Yamamoto F, Steinberg R H
Department of Ophthalmology, University of California, San Francisco 94143-0444.
Exp Eye Res. 1992 May;54(5):699-709. doi: 10.1016/0014-4835(92)90024-m.
We studied the effect of systemic hypoxia on intraretinal pH in the intact cat eye using double-barreled H(+)-sensitive microelectrodes. Hypoxia in the dark further acidified the extracellular space surrounding rods in the distal retina and this effect was maximal in the outer nuclear layer (ONL). An acidification occurred in response to essentially any decrease in PaO2 below the normoxic level. Light-evoked alkalinizations in the ONL were larger in amplitude during hypoxia than in normoxia and this difference increased with the severity of hypoxia. Background illumination suppressed the hypoxic acidification of the ONL, completely inhibiting it at rod saturating intensities, at levels of hypoxia down to PaO2s of 40 mmHg. Systemic hyperoxia produced a small alkalinization in the ONL, and a reduction in the amplitude of the light-evoked alkalinizations. This suggests that systemic hyperoxia can partially suppress the ongoing glycolysis of dark-adapted rods. Changes in blood flow during hypoxia also altered intraretinal pH. Hypoxia led to an alkalinization in the choroid in both dark and light adaptation that spread into the distal retina. This alkalinization is most likely caused by the increase in CO2 removal that occurs as systemic blood pressure, and as a consequence, choriocapillaris blood flow increase during hypoxia. The alkalinization attenuated the acidification that was observed outside rods during hypoxia. There was also an alkalinization of the proximal portion of the retina, which spread into the vitreous. This alkalinization was attributed to the autoregulatory increase in blood flow that occurs in the retinal vessels during hypoxia. These findings provide further evidence for the hypothesis that the energy metabolism of dark-adapted rods is exquisitely sensitive to systemic hypoxia so that any small decrease in PaO2 increases rod glycolysis. Rod-saturating illumination can completely suppress this increase in glycolysis for all but severe hypoxia. An increase in blood flow in the choriocapillaris during hypoxia appears to mitigate the effects of hypoxia on the distal retina.
我们使用双管氢离子敏感微电极研究了全身缺氧对完整猫眼视网膜内pH值的影响。黑暗中的缺氧进一步使视网膜远端视杆细胞周围的细胞外空间酸化,这种效应在外核层(ONL)最为明显。基本上,只要动脉血氧分压(PaO2)低于正常水平,就会发生酸化。缺氧时,ONL中光诱发的碱化幅度比正常氧合时更大,且这种差异随着缺氧程度的加重而增大。背景光照抑制了ONL的缺氧酸化,在视杆细胞饱和强度下,即在低至40 mmHg的PaO2水平的缺氧情况下,完全抑制了这种酸化。全身高氧在ONL中产生了轻微的碱化,并降低了光诱发碱化的幅度。这表明全身高氧可部分抑制暗适应视杆细胞正在进行的糖酵解。缺氧期间血流量的变化也改变了视网膜内pH值。缺氧在暗适应和明适应状态下均导致脉络膜碱化,并扩散至视网膜远端。这种碱化很可能是由于缺氧时全身血压升高,进而脉络膜毛细血管血流量增加,导致二氧化碳排出增加所致。这种碱化减弱了缺氧时在视杆细胞外观察到的酸化。视网膜近端部分也出现了碱化,并扩散至玻璃体。这种碱化归因于缺氧时视网膜血管中发生的血流自动调节性增加。这些发现为以下假说提供了进一步的证据:暗适应视杆细胞的能量代谢对全身缺氧极为敏感,以至于PaO2的任何微小降低都会增加视杆细胞的糖酵解。除了严重缺氧外,视杆细胞饱和光照可完全抑制糖酵解的这种增加。缺氧时脉络膜毛细血管血流量的增加似乎减轻了缺氧对视网膜远端的影响。