View clinical trials related to Regional Blood Flow.
Filter by:The aim of this project is to demonstrate that fluorescence-mediated photoplethysmography (FM-PPG) is capable of routinely acquiring the tissue perfusion data sufficient to detect and monitor skin tissue perfusion anomalies.
Ultrasound-guided regional anesthesia is increasingly being used in the modern surgical environment to provide specific intraoperative anesthesia and postoperative analgesia. Infiltration of local anesthesics around peripheral nerves firs blocks sympathetic, then sensory, then motor nerve function. Sympathectomy-induced vasodilation following brachial plexus block results in increased skin temperature and arterial flow within minutes. Although it has not been shown to reliably increase diameter or cross-sectional area of distal arteries, brachial plexus block does change the pattern and quantity of blood flow to the hand. Given that the magnitude of change of flow cannot be attributed to vessel radius, the investigators suspect that the more laminar fluid dynamics are due to vascular tone. The investigators study aims to quantify alterations in physiology and peripheral vasodilator response. The investigators anticipate that axially block will significantly improve regional blood flow.
With age, muscles tend to waste at 0.5-1% per year, so that an 80 year old may have only 70% of the muscle possessed at 50. Muscle loss makes it harder to carry out tasks that require strength, keep the body balanced and continue activity for a prolonged period, which together may contribute to a loss of independence and an increased risk of falls. The cause of some of this muscle loss with ageing appears to be a reduction in muscle building in response to food. The known decreased limb blood flow in ageing muscle may go some way to explain this as there may be less nutrient delivery to the muscles. The investigators want to test if the known decrease in limb blood flow with age is matched with a decrease in the proportion of blood being delivered directly to the muscles, rather than fat and connective tissue. If so the investigators expect to see an improvement in the ability of muscles to maintain themselves via better capture of amino acids into protein. The investigators also want to test if 20 weeks resistance exercise training or drinking a cocktail of mixture of high flavanol cocoa (which can increase blood flow) and vitamin C can improve limb blood flow to older muscles and help reduce muscle wasting.
Impaired retinal blood flow has been implicated in the pathogenesis of diabetic retinopathy. Patel et al. (1992) showed that retinal blood flow increases with the level of diabetic retinopathy. Grunwald et al. (1996) reported that patients with insulin dependent diabetes mellitus (IDDM) of relatively short duration have increased retinal blood flow, even before the onset of diabetic retinopathy. On the other hand the data of Bursell et al. (1996) indicate that IDDM patients have reduced retinal blood flow, when they have normal blood glucose levels, but this study may have considerable methodological limitations. Acute elevations of blood glucose levels, however, result in an increase in retinal blood flow (Grunwald et al. 1987, Bursell et al. 1996). Based on previous experimental data the investigators hypothesize that ocular blood flow is increased in early diabetes and reduced at later stages of the disease. Previous studies have demonstrated that metabolic conditions such as hyperglycemia influence outcome parameters and thereby might have confounded results regarding ocular blood flow in diabetic retinopathy. The investigators will therefore study patients with IDDM during euglycemic conditions.
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. However, the mechanism behind choroidal autoregulation remains unclear. In the present study autoregulation of the choroid will be investigated during a decrease in ocular perfusion pressure, which will be achieved by an increase in intraocular pressure. Pressure/flow relationships will be investigated in the absence or presence of a NO synthase inhibitor. As a control substance the alpha-receptor agonist phenylephrine will be used.
