Zou Y Y, Lu J, Poon D J F, Kaur C, Cao Q, Teo A L, Ling E A
Department of Pathology, Faculty of Basic Medical Sciences, Kunming Medical College, Kunming, People's Republic of China.
Neuroscience. 2009 May 19;160(3):698-709. doi: 10.1016/j.neuroscience.2009.03.007. Epub 2009 Mar 12.
Retinal cells respond to various experimental stimuli including hypoxia, yet it remains to be investigated whether they react to smoke inhalation. We show here that retinal cells in rats, notably the ganglion cells, Müller cells, astrocytes and blood vessels responded vigorously to a smoke challenge. The major changes included up-regulated expression of vascular endothelial growth factor (VEGF), aquaporin 4 (AQP4) and nitric oxide synthase (NOS). VEGF expression was localized in the ganglion cells, Müller cells, astrocytes and associated blood vessels. AQP4 was markedly enhanced in both astrocytes and Müller cells. Increase in vascular permeability after smoke exposure was evidenced by extravasation of serum derived rhodamine isothiocyanate which was internalized by Müller cells and ganglion cells. The tracer leakage was attenuated by aminoguanidine and N(G)-nitro-L-arginine methyl ester (L-NAME) treatment which suppressed retinal tissue NOS and nitric oxide (NO) levels concomitantly. It is suggested that VEGF, AQP4 and NO are involved in increased vascular permeability following acute smoke exposure in which hypoxia was ultimately implicated as shown by blood gases analysis. NOS inhibitors effectively reduced the vascular leakage and hence may ameliorate possible retinal edema in smoke inhalation.
视网膜细胞对包括缺氧在内的各种实验刺激有反应，但它们是否对吸入烟雾有反应仍有待研究。我们在此表明，大鼠的视网膜细胞，尤其是神经节细胞、穆勒细胞、星形胶质细胞和血管，对烟雾刺激有强烈反应。主要变化包括血管内皮生长因子（VEGF）、水通道蛋白4（AQP4）和一氧化氮合酶（NOS）的表达上调。VEGF表达定位于神经节细胞、穆勒细胞、星形胶质细胞及相关血管。AQP4在星形胶质细胞和穆勒细胞中均显著增强。烟雾暴露后血管通透性增加通过血清来源的异硫氰酸罗丹明外渗得以证实，该物质被穆勒细胞和神经节细胞内化。氨基胍和N（G）-硝基-L-精氨酸甲酯（L-NAME）处理可抑制视网膜组织NOS和一氧化氮（NO）水平，从而减轻示踪剂渗漏。提示VEGF、AQP4和NO参与急性烟雾暴露后血管通透性增加，血气分析显示最终涉及缺氧。NOS抑制剂有效减少血管渗漏，因此可能改善烟雾吸入时可能出现的视网膜水肿。
