View clinical trials related to Blood Flow Velocity.
Filter by:Blood flow autoregulation is defined as the ability of a tissue to maintain a relatively constant flow, despite moderate alterations in perfusion pressure. Similar to the cerebral, renal, coronary and skeletal muscle circulations, the ocular vascular bed shows the property of flow autoregulation. This homeostatic mechanism allows blood supply to the eye to match metabolic demand during daily activities, such as changes in posture, or in more critical conditions. Autoregulation has been found to be a complex phenomenon, showing heterogeneity in its site and time course of action. Since metabolic, myogenic, neurogenic and possibly endothelium-related mechanisms may be involved, several factors may vary depending on the challenging stimulus, the vessel tone, or the degree of impairment of autoregulation. To study the dynamics of ocular autoregulation, it is necessary to introduce a step disturbance (stimulus) in ocular perfusion pressure and to record the responses of ocular blood flow continuously before and after this step disturbance. The investigators have employed a mechanical noninvasive technique to induce an ocular perfusion pressure step disturbance without drugs or changes in the concentration of vasoactive substances in the blood by using the thigh cuff technique inducing a small step decrease in ocular perfusion pressure. With this technique the investigators could show significant differences in the time response of blood velocities in the ophthalmic and middle cerebral artery. This clearly indicates different mechanisms to be responsible for autoregulatory mechanisms distal to the vessels. Interestingly our results indicate that in the ophthalmic artery a late vasoconstriction occurs. Many previous investigations have demonstrated that sympathetic nerve stimulation causes vasoconstriction in the ocular circulation. Accordingly, the present study tests the hypothesis that α2-adrenoceptors are involved in the dynamic regulation of blood flow in the ophthalmic and middle cerebral artery after a step decrease in perfusion pressure.
Several lines of evidence suggest now that ocular perfusion abnormalities may contribute to the progression of glaucoma. It has been hypothesised that increased endothelin-1 plasma levels, as seen in patients with glaucoma, may be related to these alterations in ocular blood flow. We could show in recent experiments that administration of ET-1 decreases ocular blood flow, whereas blocking of the ET-A receptors do not affect basal vascular tone in healthy subjects. In the current study we set out to evaluate the effect Bosentan, a non-selective ETA-receptor antagonist in patients with open-angle glaucoma. This should allow us to test the hypothesis that administration of an ET-1 receptor antagonist increases ocular blood flow in patients with glaucoma. Investigations will be done with a retinal vessel analyzer to determine retinal vessel cross-sectional diameters, with laser Doppler flowmetry and laser Doppler velocimetry to determine subfoveal macular blood flow and optic nerve head blood flow and with laser interferometric measurements to determine fundus pulsation amplitude in the macula. The intraocular pressure will be measured with applanation tonometry. This will be assessed at baseline and in response to peroral application of Bosentan or placebo. The study objective is therefor, to evaluate the contribution of ET-1 to ocular blood flow dysregulation in patients with open-angle glaucoma.
Habitual smoking is associated with an increased risk of coronary artery disease, cerebral and peripheral vascular disease, including ocular diseases like age-related macular degeneration or diabetic retinopathy. Data of a recent study performed in the investigators lab revealed abnormal choroidal blood flow regulation in chronic smokers as compared to age-matched non-smoking subjects during isometric exercise. However, no information is yet available about the regulation of retinal vascular tone in habitual smokers. Thus, in the current study, the investigators set out to investigate whether the regulation of retinal vessels diameters is affected in habitual smokers. It has been shown in several reports that stimulation with diffuse luminance flicker, increases retinal arterial and venous diameters, indicating for the ability of the retina to adapt to changing metabolic demands. In the current study we use this effect as a tool to investigate whether the flicker induced vasodilatation is affected in habitual smokers. This would indicate for an impaired vascular regulation process in smokers.