PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 2406959

The vascular laboratory. Standards and certification.

B L Thiele
View original source ↗Export metadata ↓

Abstract

The diversity of testing methodologies and reporting practices has necessitated that standards be defined for both performance of testing as well as interpretation and reporting of results. The guidelines to be used for the noninvasive diagnosis of extracranial vascular disease and the rationale for their use are presented. Emphasis is placed upon realistic diagnostic features that have clinical relevance and the use of testing methods that can identity these features. Further developments in this field, particularly those addressing the overall performance of vascular diagnostic laboratories, are to be defined by a multiprofessional inter-societal commission in the near future. It is anticipated that a voluntary accreditation process will insure high quality of testing.

Explore related subjects

Blood Flow VelocityCerebrovascular CirculationCerebrovascular DisordersCertificationHumansTerminology as TopicUltrasonicsUltrasonographyJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

B L Thiele. 1990. The vascular laboratory. Standards and certification.. https://doi.org/10.1016/s0039-6109(16)45029-2

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Vascular bed origin dictates flow pattern regulation of endothelial adhesion molecule expression.

Endothelial cell phenotypes markedly differ, depending upon function and vascular bed of origin. Differences might account for specific susceptibility to pathological conditions. As leukocyte adhesion to activated endothelium is the initiating event in a range of diseases, we compared the influence of vascular bed-specific flow patterns on adhesion molecule expression in human saphenous vein (HSVEC) and coronary artery endothelial cells (HCAEC). In vitro, immune cell attachment was increased 1.6-fold when tumor necrosis factor (TNF)-alpha-stimulated HSVEC were exposed to coronary artery flow in place of physiological venous flow and 1.9-fold higher compared with attachment to cytokine-stimulated HCAEC exposed to coronary artery flow. This was associated with increased concentrations of soluble E-selectin, VCAM-1, and ICAM-1 in supernatants of HSVEC exposed to coronary artery flow compared with HCAEC exposed to the same flow pattern. Venous and coronary artery flow both increased TNF-alpha-induced E-selectin and ICAM-1 expression on HSVEC, but only coronary artery flow increased VCAM-1 expression. In marked contrast to HSVEC, venous and coronary artery flow attenuated TNF-alpha-induced E-selectin and VCAM-1 expression on HCAEC, whereas coronary artery flow further induced ICAM-1 on cytokine-stimulated HCAEC. With the exception of cytokine-induced ICAM-1, adhesion molecule expression on HSVEC exposed to coronary artery flow exceeded expression on HCAEC. Thus ICAM-1 expression involves complex flow-dependent and -independent pathways with marked dissimilarities between the two endothelial cell types studied. Interestingly, Kruppel-like factor (KLF) 4 overexpression in HCAEC and HSVEC significantly reduced TNF-alpha-induced E-selectin and VCAM-1 expression in static conditions, while ICAM-1 expression remained constant. Furthermore, both flow patterns induced KLF2 and KLF4 expression in HCAEC and HSVEC. Venous and coronary artery flow differentially influence endothelial adhesion molecule and transcription factor expression, depending on the vascular bed of origin. Differences in adhesion molecule expression and subsequent immune cell adhesion between HSVEC and HCAEC may contribute to different susceptibility to pathological conditions.

Blood Flow Velocity↗
PubMed2007

Mesoscale simulation of blood flow in small vessels.

Computational modeling of blood flow in microvessels with internal diameter 20-500 microm is a major challenge. It is because blood in such vessels behaves as a multiphase suspension of deformable particles. A continuum model of blood is not adequate if the motion of individual red blood cells in the suspension is of interest. At the same time, multiple cells, often a few thousands in number, must also be considered to account for cell-cell hydrodynamic interaction. Moreover, the red blood cells (RBCs) are highly deformable. Deformation of the cells must also be considered in the model, as it is a major determinant of many physiologically significant phenomena, such as formation of a cell-free layer, and the Fahraeus-Lindqvist effect. In this article, we present two-dimensional computational simulation of blood flow in vessels of size 20-300 microm at discharge hematocrit of 10-60%, taking into consideration the particulate nature of blood and cell deformation. The numerical model is based on the immersed boundary method, and the red blood cells are modeled as liquid capsules. A large RBC population comprising of as many as 2500 cells are simulated. Migration of the cells normal to the wall of the vessel and the formation of the cell-free layer are studied. Results on the trajectory and velocity traces of the RBCs, and their fluctuations are presented. Also presented are the results on the plug-flow velocity profile of blood, the apparent viscosity, and the Fahraeus-Lindqvist effect. The numerical results also allow us to investigate the variation of apparent blood viscosity along the cross-section of a vessel. The computational results are compared with the experimental results. To the best of our knowledge, this article presents the first simulation to simultaneously consider a large ensemble of red blood cells and the cell deformation.

Blood Flow Velocity↗
PubMed2007

Doppler sonography evaluation of flow velocity and volume of the extracranial internal carotid and vertebral arteries in healthy adults.

PURPOSE: To measure with Doppler sonography the velocity and volume of blood flow in the extracranial internal carotid artery (ICA) and vertebral artery (VA) of healthy adults and to calculate total cerebral blood flow volume (tCBFV). METHODS: Bilateral ICA and VA were examined sonographically in 180 healthy adults. Angle-corrected peak systolic (Vps), end-diastolic (Ved), and time-averaged maximum blood flow velocity (TAV) were measured in pulsed Doppler mode, and the resistance index (RI) and pulsatility index (PI) were calculated. The cross-sectional area (A) was measured on gray-scale images. Volume flow was calculated as FV = TAV x A, and tCBFV was calculated as the sum of the right and left ICA and VA volume flow. RESULTS: tCBFV was 651 +/- 96 ml/min for the entire population. There was a significant decrease in Vps, Ved, TAV, and tCBFV with age in all arteries. RI and PI values initially declined and then increased with age. Cross-sectional area increased with age in ICA but not in VA. PI and RI were higher in men than in women. Blood flow velocity and volume were higher, and RI was lower in the left than in the right VA. CONCLUSION: The Doppler sonographic assessment of extracranial ICA and VA blood flow volume may be useful for the study of cerebral hemodynamic changes in patients with cerebrovascular disorders. Age-dependent changes should be considered, for instance, in the management of intensive care patients with impaired cerebral perfusion.

Blood Flow Velocity↗