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Vessel Reactivity (vessel + reactivity)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Effects of a high-fat meal on resistance vessel reactivity and on indicators of oxidative stress in healthy volunteers

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 4 2001
Andreas Schinkovitz
High fat meals postprandially impair macrovascular endothelial function and a link to increased oxidative stress is suggested. Few information, on the other hand, exists on the effect of postprandial hyperlipidaemia on resistance vessel function. Under normal circumstances this vascular bed regulates tissue perfusion and, by controlling flow, impacts on macrovascular nitric oxide formation. The impact of a high fat meal (1200 kcal, 90 g fat, 46 g protein and 47 g carbohydrates) on postprandial resistance vessel reactivity and on indicators of oxidative stress was studied in 11 healthy subjects by venous-occlusion plethysmography using another six subjects as time control group. Ingestion of the test meal resulted in a pronounced increase of serum triglycerides from 1·05 ± 0·61 mmol l,1 in the fasting state to peak postprandial values of 1·94 ± 0·41 mmol l,1 (P < 0·001) reached after 4 h and a return to baseline after 8 h. Fasting peak reactive hyperaemia (RH) was 19·6 ± 2·4 ml min,1 (100 ml),1. Two hours after ingestion of the test meal peak RH was transiently reduced to 16·8 ± 2·2 ml min,1 (100 ml),1 (P < 0·05). No alteration of resting forearm perfusion was observed. The time course of peak RH suggested a potential biphasic effect of the test meal with an early impairment and a late increase of RH. Ingestion of a lipid rich test meal did not exert any influence on either total plasma antioxidant capacity given in trolox equivalents (513 ± 26 ,mol l,1 at baseline) or on plasma peroxides measured as H2O2 equivalents (469 ± 117 ,mol l,1). Our results suggest that ingestion of a meal containing 90 g of fat results in a transient impairment of reactive hyperaemia in healthy subjects but these vascular alterations are not accompanied by signs of systemically increased oxidative stress. [source]

2412: Laser and oxygen

ACTA OPHTHALMOLOGICA, Issue 2010
CJ POURNARAS
Purpose To evaluate the changes in the retinal oxygen partial pressure (PO2) following photocoagulation as well as the resulting effect of the laser induced improved oxygenation, on the retinal vessels hemodynamics. Methods Measurements of the partial pressure of oxygen (PO2) distribution within the retina in various animal species using oxygen sensitive microelectrodes and evaluation of changes on the retinal vessels reactivity, following laser treatment, gave additional insights concerning photocoagulation mechanisms. Results Preretinal intervascular PO2 , far away from vessels, remain constant in all retinal areas. Intervascular intraretinal PO2 gradually decreases from both the vitreo-retinal interface and the choroid towards the mid-retina. Close to the pigment epithelium, it is significantly higher than at the vitreoretinal interface due to the much higher O2 supply provided by choroidal compaires to retinal circulation. Laser photocoagulation reduces the outer retina O2 consumption and allows O2 diffusion into the inner retina from the choroid raising the PO2 in the inner healthy retinal layers and in the preretinal intervascular normal areas. In this way, laser treatment relieves retinal hypoxia in experimental branch vein occlusion (BRVO). In patients with diabetic retinopathy (DR), the retinal PO2 is also higher in areas previously treated with laser. Following photocoagulation, the resulting reversal of hypoxia, the down-regulation of the VEGF expression, the retinal vasculature constriction and the improvement of the auto-regulatory response to physiological stimuli, all affect favorably both the retinal neovascularisation and macular edema. Conclusion Photocoagulation induces an increase of the inner retinal oxygenation resulting to an improvement of the autoregulatory retinal vessels response. [source]

Retinal photocoagulation and oxygenation

ACTA OPHTHALMOLOGICA, Issue 2009
CJ POURNARAS
Purpose The clinical role of photocoagulation for the treatment of hypoxia related complications of retinal ischemic microangiopathies is well established. Methods Measurements of the partial pressure of oxygen (PO2) distribution within the the retina in various animal species using oxygen sensitive microelectrodes and evaluation of the retinal vessels reactivity by laser doppler velocimetry gave additional insights concerning photocoagulation mechanisms. Results The PO2 within the vitreo-retinal interface is heterogeneous. Preretinal and trans-retinal PO2 profiles indicate that the preretinal PO2 far away from vessels remain constant in all retinal areas. Intervascular intraretinal PO2 gradually decreases from both the vitreo-retinal interface and the choroid towards the mid-retina. Close to the pigment epithelium, it is significantly higher than at the vitreoretinal interface due to the much higher O2 supply provided by choroidal compaires to retinal circulation. Laser photocoagulation reduces the outer retina O2 consumption and allows O2 diffusion into the inner retina from the choroid raising the PO2 in the inner healthy retinal layers and in the preretinal intervascular normal areas. In this way laser treatment relieves retinal hypoxia in experimental branch vein occlusion (BRVO). In patients with diabetic retinopathy (DR), the retinal PO2 is higher in areas previously treated with laser. Following photocoagulation, the resulting reversal of hypoxia, the retinal vasculature constriction and the improvement of the regulatory response to hyperoxia all affect favorably both the retinal neovascularisation and macular edema. Conclusion Photocoagulation induces an increase of the inner retinal oxygenation reversing the retinal hypoxia and improving the regulatory response of the retinal vessels [source]