Department of Biomedical Engineering, Illinois Institute of Technology, 3255 South Dearborn Street, Wishnick Hall 314, Chicago, IL 60616 USA.
Exp Eye Res. 2009 Nov;89(5):801-9. doi: 10.1016/j.exer.2009.07.014. Epub 2009 Jul 30.
Nitric oxide (NO) has been observed to regulate blood flow under basal and stimulated conditions in the retina. Recent evidence suggests that NO produced by neuronal nitric oxide synthase (nNOS) may regulate blood flow in addition to that produced by endothelial nitric oxide synthase (eNOS). The objective of the current study was to investigate the contribution of NO produced by nNOS in the regulation of basal retinal blood flow. A non-specific NOS inhibitor N (G)-nitro-l-arginine methyl ester (l-NAME) and the specific nNOS inhibitors 1-(2-trifluoromethylphenyl) imidazole (TRIM) and (4S)-N-(4-amino-5 [aminoethyl] aminopentyl)-N-nitroguanidine (AAAN) were injected into the vitreous (intravitreal) of Long-Evans rats. Vessel diameters, velocities and volumetric blood flow rates (VBF) in the retinal circulation were determined prior to and in 30-min intervals for 4-4.5h after injection. In addition, the basal amount of nNOS in the rat retina was quantified using a specific enzyme linked immunoassay (ELISA). Treatment with l-NAME and TRIM significantly decreased diameters and VBF. Compared with saline, treatment with l-NAME and TRIM produced a significant (p<0.001) decrease of approximately 12-17% in vessel diameters. Treatment with AAAN significantly decreased vessel diameters and venous VBF. Compared with saline AAAN produced a significant decrease of approximately 7% in arterial (p<0.001) and 5% in venous (p=0.011) diameters, respectively. The amount of nNOS in the rat retina was 0.17+/- 0.0147 pmol mg(-1) of dry retina. The results suggest that though inhibition of nNOS decreases basal diameters, constant VBF is maintained in the retinal circulation.
一氧化氮（NO）已被观察到在视网膜的基础和刺激条件下调节血液流动。最近的证据表明，神经元型一氧化氮合酶（nNOS）产生的 NO 除了内皮型一氧化氮合酶（eNOS）产生的 NO 之外，还可能调节血液流动。本研究的目的是研究 nNOS 产生的 NO 在调节基础视网膜血流中的作用。非特异性 NOS 抑制剂 N（G）-硝基-L-精氨酸甲酯（l-NAME）和特异性 nNOS 抑制剂 1-（2-三氟甲基苯基）咪唑（TRIM）和（4S）-N-（4-氨基-5-[氨基乙基]氨基戊基）-N-硝基胍（AAAN）被注入到长耳大鼠的玻璃体（眼内）中。在注射前和注射后 4-4.5 小时内的 30 分钟间隔内，确定视网膜循环中的血管直径、速度和容积血流速度（VBF）。此外，使用特定的酶联免疫吸附测定（ELISA）定量大鼠视网膜中的基础 nNOS 量。l-NAME 和 TRIM 的处理显著降低了直径和 VBF。与生理盐水相比，l-NAME 和 TRIM 的处理导致血管直径显著降低（p<0.001），约为 12-17%。AAAN 的处理显著降低了血管直径和静脉 VBF。与生理盐水相比，AAAN 导致动脉（p<0.001）和静脉（p=0.011）直径分别显著降低约 7%和 5%。大鼠视网膜中的 nNOS 量为 0.17+/-0.0147 pmol mg(-1)干视网膜。结果表明，尽管抑制 nNOS 会降低基础直径，但视网膜循环中的恒定 VBF 得以维持。
