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[急性胰腺炎肺损伤的临床研究]

[Clinical study of lung injury in acute pancreatitis].

作者信息

Liao C X

机构信息

Southwest Hospital, Third Military Medical University, Chongqing.

出版信息

Zhonghua Wai Ke Za Zhi. 1990 Jun;28(6):325-7, 380.

PMID:2096052
Abstract

Lung injury is a common and severe complication in acute pancreatitis. The pathogenesis of which has not been completely understood. To explore the mechanism of lung injury, ST and FFA and PLA in bronchoalveolar perfusate, FFA and PLA in blood were measured; clinical symptoms and chest film were analysed; blood gas analysis was performed. The results indicated that lung injury mostly occurs in ABNP and less in AEP. Pulmonary edema and atelectasis are essential changes of lung injury. It is believed that FFA is an important factor responsible for pulmonary edema. PLA, which plays the most important role in lung injury, not only results in atelectasis by degradating the SA in alveolar, but also induces pulmonary edema. The main reason for the increase of ST is the degradation of SA in alveolar. The levels of FFA and PLA in the blood may indicate the severity of acute pancreatitis. However, it remains unknown whether the synthesis of SA in patient with acute pancreatitis is inhibited.

摘要

肺损伤是急性胰腺炎常见且严重的并发症。其发病机制尚未完全明确。为探究肺损伤的机制,检测了支气管肺泡灌洗液中的ST、FFA和PLA、血液中的FFA和PLA;分析了临床症状及胸部X线片;进行了血气分析。结果表明,肺损伤多发生于ABNP,较少发生于AEP。肺水肿和肺不张是肺损伤的基本改变。认为FFA是导致肺水肿的重要因素。PLA在肺损伤中起最重要作用,不仅通过降解肺泡表面活性物质(SA)导致肺不张,还可诱发肺水肿。ST升高的主要原因是肺泡SA降解。血液中FFA和PLA的水平可提示急性胰腺炎的严重程度。然而,急性胰腺炎患者SA的合成是否受到抑制仍不清楚。

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