Seven-degree head-down tilt reduces choroidal pulsatile ocular blood flow.

INTRODUCTION: We investigated the effects of head-down tilt (HDT), which simulates microgravity during spaceflights, on the choroidal pulsatile ocular blood flow (POBF). This investigation is important because alterations in the choroidal blood flow can affect the function of retinal rods and cones that rely totally on the choroid for metabolites. METHODS: Nineteen healthy adults between 20 and 38 yr of age participated in this study. The POBF was compared for: 1) baseline, wherein subjects were declined 30 degrees from vertical; 2) microgravity simulation where subjects were in a 7 degrees HDT for 2 min; 3) 90 min of the 7 degrees HDT; and 4) recovery, i.e., back at 30 degrees for 2 min. RESULTS: The group averaged POBF (Mean +/- SEM values: 828.43 +/- 48.88 microL x min(-1)) decreased immediately during the 2-min microgravity simulation (582.18 +/- 43.62 microL x min(-1)), remained at that inferior level at the 90-min mark of HDT (542.26 +/- 45.35 microL x min(-1)), and came back toward baseline POBF during the recovery period (760.11 +/- 46.03 microL x min(-1)) (p = 0.0001). DISCUSSION: The results show that simulated-microgravity of relatively short duration induces retinal hypoperfusion throughout the microgravity interval through the reduction in the POBF. This finding may have important implications regarding visual performance in space crewmembers placed in prolonged microgravity environments.

Night blindness in Sorsby's fundus dystrophy reversed by vitamin A.

Sorsby's fundus dystrophy (SFD) is an autosomal dominant retinal degeneration caused by mutations in the tissue inhibitor of metalloproteinases-3 (TIMP3) gene. Mechanisms of the visual loss in SFD, however, remain unknown. In a SFD family with a novel TIMP3 point mutation, we tested a hypothesis that their night blindness is due to a chronic deprivation of vitamin A at the level of the photoreceptors caused by a thickened membrane barrier between the photoreceptor layer and its blood supply. Vitamin A at 50,000 IU/d was administered orally. Within a week, the night blindness disappeared in patients at early stages of disease. Nutritional night blindness is thus part of the pathophysiology of this genetic disease and vitamin A supplementation can lead to dramatic restoration of photoreceptor function.