Stefansson E
Department of Ophthalmology, Duke University Medical Center, Durham, NC.
Graefes Arch Clin Exp Ophthalmol. 1990;228(2):120-3. doi: 10.1007/BF00935719.
In 1956, Wise suggested that retinal hypoxia stimulated retinal neovascularization in the ischemic proliferative retinopathies. Although not directly proven, this theory is strongly supported by a wealth of circumstantial information. Two treatment modalities, vitrectomy and panretinal photocoagulation, have been shown to be effective against retinal neovascularization in diabetics. Both of these treatment modalities improve retinal oxygenation, and we propose that this is the mechanism through which they halt retinal neovascularization. The mechanism for improving retinal oxygenation is different for the two treatment modalities. In the case of panretinal photocoagulation, the new oxygen supply comes from the choroid through the laser scar in the outer retina. In the case of vitrectomy, it comes from the vitreous cavity itself, but the end result is the same. We have expanded Wise's hypothesis to include these two treatment modalities, which were not known at the time of Wise's original paper.
1956年,怀斯提出视网膜缺氧会刺激缺血性增殖性视网膜病变中的视网膜新生血管形成。尽管该理论尚未得到直接证实,但大量的间接信息为其提供了有力支持。两种治疗方式,即玻璃体切除术和全视网膜光凝术,已被证明对糖尿病患者的视网膜新生血管形成有效。这两种治疗方式均能改善视网膜氧合,我们认为这就是它们阻止视网膜新生血管形成的机制。两种治疗方式改善视网膜氧合的机制不同。对于全视网膜光凝术,新的氧气供应来自脉络膜,通过外层视网膜的激光瘢痕进入。对于玻璃体切除术,氧气来自玻璃体腔本身,但最终结果是相同的。我们扩展了怀斯的假说,将这两种在怀斯最初发表论文时尚不为人知的治疗方式纳入其中。