Pournaras C J, Tsacopoulos M, Bovet J, Roth A
Clinique d'Ophatalmologie, Laboratoire d'Ophtalmologie expérimentale, Genève.
Ophtalmologie. 1990 Jan-Feb;4(1):17-9.
Transretinal PO2 profiles were recorded during normoxia and hyperoxia in normal and ischemic retinal territories in anesthetized miniature pigs using double barrelled recess type microelectrodes. In normoxia and hyperoxia the PO2 in the normal territory decreased from the inner retina and the choroid towards the mid-retina, indicating that the choroid cannot supply O2 to the whole normal retina. Preretinal and transretinal PO2 measurements in ischemic territories following a laser occlusion of a retinal branch vein demonstrated that in normoxia the direction of PO2 gradients prevents O2 diffusing from the choroid to reach the inner retina. This explains why the ischemic territories are hypoxic. In the contrary, during hyperoxia the intraretinal PO2 gradient indicates an O2 flux from the choroid to the inner retina resulting to marked preretinal PO2 increase at the affected territories. We proposed the hypothesis that in the ischemic retinas the hyperoxia does not induce a rise of the O2 consumption of the outer retina. Hence hyperoxia could be a useful tool to restore the oxygenation of the inner hypoxic retinal layers.
使用双管凹槽型微电极，在麻醉的小型猪的正常和缺血性视网膜区域，记录了常氧和高氧状态下的经视网膜氧分压（PO2）分布。在常氧和高氧状态下，正常区域的PO2从视网膜内层和脉络膜向视网膜中层降低，这表明脉络膜不能为整个正常视网膜提供氧气。视网膜分支静脉激光闭塞后，对缺血区域进行视网膜前和经视网膜PO2测量表明，在常氧状态下，PO2梯度方向阻止了氧气从脉络膜扩散到视网膜内层。这解释了为什么缺血区域会缺氧。相反，在高氧状态下，视网膜内PO2梯度表明有氧气从脉络膜流向视网膜内层，导致受影响区域的视网膜前PO2显著增加。我们提出了一个假设，即在缺血性视网膜中，高氧不会导致外层视网膜氧消耗增加。因此，高氧可能是恢复内层缺氧视网膜层氧合的有用工具。
