水通道蛋白1基因敲除对胸腔液体转运的影响

Effect of Aquaporin-1 (AQP1) Deletion on Pleural Fluid Transport

目的:探讨水通道蛋白1在小鼠胸腔液体转运的作用。方法:实验小鼠分为野生型组和基因敲除型组,每组基因型各分为高渗组和低渗组。小鼠吸入麻醉后,胸膜腔内分别注入高渗或等渗液体,处理组液体中含特布他林100μmol·L-1或阿米吡嗪200μmol·L-1。在不同时间收集胸腔液体,测量渗透压或体积。结果:胸膜腔内注入500mOsm液体后,在1,2和5min时收集胸腔液体测渗透压,野生型组中渗透压均明显高于基因敲除组(P<0.01)。胸腔内注入等渗液体后,在30,60和90min时收集胸腔液体测量体积,野生型组和基因敲除型组间无明显差异(P>0.05)。特布他林增加高渗和等渗液体胸腔转运(P<0.05),不受水通道蛋白1敲除的影响。阿米吡嗪抑制高渗和等渗液体胸腔转运(P<0.05),也不受水通道蛋白1敲除的影响。结论:水通道蛋白1促进渗透压引起的小鼠胸腔液体转运,对胸腔等渗液体清除无影响。钠通道影响胸腔高渗和等渗液体转运,水通道蛋白1基因敲除不影响钠通道的这种作用。

Objective：To investigate the role of aquaporin-1 （AQP1） on pleural fluid transport. Methods：Wild-type and AQP1 null mice were used in this study. After the mice were briefly anesthetized, 0.25 mL of hyperosmolar or isosmolar solution （containing terbutaline, amiloride or saline only） was infused into the pleural space. Then mice were sacrificed at scheduled times for measurement of pleural fluid osmolality or volume. Results： After instillation of hyperosmolar fluid into the pleural space, the osmolality of pleural fluid in wild-type mice was higher than that in AQP1 null mice killed at the same time （1, 2, 5 rain）. There was no difference in the isosmolar clearance between the wild type and AQP1 null mice after injection of 0.25 mL isosmolar fluid into the pleural space. Terbutaline could increase the osmotic and isosmolar fluid transport across pleura, but these effects were not influenced by AQP1 deletion. In contrast, amiloride could reduced osmotic and isosmolar pleural fluid transport, and these effects were not influenced by AQP1 deletion. Conclusion： The results indicats osmotic fluid transport across the pleural surface is facilitated by AQP1 water channels. However, AQP1 does not play an important role in pleural isosmolar fluid clearance. Sodium channel may play a role in osmotic and isosmolar pleural fluid transport. The effects of sodium channel on fluid transport across pleural space are not influenced by aquaporin-1 deletion.