Preretinal Partial Pressure of Oxygen Gradients Before and After Experimental Pars Plana Vitrectomy

Abstract

Preretinal PO2 gradients are not eliminated after pars plana vitrectomy. During BSS perfusion, vitreous cavity PO2 is very high. Interruption of BSS perfusion evokes progressive equilibration of vitreous cavity PO2 with concomitant progressive return of preretinal PO2 gradients to their previtrectomy patterns. This indicates that preretinal diffusion of oxygen is not altered after vitrectomy. The beneficial effect of vitrectomy in ischemic retinal diseases or macular edema may be related to other mechanisms, such as increased oxygen convection currents or removal of growth factors and cytokines secreted in the vitreous.

Retinal oxygen: from animals to humans

“…The gelled vitreous is 99% water, so after vitrectomy, when the vitreous is 100% water, would not matter. Consistent with this, Petropolous et al (Petropoulos et al, 2013) convincingly showed experimentally that O 2 gradients do not change after vitrectomy. Arguments that it does change (Gisladottir et al, 2009; Stefansson and Loftsson, 2006) are based on considering the vitreous as a viscous fluid rather than a gel and are not valid (Barton et al, 2007).…”

“…However, the preretinal vitreous PO 2 is not always sufficient for understanding inner retinal PO 2 . Alder and Cringle (Alder and Cringle, 1985, 1990) and others (Buerk et al, 1993; Petropoulos et al, 2013) have shown that gradients of PO 2 extend for several hundred μm into the vitreous and they depend on the proximity to retinal vessels. PO 2 is higher at the retina near arterioles, and decreases with distance into the vitreous from the retina.…”

“…Lange et al (Lange et al, 2011) confirmed this result for the midvitreous of diabetics with macular retinal detachment (about 7 mmHg) compared to non-diabetics (about 11 mmHg). Much of the O 2 in the vitreous comes from the retina, according to animal studies (Alder and Cringle, 1985, 1990; Alder et al, 1991; Linsenmeier et al, 1981; Petropoulos et al, 2013), but in the midvitreous there is a great deal of spatial averaging, so midvitreal measurements are not good for resolving details at the retina, as noted in section 3.3. Consequently, Lange et al (Lange et al, 2011) also made two measurements “at the retinal surface,” one near the macula and one superior to the superior artery, and averaged them, because they were reported to be similar.…”

“…A third indirect line of evidence about hypoxia is that two treatments that can reduce or halt neovascularization in diabetic retinopathy, vitrectomy and panretinal photocoagulation, are most easily understood in terms of their ability to increase O 2 in the inner retina (Grunwald et al, 1989; Grunwald et al, 1986; Molnar et al, 1985; Petropoulos et al, 2013; Pournaras et al, 2008; Stefansson, 2006; Stefansson et al, 1981; Stefansson et al, 1992). The evidence for panretinal photocoagulation and vitrectomy is complicated and relies on both human and animal measurements, so these topics will be discussed further in sections 6.3 and section 6.4.…”

“…In cats, Stefansson et al (Stefansson et al, 1990) showed that a prior vitrectomy allowed preretinal PO 2 to remain close to normal when a branch retinal vein was occluded, whereas average PO 2 fell dramatically following venous occlusion if no vitrectomy had been done. Petropoulos et al (Petropoulos et al, 2013) recorded gradients in the vitreous near arterioles, venules, and intravascular zones in normal eyes of minipigs. While vitrectomy initially increased the PO 2 s in all areas, this was attributed to the oxygenated perfusion fluid, and over the next 2.5 hours, the PO 2 s and the gradients returned to initial levels.…”