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Vessel Regression (vessel + regression)
Selected AbstractsStructural and biophysical simulation of angiogenesis and vascular remodeling ,DEVELOPMENTAL DYNAMICS, Issue 4 2001Ralf Gödde Abstract The purpose of this report is to introduce a new computer model for the simulation of microvascular growth and remodeling into arteries and veins that imitates angiogenesis and blood flow in real vascular plexuses. A C++ computer program was developed based on geometric and biophysical initial and boundary conditions. Geometry was defined on a two-dimensional isometric grid by using defined sources and drains and elementary bifurcations that were able to proliferate or to regress under the influence of random and deterministic processes. Biophysics was defined by pressure, flow, and velocity distributions in the network by using the nodal-admittance-matrix-method, and accounting for hemodynamic peculiarities like Fahraeus-Lindqvist effect and exchange with extravascular tissue. The proposed model is the first to simulate interdigitation between the terminal branches of arterial and venous trees. This was achieved by inclusion of vessel regression and anastomosis in the capillary plexus and by remodeling in dependence from hemodynamics. The choice of regulatory properties influences the resulting vascular patterns. The model predicts interdigitating arteriovenous patterning if shear stress-dependent but not pressure-dependent remodeling was applied. By approximating the variability of natural vascular patterns, we hope to better understand homogeneity of transport, spatial distribution of hemodynamic properties and biomass allocation to the vascular wall or blood during development, or during evolution of circulatory systems. © 2001 Wiley-Liss, Inc. [source] Regression of blood vessels in the ventral velum of Xenopus laevis Daudin during metamorphosis: light microscopic and transmission electron microscopic studyJOURNAL OF ANATOMY, Issue 2 2000H. BARTEL Structural changes of the ventral velum of Xenopus laevis tadpoles from late prometamorphosis (stage 58) to the height of metamorphic climax (stage 62) were examined by light and transmission electron microscopy. Special emphasis was given to the blood vessel regression. Early changes of velar capillaries were formation of luminal and abluminal endothelial cell processes, vacuolation, and cytoplasmic and nuclear chromatin condensation. At the height of metamorphic climax, transmission electron microscopy revealed apoptotic endothelial cells with nuclear condensation and fragmentation, intraluminal bulging of rounded endothelial cells which narrowed or even plugged the capillary, and different stages of endothelial cell detachment (,shedding') into the vessel lumen. These changes explain the ,miniaturisation' of the velar microvascular bed as well as the typical features found in resin-casts of regressing velar vessels which have been observed in a previous scanning electron microscopy study of the ventral velum. [source] Long-term study of vascular perfusion effects following arteriovenous sheathotomy for branch retinal vein occlusionACTA OPHTHALMOLOGICA, Issue 3 2010Mahiul M. K. Muqit Abstract. Purpose:, To evaluate the perfusion effects and long-term visual outcome of pars plana vitrectomy (PPV) combined with arteriovenous sheathotomy (AVS) with or without triamcinolone for nonischaemic branch retinal vein occlusion (NI-BRVO). Methods:, Prospective, interventional case series of eight patients with NI-BRVO and haemorrhagic macular oedema. Patients underwent PPV and AVS (n = 5), or PPV, AVS and intravitreal triamcinolone (IVT, n = 3). A masked grading technique assessed fundus photographs and fluorescein angiography (FFA) following surgery. Scanning laser ophthalmoscopy/optical coherence tomography (SLO/OCT) evaluated macular oedema and outer retinal architecture. Main outcomes examined included visual acuity (VA), retinal reperfusion, collateral vessel regression, vascular dilatation, cystoid macular oedema (CMO), and ocular neovascularization. Results:, Seven of eight patients underwent uncomplicated surgery, with increased intraretinal perfusion and reduced engorgement of distal retinal veins. The mean pre-logMAR VA was 0.8 (SD 0.17) and did not improve significantly after surgery (post-logMAR 0.6, SD 0.38; p = 0.11, paired t -test). SLO/OCT showed persistent CMO in four patients, and subfoveal thinning of the photoreceptor layer. Collateral vessels disappeared at the blockage site post-AVS in 7/8 eyes, and this was associated with improved retinal perfusion. Six of eight patients developed epiretinal membrane. No patients developed ocular neovascularization. The average follow-up was 34.5 months. Conclusions:, PPV with AVS is a safe procedure, and adjunctive IVT had no additional effects on vascular perfusion. Successful decompressive surgery was followed by disappearance of collateral vessels at the BRVO blockage site and was a clinical marker for intravascular reperfusion. Long-term epiretinal gliosis and subfoveal photoreceptor atrophy limited functional and visual recovery. [source] The role of HIF-1 alfa in apoptosis and proliferative retinopathyACTA OPHTHALMOLOGICA, Issue 2009R FERNANDES Purpose In diabetic retinal capillaries, the earlier morphological changes include pericyte loss and acellular capillary formation. These processes are regulated by interactions among a number of pro- and antiangiogenic factors, including vascular endothelial growth factor (VEGF) and Angiopoietin-2 (Ang-2). We hypothesize that increased levels of methylglyoxal (MGO) in RPE cells disrupts the balance of VEGF/Ang-2 promoting endothelial cell death and vessel regression. Methods Rats with moderate T2D, and retinal cell lines of epithelium (RPE) and endothelium (EC) were used. MGO levels were determined by HPLC. Immunohistochemical analysis was performed in retinas stained for VEGF and Ang-2. RPE cells were incubated with MGO in hypoxic conditions and the level of VEGF and Ang-2 was assessed by ELISA. EC were subsequently treated with the pre-conditioned media of the RPE cells. Cell death was determined by WB against Bax and Bcl-2, while EC proliferation was assessed by BrdU-incorporation and fibrin gel angiogenic assays. Results Hyperglycemia increases the levels of MGO in retinas and RPE cells. MGO increases the levels of Ang-2 and strongly decreases the levels of VEGF in response to hypoxia. VEGF downregulation appears to result both from increased HIF-1, degradation and low HIF-1 transcriptional activity. The MGO-induced imbalance in the VEGF/Ang-2 significantly increases the expression of Bax and decreases the levels of Bcl-2. Consistently, this imbalance leads to decreased proliferation of the EC. Conclusion In diabetic retinopathy, accumulation of MGO may play a role in VEGF/Ang-2 imbalance, triggering the activation of the apoptotic cascade which induces decreased proliferation of retinal endothelial cells and as a consequence vessels regression [source] | ||||||||||