Moretti Ana Iochabel Soares, Rios Ester Correia Sarmento, Soriano Francisco Garcia, de Souza Heraldo Possolo, Abatepaulo Fátima, Barbeiro Denise Frediani, Velasco Irineu Tadeu
Emergency Medicine Department, Medical School, University of São Paulo, São Paulo, Brazil.
Pancreas. 2009 Jul;38(5):507-14. doi: 10.1097/MPA.0b013e31819fef75.
Acute pancreatitis (AP) protease release induces lung parenchymal destruction via matrix metalloproteinases (MMPs), a neutrophil (polymorphonuclear leukocyte)-dependent process. Recent studies in hemorrhagic shock revealed that hypertonic saline (HTS) has an anti-inflammatory effect and can inhibit a variety of neutrophil functions. The aim of this study was to determine whether HTS and its actions in the pathway of neutrophil migration, MMPs, and heat shock proteins (HSPs) are effective in protecting the lung from injury associated with AP.
We determined neutrophil infiltration and expressions of MMPs and HSPs in the lung tissue after AP induced by retrograde infusion of 2.5% of sodium taurocholate.
Animals submitted to AP that received HTS compared with those who received normal saline presented with increased HSP70 and HSP90 expressions and reduced myeloperoxidase levels and MMP-9 expression and activity.
Our data raised the hypothesis that a sequence of HTS lung protection events increases HSP70 and HSP90, inhibiting infiltration of neutrophils and their protease actions in the lung.
急性胰腺炎（AP）蛋白酶释放通过基质金属蛋白酶（MMPs）诱导肺实质破坏，这是一个中性粒细胞（多形核白细胞）依赖的过程。最近关于失血性休克的研究表明，高渗盐水（HTS）具有抗炎作用，可抑制多种中性粒细胞功能。本研究的目的是确定HTS及其在中性粒细胞迁移、MMPs和热休克蛋白（HSPs）途径中的作用是否能有效保护肺免受与AP相关的损伤。
我们通过逆行输注2.5%牛磺胆酸钠诱导AP后，测定肺组织中的中性粒细胞浸润以及MMPs和HSPs的表达。
与接受生理盐水的动物相比，接受HTS的AP动物呈现出HSP70和HSP90表达增加，髓过氧化物酶水平降低，MMP-9表达及活性降低。
我们的数据提出了一个假设，即一系列HTS肺保护事件会增加HSP70和HSP90，抑制中性粒细胞在肺中的浸润及其蛋白酶作用。
