Functional ex-vivo Imaging of Arterial Cellular Recruitment and Lipid Extravasation.

The main purpose of this sophisticated and highly versatile method is to visualize and quantify structural vessel wall properties, cellular recruitment, and lipid/dextran extravasation under physiological conditions in living arteries. This will be of interest for a broad range of researchers within the field of inflammation, hypertension, atherosclerosis, and even the pharmaceutical industry. Currently, many researchers are using in vitro techniques to evaluate cellular recruitment, like transwell or flow chamber systems with cultured cells, with unclear physiological comparability. The here introduced method describes in detail the use of a sophisticated and flexible method to study arterial wall properties and leukocyte recruitment in fresh and viable murine carotid arteries ex vivo under arterial flow conditions. This model mimics the in vivo situation and allows the use of cells and arteries isolated from two different donors (for example, wildtype vs. specific knockouts) to be combined into one experiments, thereby providing information on both leukocyte and/or endothelial cell properties of both donors. As such, this model can be considered an alternative for the complicated and invasive in vivo studies, such as parabiotic experiments.

The effect of flow changes on the arterial system proximal to an arteriovenous fistula for hemodialysis.

Arterial remodeling in response to flow changes is controlled by the endothelium, sensing wall shear stress (SS) changes. The present study focuses on the remodeling capacities of the brachial (BA) and radial artery (RA) of 16 renal failure patients after arteriovenous fistula creation. Pre- and postoperatively at predetermined time-points, diameter, wall thickness and peak and mean SS were assessed. After arteriovenous fistula creation, acute increases in BA SS (p = 0.018) and lumen diameter (p = 0.028) were observed. The diameter further increased in the next year (p = 0.023), whereas BA SS remained unchanged. RA SS and diameter increased acutely (p = 0.005) and remained unaltered after 1 y. RA wall thickness tended to decrease acutely (p = 0.059) and increased steadily during 1 y (p = 0.008). BA and RA diameter acutely increased after an acute SS rise and remained augmented after 1 y. Also, the RA vessel wall thickness enlarged, indicating structural remodeling. After 1 y, however, these changes did not result in SS restoration.

Shear stress depends on vascular territory: comparison between common carotid and brachial artery.

Shear stress (SS) is thought to be constant throughout the vascular system. Evidence for this supposition is scarce, however. To verify this hypothesis in vivo, we assessed common carotid (CCA) and brachial artery (BA) peak and mean wall shear rate (SR) noninvasively in 10 healthy volunteers (23.7 +/- 3.4 yr) with an ultrasound SR estimation system. SS was estimated from SR and calculated whole blood viscosity. SR was higher (P < 0.05) in the CCA (mean: 359 +/- 111 s(-1); peak: 1,047 +/- 345 s(-1)) than in the BA (mean: 95 +/- 24 s(-1); peak: 770 +/- 170 s(-1)). Whole blood viscosity was higher in the BA than in the CCA (5.1 +/- 0.7 vs. 3.3 +/- 0.6 mPa. s; P < 0.001). Peak SS did not differ between the CCA and the BA, whereas mean SS was significantly higher in the CCA (1.15 +/- 0.21 Pa) than in the BA (0.48 +/- 0.15 Pa; P < 0.001). These results demonstrate that BA SS strongly deviates from CCA SS in vivo.

Brachial artery shear stress is independent of gender or age and does not modify vessel wall mechanical properties.

The objective of the present study was to obtain brachial artery (BA) baseline shear stress (SS) values in healthy volunteers and to relate this to gender and age. Peak and mean wall shear rate (SR) were noninvasively measured in 30 healthy subjects using an SR estimation system. Arterial diameter and wall characteristics were obtained with a wall tracking system. SS was estimated from SR and calculated whole blood viscosity. Intrasubject variability and the effects of age and gender were assessed. Intrasubject variability of BA peak and mean SR were 16.2% and 28.6%. Baseline peak ( approximately 3.0 +/- 0.7 Pa) and mean SS ( approximately 0.5 +/- 0.2 Pa) were not gender-dependent, nor were they influenced by age. No vessel wall parameter related to BA SS. No differences in BA SS were observed between the genders and no influence of age was apparent. Our results indicate that the BA adequately responds to chronic changes in blood flow.