High intraocular pressure following anti-vascular endothelial growth factor therapy: proposed pathophysiology due to altered nitric oxide metabolism.

摘要: Abstract The nitric oxide (NO) pathway and its physiological significance on relaxing smooth muscle endothelial cells throughout the body is well outlined understood. Components of this have been located in ocular anterior posterior chambers, they connected with vascular, retinal, trabecular meshwork normal physiology. Nitric has shown to increase chamber aqueous outflow via reduction trabeculocyte size contractility, Schlemm's canal vasodilation. Anti-vascular growth factor (VEGF) therapy disrupt signaling pathway, producing systemic arterial hypertension following systemically administered anti-VEGF oncology by exactly that mechanism. Intravitreal now considered a standard care several retinal diseases. Sustained elevated intraocular pressure (IOP) described as potential adverse effect appears related ...