Huemer Karl-Heinz, Garhofer Gerhard, Aggermann Tina, Kolodjaschna Julia, Schmetterer Leopold, Fuchsjäger-Mayrl Gabriele
Department of Clinical Pharmacology, Medical University of Vienna, Vienna, USA.
Invest Ophthalmol Vis Sci. 2007 Sep;48(9):4215-9. doi: 10.1167/iovs.07-0176.
Several studies have recently shown that a transition from light to dark is associated with a reduction in choroidal blood flow. The mechanism underlying this effect is unclear but may be related to changes in neural input. In the present study, the authors hypothesized that either the alpha-receptor agonist phenylephrine or the nitric oxide synthase (NOS) inhibitor L-NMMA may alter the choroidal blood flow response during a transition from light to dark.
In 15 healthy male nonsmoking subjects, the response of choroidal perfusion was studied in a randomized placebo-controlled three-way crossover study. Phenylephrine, L-NMMA or placebo was administered on different study days, and the effect of a light/dark transition on choroidal perfusion parameters was studied. Subfoveal choroidal blood flow and fundus pulsation amplitude were assessed with laser Doppler flowmetry and laser interferometry, respectively.
Before drug administration, a transition from light to dark reduced both choroidal hemodynamic parameters by 11% to 20%. Neither phenylephrine nor placebo altered basal choroidal blood flow or choroidal blood flow responses to the light/dark transitions. By contrast, the NOS inhibitor L-NMMA significantly reduced basal choroidal blood flow by 20.5% +/- 5.9% (P < 0.001) and basal fundus pulsation amplitude by 21.5% +/- 4.8% (P < 0.001). In addition, the response of subfoveal choroidal blood flow (-6.2% +/- 3.2%; P = 0.008) and fundus pulsation amplitude (-4.2% +/- 2.4%; P < 0.001) to the light/dark transition was significantly diminished.
The present study indicates that NO plays a role in the choroidal blood flow decrease during a transition from light to dark. Given that L-NMMA is a nonspecific inhibitor of NOS, the present study does not clarify whether this NO is from endothelial or neural sources.
最近的几项研究表明,从明到暗的转变与脉络膜血流减少有关。这种效应的潜在机制尚不清楚,但可能与神经输入的变化有关。在本研究中,作者假设α受体激动剂去氧肾上腺素或一氧化氮合酶(NOS)抑制剂L-NMMA可能会改变从明到暗转变过程中的脉络膜血流反应。
在15名健康男性非吸烟受试者中,采用随机、安慰剂对照的三向交叉研究来研究脉络膜灌注反应。在不同的研究日给予去氧肾上腺素、L-NMMA或安慰剂,并研究明/暗转变对脉络膜灌注参数的影响。分别用激光多普勒血流仪和激光干涉仪评估黄斑下脉络膜血流和眼底搏动幅度。
给药前,从明到暗的转变使两个脉络膜血流动力学参数降低了11%至20%。去氧肾上腺素和安慰剂均未改变基础脉络膜血流或脉络膜血流对明/暗转变的反应。相比之下,NOS抑制剂L-NMMA使基础脉络膜血流显著降低了20.5%±5.9%(P<0.001),基础眼底搏动幅度降低了21.5%±4.8%(P<0.001)。此外,黄斑下脉络膜血流(-6.2%±3.2%;P=0.008)和眼底搏动幅度(-4.2%±2.4%;P<0.001)对明/暗转变的反应显著减弱。
本研究表明,一氧化氮在从明到暗转变过程中脉络膜血流减少中起作用。鉴于L-NMMA是NOS的非特异性抑制剂,本研究并未阐明这种一氧化氮是来自内皮还是神经来源。