There is also the maintenance of the function of thrombocytes (without interference with coagulation) and its action as a stabilizer of cellular junctions and a free radical scavenger, in particular in vascular occlusion studies. When administered during reperfusion in the stroke rats, BPC 157 therapy counteracted both early and delayed neural hippocampal damage and completely recovered debilitated functions in the stroke rats. This was likely due to its modulatory effects on NO system and prostaglandins system, maintained vasomotor tone through the activation of Src-Caveolin-1-eNOS pathway and interaction with several molecular pathways. Thereby, through BPC 157 therapy, both as a rapid effect and then sustained beneficial effect, one remaining episcleral vein should be upgraded to compensate otherwise inescapable venous congestion and counteract and avoid the increased intraocular pressure and consequent injurious course, thus preventing otherwise rapidly imminent glaucoma course and an advanced increased intraocular course reversal.įurthermore, taking retinal ischemia as the final drawback, the nitric oxide synthase (NOS)-blocker L-NAME retrobulbar administration-induced retinal ischemia in rats was counteracted by BPC 157 application. Consequently, we theorized that all BPC 157 regimens in rats with cauterized three episcleral veins and increased intraocular pressure would immediately normalize intraocular pressure. Its applicability in the rapid upgrading of the collateral pathways may likely provide an additional beneficial effect in various vessel tributaries and normalization/attenuation of the intracranial (sinus sagittal) hypertension, portal and caval hypertension and aortal hypotension, and counteraction of the multiorgan failure syndrome. Recently, the rapid upgrading of the collateral pathways by a stable gastric pentadecapeptide BPC 157 has cured many severe syndromes induced by permanent occlusion of major vessels, veins and/or arteries, peripherally and centrally, major intoxication (alcohol, lithium) and maintained intra-abdominal hypertension. As a novel therapeutic approach, we investigated the stable gastric pentadecapeptide BPC 157 therapy (for review, see ).
If not upgraded, one episcleral vein is regularly unable to acquire and take over the whole function, and glaucoma-like features persist.
In conclusion, we claim that the reversal of the episcleral veins cauterization glaucoma appeared as a consequence of the BPC 157 therapy of the vessel occlusion-induced perilous syndrome.Ĭauterization of three episcleral veins (open-angle glaucoma model) induces venous congestion and increases intraocular pressure in rats. As leading symptoms, increased intraocular pressure and mydriasis, as well as degeneration of retinal ganglion cells, optic nerve head excavation and reduction in optic nerve thickness, generalized severe irregularity of retinal vessels, faint presentation of choroidal vessels and severe optic nerve disc atrophy were all counteracted. BPC 157-treated rats exhibited normal pupil diameter, microscopically well-preserved ganglion cells and optic nerve presentation, normal fundus presentation, normal retinal and choroidal blood vessel presentation and normal optic nerve presentation. Consequently, all BPC 157 regimens immediately normalized intraocular pressure. The daily regimen of BPC 157 (0.4 µg/eye, 0.4 ng/eye 10 µg/kg, 10 ng/kg) was administered locally as drops in each eye, intraperitoneally (last application at 24 h before sacrifice) or per-orally in drinking water (0.16 µg/mL, 0.16 ng/mL, 12 mL/rat until the sacrifice, first application being intragastric). In a six-week study, medication was given prophylactically (immediately before glaucoma surgery, i.e., three episcleral veins cauterization) or as curative treatment (starting at 24 h after glaucoma surgery). Recently, the rapid upgrading of the collateral pathways by a stable gastric pentadecapeptide BPC 157 has cured many severe syndromes induced by permanent occlusion of major vessels, veins and/or arteries, peripherally and centrally. Cauterization of three episcleral veins (open-angle glaucoma model) induces venous congestion and increases intraocular pressure in rats.