Age-related macular degeneration (AMD) is the chief cause of severe and irreversible loss of vision in developed countries. The prevalence of AMD increases dramatically with age. The early stage (or dry AMD) is associated with minimal visual impairment and is characterized by large drusen and pigmentary abnormalities in the macula. The late stage is a neovascular, exudative form. This so called exudative AMD includes serous or hemorrhagic detachment of retinal pigment epithelium and choroidal neovascularization leading to severe loss of vision (20/200 or worse). Patients with unilateral CNV (choroidal neovascularisation) have a significant risk of CNV developing in the second eye. Choroidal blood flow is of great importance for normal visual function. Several reports have provided evidence suggesting that choroidal blood flow is decreased in subjects with AMD. In late stages of AMD angiogenesis leads to the formation of choroidal neovascularization that can cause severe visual impairment by disrupting normal macular function. The purpose of this evaluation is to investigate a possible link between alterations in choroidal blood flow and the development of CNV and serous detachment in the fellow eye of patients with AMD and unilateral neovascular maculopathy. This longitudinal study may provide important findings with respect to natural history and visual prognosis of patients with neovascularized AMD. Ocular blood flow will be determined by non-invasive methods, including laser Doppler flowmetry and laser interferometry
Very low birth weight infants has increased dramatically their survival. Survival without neurologic disturbance varies a lot between centers.There is evidence that fluctuations in cerebral blood flow influences the appearance of intraventricular hemorrhage and itself implies a detrimental neurologic developing.The electroencephalography is the result of electric base membrane activity on rest, and it's influenced by the blood flow either. The Amplitude-integrated electroencephalography is a novel tool, that is capable to be continuously used at the patient bed and is easily to be read by the trained clinician.The hypothesis is that common procedures as Surfactant instilation, Indomethacin and Aminophyline infusion as the appearance of apneas alters the aEEG register. It is a prospective study that tries to recruit 10 < 30 weeks of gestational age with aprofen consent to monitorize the aEEG since birth to the seventh day of live.
High arterial blood oxygen tension leads to vasoconstriction of retinal vessels, possibly related to an interaction between reactive oxygen species and endothelium-derived vasoactive factors. Vitamin C is a potent antioxidant capable of reversing endothelial dysfunction due to increased oxidant stress. Vitamin C appears to have vasodilatory properties, but the underlying mechanisms are not well understood. In the present study we hypothesized that hyperoxic vasoconstriction of retinal vessels could be diminished by vitamin C. Ocular blood flow will be determined by non-invasive methods, including laser Doppler velocimetry and the Zeiss retinal vessel analyser.
Latanoprost is a synthetic prodrug of 17-phenyl-substituted prostaglandin F2α analog. Used at a dose of one drop per day, it has been reported to produce a 30 to 35% reduction in intraocular pressure. Its mechanism of activation involves augmentation of the eye's natural uveoscleral outflow capacity . There is evidence that ocular blood flow plays a role in the clinical course of glaucoma. Glaucoma medication that lowers IOP simultaneously increases ocular blood perfusion pressure, which in turn may increase ocular blood flow. This could well contribute to the partially contradicting results concerning ocular hemodynamic effects of latanoprost. In vitro studies indicate that latanoprost has no effect on ocular vascular tone in therapeutical doses. By contrast, it has been reported in several studies that latanoprost 0.005% increases pulsatile ocular blood flow in patients with primary open angle glaucoma and normal tension glaucoma. This increase in pulsatile ocular blood flow mainly reflects an increase in the choroidal circulation. Little is known about the potential effect of latanoprost on choroidal blood flow regulation in humans. The present study therefore tries to elucidate whether treatment with latanoprost may alter choroidal blood flow regulation during artificial changes in ocular perfusion pressure. In addition, the present study aims to clarify whether the change in choroidal blood flow after latanoprost administration are due to direct vasoactive effects or due to the increase in ocular perfusion pressure. The second alternative may have important implications on our understanding of glaucoma treatment, because reduction of IOP may then per se result in normalization of ocular blood flow regulation.
Age related macula degeneration is one of the most common sight threatening diseases of the elderly. The so called wet form of AMD is caused by choroidal neovascularisation (CNV) of pathological vessels, which lead to leakage, bleeding and macular edema. Several lines of evidence suggest that vascular endothelial growth factor (VEGF) plays a key role in the induction CNV. Recent evidence indicates that overexpression of VEGF in the retinal pigment epithelium may lead to the development of CNV in experimental models, and intravitreal injection of a VEGF blocker prevents the development of experimental CNV. This hypothesis is also supported by the promising effects of anti-VEGF treatment in patients with choroidal neovascularisation. The substances currently in clinical use include ranibizumab (Lucentis®), bevacizumab (Avastin®) and pegaptanib (Macugen®). However, from a physiological point of view, VEGF also serves as a survival factor for existing vessels and for neuronal cells. Moreover, it has been reported that VEGF induces vasodilatation, most probably by an increased production of nitric oxide. Accordingly one may hypothesize that anti-VEGF treatment is associated with ocular vasoconstriction with unknown long term results. Thus, in the current study, the investigators set out to investigate whether the ocular perfusion is affected by a single intravitreal anti-VEGF.