Effects of shenmai injection on pulmonary aquaporin 1 in rats following traumatic brain injury.

Background: Aquaporin-1 (AQP1) has involved in fluid transport in diverse pulmonary edema diseases. Our study aimed to explore the dynamic changes of AQP1 in pulmonary water metabolism in rats following traumatic brain injury (TBI) and the protective effect provided by shenmai injection.

Methods: Sixty male Sprague Dawley rats weighting 280 - 300 g were randomly divided into three groups: the normal control group, the model group and the shenmai injection (SMI) group. One piece skull was taken away without injuring cerebral tissue in normal control group, while rats in model group and SMI group were subject to free fall injury in the cerebral hemisphere. Rats in model group received intraperitoneal normal sodium (15 ml/kg) at one hour post-injury and the same dose of shenmai injection instead in SMI group, respectively. The expression of AQP1 was detected by immunohistochemical analysis and semi-quantitative RT-PCR at 0 hour, 10 hours, 72 hours and 120 hours after TBI. Arterial blood gas analysis and lung wet to dry were also measured.

Results: AQP1 was mainly presented in the capillary endothelium and slightly alveolar epithelial cells in three groups, but the expression of AQP1 in the normal control group was positive and tenuous, weakly positive in the model and SMI groups, respectively. Compared with normal control group, AQP1 mRNA levels were down regulated in the model and SMI groups at 10 hours, 72 hours and 120 hours (P < 0.05). While AQP1 mRNA levels in the SMI group was up-regulated than that in the model group (P < 0.05). Lung wet to dry weight ratio (W/D) in the model and SMI groups at 10 hours were higher than that in normal control group (P < 0.05). Compared with normal control group, PaO2 was markedly lower in the model and SMI groups (P < 0.05), but there were no statistically significant differences between model and SMI groups (P > 0.05).

Conclusions: The decreased AQP1 expression may be involved in the increased lung water content and dysfunction of pulmonary water metabolism following TBI. The treatment with SMI could improve water metabolism by promoting AQP1 expression.