Donati G, Pournaras C J, Munoz J L, Tsacopoulos M
Clinique d'Ophtalmologie, Hôpital Cantonal Universitaire, Genève.
Klin Monbl Augenheilkd. 1995 May;206(5):373-5. doi: 10.1055/s-2008-1035467.
NO is a nonpolar gas, which diffuses across cell membranes in an isotropic fashion. In relatively large arteries NO has been identified as the endothelium-derived releasing factor and the current hypothesis is that NO controls the vascular tone. We are investigating an alternative hypothesis proposing that the retinal tissues surrounding the arterioles contribute in the process of NO production.
We performed flicker light stimulation in anesthetized minipigs (hypnodyl 100 mg/hr, tubocurarine 0.1 mg/hr und N2O) in steady-state of normoxia-normocapnia. An NO-microprobe mounted on a micromanipulator was introduced into the eye through the pars plana and positioned on the preretinal space in a zone free of visible vessels. Preretinal NO gradient and recording of NO release variations in response to flicker light stimulation were performed so as periarteriolar microinjections of nitro-L-arginine.
When advancing the NO-probe from the vitreous towards the retina we recorded an NO-gradient corresponding to an efflux of 7.1 pMol x min-1 x cm-2 (N = 9). With the microprobe positioned close to the retina and after 60 min dark adaptation we recorded a mean increase in NO release of 1.59 muMol +/- 0.13 SE. After periarteriolar microinjection of nitro-Larginine we recorded a transitory reversible vasoconstriction.
These results indicate that a process occurring in the extravascular tissue of the retina modulates the production of NO and that constitutional NO release by the retina is a major determinant of the basal retinal arteriolar tone.
一氧化氮(NO)是一种非极性气体,以各向同性方式跨细胞膜扩散。在相对较大的动脉中,NO已被确认为内皮源性舒张因子,目前的假说是NO控制血管张力。我们正在研究另一种假说,即围绕小动脉的视网膜组织在NO产生过程中发挥作用。
在处于常氧 - 常碳酸血症稳态的麻醉小型猪(氯胺酮100mg/小时、筒箭毒碱0.1mg/小时和N₂O)中进行闪光刺激。将安装在微操纵器上的NO微探针通过睫状体扁平部插入眼内,并置于无可见血管区域的视网膜前间隙。进行视网膜前NO梯度测量以及记录对闪光刺激的NO释放变化,同时进行小动脉周围硝基 - L - 精氨酸的微量注射。
当将NO探针从玻璃体向视网膜推进时,我们记录到一个NO梯度,相当于7.1皮摩尔×分钟⁻¹×厘米⁻²的外流(N = 9)。将微探针靠近视网膜放置并经过60分钟暗适应后,我们记录到NO释放平均增加1.59微摩尔±0.13标准误。在小动脉周围微量注射硝基 - L - 精氨酸后,我们记录到短暂的可逆性血管收缩。
这些结果表明,视网膜血管外组织中发生的一个过程调节了NO的产生,并且视网膜的固有NO释放是视网膜小动脉基础张力的主要决定因素。