呼吸力学改变。

Caerulein-induced acute pancreatitis results in mild lung inflammation and altered respiratory mechanics.

作者信息

Elder Alison S F, Saccone Gino T P, Bersten Andrew D, Dixon Dani-Louise

机构信息

Department of Intensive and Critical Care Medicine, Flinders Medical Centre, Flinders University, Adelaide, Australia.

出版信息

Exp Lung Res. 2011 Mar;37(2):69-77. doi: 10.3109/01902148.2010.516307. Epub 2010 Nov 15.

Abstract

Acute lung injury is a common complication of acute pancreatitis (AP) and contributes to the majority of AP-associated deaths. Although some aspects of AP-induced lung inflammation have been demonstrated, investigation of resultant changes in lung function is limited. The aim of this study was to characterize lung injury in caerulein-induced AP. Male Sprague Dawley rats (n = 7-8/group) received 7 injections of caerulein (50 μg/kg) at 12, 24, 48, 72, 96, or 120 hours before measurement of lung impedance mechanics. Bronchoalveolar lavage (BAL), plasma, pancreatic, and lung tissue were collected to determine pancreatic and lung measures of acute inflammation. AP developed between 12 and 24 hours, as indicated by increased plasma amylase activity and pancreatic myeloperoxidase (MPO) activity, edema, and abnormal acinar cells, before beginning to resolve by 48 hours. In the lung, MPO activity peaked at 12 and 96 hours, with BAL cytokine concentrations peaking at 12 hours, followed by lung edema at 24 hours, and BAL cell count at 48 hours. Importantly, no significant changes in BAL protein concentration or arterial blood gas-pH levels were evident over the same period, and only modest changes were observed in respiratory mechanics. Caerulein-induced AP results in minor lung injury, which is not sufficient to allow protein permeability and substantially alter respiratory mechanics.

摘要

急性肺损伤是急性胰腺炎(AP)的常见并发症,也是大多数与AP相关死亡的原因。尽管AP诱发的肺部炎症的某些方面已得到证实,但对由此导致的肺功能变化的研究却很有限。本研究的目的是描述蛙皮素诱导的AP中的肺损伤特征。雄性Sprague Dawley大鼠(每组n = 7 - 8只)在测量肺阻抗力学前12、24、48、72、96或120小时接受7次蛙皮素注射(50μg/kg)。收集支气管肺泡灌洗(BAL)液、血浆、胰腺和肺组织,以确定胰腺和肺部急性炎症的指标。AP在12至24小时内发展,表现为血浆淀粉酶活性和胰腺髓过氧化物酶(MPO)活性增加、水肿和腺泡细胞异常,48小时后开始缓解。在肺部,MPO活性在12小时和96小时达到峰值,BAL细胞因子浓度在12小时达到峰值,随后在24小时出现肺水肿,48小时出现BAL细胞计数增加。重要的是,同期BAL蛋白浓度或动脉血气pH水平无明显变化,呼吸力学仅出现轻微变化。蛙皮素诱导的AP导致轻微的肺损伤,不足以引起蛋白质通透性增加和显著改变呼吸力学。

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