Methods:  Visualization of arteriolar blood flow in rat cremaster muscle was carried out in both normal and reduced flow conditions before and after Dextran 500 infusion to simulate physiological and pathological levels of red blood cell aggregation

in humans. Results:  Both normalized mean (p < 0.0001) and SD (p < 0.002) of the layer width were significantly enhanced after hyper-aggregation induction in reduced flow conditions (mean pseudoshear rate = 57.3 ± 7.2/sec). Normalized mean and SD of the layer width generally increased with decreasing vessel radius and this effect was most pronounced with hyper-aggregation in reduced flow conditions. The threshold pseudoshear rate at which the layer formation became more pronounced when compared with non-aggregating condition was higher with hyper-aggregation (217/sec) than normal-aggregation induction (139/sec). Conclusion:  Our findings confirmed the formation FK506 of a prominent Apoptosis inhibitor cell-free layer in the arterioles under higher shear conditions at pathological aggregation levels and this effect became more pronounced in smaller arterioles in normalizing the layer to the vessel radius. “
“Microcirculation (2010) 17, 59–68. doi: 10.1111/j.1549-8719.2009.00009.x Purpose:  To quantitatively assess microvascular dimensions in the eyes of neonatal wild-type and

VEGF120-tg mice, using a novel combination of techniques which permit three-dimensional (3D) image reconstruction. Methods:  A novel combination of techniques was

developed for the accurate 3D imaging of the microvasculature and demonstrated on the hyaloid vasculature of the neonatal mouse eye. Vascular corrosion casting is used to create a stable replica of the vascular network and X-ray microcomputed tomography (μCT) to obtain the 3D images. In-house computer-aided image analysis techniques were then used to perform a quantitative morphological analysis of the images. Results:  With the use of these methods, differences in the numbers of vessel segments, their diameter, and volume of vessels in the vitreous compartment were quantitated in wild-type neonatal mice or littermates over-expressing a labile (nonheparin binding) isoform of vascular endothelial growth factor (VEGF120) from the developing lens. This methodology was instructive in demonstrating that hyaloid vascular networks in VEGFA120 over-expressing mice have Astemizole a 10-fold increase in blind-ended, a six-fold increase in connected vessel segments, in addition to a sixfold increase (0.0314 versus 0.0051 mm3) in total vitreous vessel volume compared with wild type. These parameters are not readily quantified via histological, ultrastructural, or stereological analysis. Conclusion:  The combination of techniques described here provides the first 3D quantitative characterization of vasculature in an organ system; i.e., the neonatal murine intra-ocular vasculature in both wild-type mice and a transgenic model of lens-specific over-expression of VEGF.