Abstract

Objective To investigate the effect of sodium tanshinone ⅡA sulphonate (STS) on rats with pulmonary edema induced by sea water drowning (PE-SWD) and the mechanism involved.Methods Forty Sprague-Dawley rats were randomly divided into 4 groups:the normal group,the STS group,the seawater group (the SW group),the seawater + STS group (the SW + STS group),each consisting of 12 animals.The PE-SWD rat model was established with seawater instillation.PaO2 level,pulmonary pathology,lung wet/dry ratio,pulmonary microvascular permeability (PMVP),the activity of Na+-K+-ATPase,as well as protein abundance and mRNA were monitored respectively.Results Seawater aspiration decreased the level of PaO2 and the activity of Na+-K+-ATPase,and at the same time increased lung wet/dry ratio and PMVP level.Two hours after aspiration of seawater,the level of PaO2 for the SW + STS group increased significantly,when compared with that of the SW group.Pulmonary lesion,W/D ratio and PMVP level for the SW + STS group all alleviated,when compared with those of the SW group.Na+-K+-ATPase activity,Na+-K+-ATPase α1 and β1 protein abundance,and Na+-K+-ATPase β1 mRNA all significantly increased,when compared with those of the SW group.However,no significant differences in the Na+-K+-ATPase α1 mRNA level could be found between the SW + STS group and the SW group.Conclusions STS could produce certain effects on pulmonary edema induced by sea water drowning,the mechanism of which might be related with the level and up-regulation of Na+-K+-ATPase. Key words: Sea water; Drowning; Acute pulmonary edema; Sodium tanshinone Ⅱ A sulphonate ; Na+-K+-ATPase

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