View clinical trials related to Ocular Physiology.
Filter by:Autoregulation is the ability of a vascular bed to maintain blood flow despite changes in perfusion pressure. The existence of an effective autoregulation in the optic nerve circulation has been shown in animals and humans. The exact mechanism behind this autoregulation is still unknown. The motive for the investigation of optic nerve head (ONH) blood flow autoregulation is to enhance the understanding of pathologic eye conditions associated with ocular vascular disorders. To clarify the regulatory mechanisms of ONH microcirculation is of critical importance to understand the pathophysiology of glaucoma because there is evidence that glaucoma is associated with optic nerve head ischemia. Several studies indicate that a disturbed autoregulation might contribute to glaucomatous optic neuropathy. Previous findings suggest endothelial dysfunction in glaucomatous optic neuropathy, in particular alterations in endothelin- and nitric oxide- system, which both play an important role in local regulation of vascular tone. In the present study, changes in ocular perfusion pressure will be performed during administration of drugs, which may potentially alter the pressure-flow relationship. These drugs include endothelin-1 and the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA).
Brimonidine tartrate is an alpha-2 agonist ocular hypotensive drug that exerts its effect by causing both a decrease in aqueous production and an increase in uveoscleral outflow. It has been proven to reduce increased intraocular pressure in glaucoma and ocular hypertension. As an alpha 2 agonist Brimonidine belongs to the same class of drugs as Clonidine; however, its molecular structure is sufficiently different to make it more selective for the alpha 2 receptor than Clonidine. Unlike Clonidine, Brimonidine does not appear to have an effect on the central nervous system and therefore does not cause sedation or systemic hypotension. In addition to their known effect of lowering intraocular pressure, alpha 2 adrenoceptor agonists are neuroprotective. It has, however, been shown that Brimonidine is a very potent vasoconstrictor in the ciliary body thus reducing aqueous humor production. Little is, however, known about potential vasoconstrictor effects of Brimonidine in the posterior pole of the eye. This is of clinical importance, because optic nerve head ischemia appears to contribute to glaucoma pathophysiology. This study is performed to investigate the effects of topical Clonidine vs. topical Brimonidine on choroidal blood flow and intraocular pressure during isometric exercise.
There is evidence from a variety of animal studies that choroidal blood flow is under neural control. By contrast, only little information is available from human studies. Recent results indicate that a light/dark transition is associated with a reduction in choroidal blood flow due to an unknown mechanism. We have shown that during unilateral dark/light transitions both eyes react with choroidal vasoconstriction strongly indicating a neural mechanism responsible for the blood flow changes. Dopamine has been discussed as a chemical messenger for light adaptation. However, dopaminergic effects in the eye are not restricted to synaptic sites of release, but dopamine also diffuses to the outer retinal layers and pigment epithelium. Accordingly, dopaminergic effects also include a modulatory role on retinal vessel diameter and animal studies provide evidence for vasodilatory effects in the choroid. There is evidence that during darkness retinal and choroidal dopamine levels decrease. Accordingly, dopamine could provide a modulatory input to the light/dark transition induced changes of choroidal circulation. The aim of the present study is to test this hypothesis.
Autoregulation is the ability of a vascular bed to maintain blood flow despite changes in perfusion pressure. For a long time it had been assumed that the choroid is a strictly passive vascular bed, which shows no autoregulation. However, recently several groups have identified some autoregulatory capacity of the human choroid. In the brain and the retina the mechanism behind autoregulation is most likely linked to changes in transmural pressure. In this model arterioles change their vascular tone depending on the pressure inside the vessel and outside the vessel. In the choroid, several observations argue against a direct involvement of arterioles. In a previous project we were able to identify that the nitric oxide (NO) - system as well as the endothelin system are involved in choroidal blood flow regulation during isometric exercise. In the present study autoregulation of the choroid during isometric exercise will be investigated and the pressure/flow relationships will be observed in the absence or presence of a calcium antagonist - nifedipine.
Prostaglandins (PG) are known to alter regional ocular blood flow and exhibit vasoactive properties in isolated ocular blood vessels. A variety of animal experiments indicate that endogenous PGs play a role in the regulation of retinal (RBF) and choroidal (ChBF) blood flow. There is also evidence that the prostaglandin pathway is involved in the activation of NO production in humans, however, the mechanisms for interactions between PG and NO in ocular vasculature are still unclear. Animal studies suggest that retinal and choroidal blood flow decrease after administration of indomethacin (a nonspecific cyclooxygenase inhibitor). More recently, it has been shown that indomethacin injected intravenously decreased optic nerve oxygen tension and reduced the CO2 reactivity. This is probably the result of decreased blood flow through vasoconstriction of vessels in the optic nerve. Systemic administration of indomethacin also diminishes cerebral, renal and mesenteric blood flow by an unknown mechanism. However, no clinical trials exist so far investigating the effects of indomethacin on ocular blood flow. Therefore, the aim of this study is to investigate the effect of indomethacin on ocular blood flow in healthy humans.