Effects of atropine on choroidal hemodynamics and VEGFA and HIF-1α expression in form-deprivation myopia guinea pigs.

We investigated the mechanism of action of atropine in myopia control by examining its effect on choroidal hemodynamics. Blood flow was evaluated using indocyanine green (ICG) fluorescence and molecular variation during the development of form-deprivation myopia (FDM) and atropine treatment in guinea pigs. Guinea pigs were divided randomly into the normal control (NC), FDM, and FDM + 1% atropine (ATR) groups, and evaluated by spherical equivalent refractive error (SE) and axial length (AL). Choroidal hemodynamic parameters were measured via ICG fluorescence imaging including the maximal ICG fluorescence intensity (Imax), rising time (Trising), blood flow index (BFI), and mean transit time (MTT). Additionally, the expression in the choroid-RPE complex of choroidal vascular endothelial growth factor A (VEGFA) and HIF-1 α were assessed via Western blotting. Atropine inhibited the development of FDM, with effects of FD on both SE and AL being reduced. ICG fluorescence hemodynamic wide-field maps and time-series curves revealed that the atropine significantly accelerated choroidal blood flow, with reduced Trising and MTT, while increasing Imax, BFI and the number of lobulated choriocapillaris structures compared with the FDM group. In terms of molecular markers, atropine inhibited the effect of FDM, increasing VEGFA levels and reducing HIF-1α expression. These findings suggest that atropine improved choroidal hemodynamics and changed vascular markers, potentially contributing to its role in inhibiting the progression of myopia in the FDM model.