PubMed Health⌕ Search

PubMed · 15501192

Vascular imaging.

Abstract

Many rheumatic diseases affect the vasculature, either as a 'primary' manifestation of the disease process (as in vasculitis or scleroderma-spectrum disorders) or as a result of accelerated atherosclerosis. Recent years have seen very major developments in, and refinements of, vascular imaging methods. It is likely that this pace of development will continue, enhancing the rheumatologist's ability to diagnose different musculoskeletal conditions and follow their progression, using minimally invasive techniques. In this chapter, we describe these recent advances in vascular imaging techniques, concentrating on those most relevant to the practising clinician, but also discussing methods which are being used in clinical research. Three main groups of imaging modalities are described: large vessel imaging (X-ray, magnetic resonance (MR) and computed tomography (CT) angiography), nailfold microscopy and thermography. For each of these, the method(s) and then the clinical and research applications are discussed. Laser Doppler, a research technique, is also described.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Ariane L Herrick, Charles Hutchinson. 2004. Vascular imaging.. https://doi.org/10.1016/j.berh.2004.06.004

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

KEEP EXPLORING

Related citations

On the role of endothelial progenitor cells in tumor neovascularization.

The exact role that bone marrow (BM)-derived endothelial progenitor cells (EPCs) play in tumor neovascularization is heavily debated. We develop a quantitative three-compartment model with predictive power regarding the dynamics of tumorigenesis. There are two distinct processes by which tumor neovasculature can be built: angiogenesis is the formation of new blood vessels from preexisting vessels; vasculogenesis is the formation of new vessels by recruiting circulating EPCs. We show that vasculogenesis-driven and angiogenesis-driven tumors grow in different ways. (i) If angiogenesis is the prevailing process, then the tumor mass (and volume) will grow as a cubic power of time, and BM-derived EPCs will stay at a constant level. (ii) If vasculogenesis is the dominant process, then the tumor mass will be characterized by a linear growth in time, and the number of circulating EPCs (after possibly increasing to a maximum) will decrease to low levels. With this information, one can identify the "signature" of each of the processes in the observations of tumor growth and the dynamics of the relevant characteristics, such as the level of BM-derived EPCs. We show how our results can help explain some apparently contradictory experimental data. We also propose ways to couple this study with directed experiments to identify the exact role of vasculogenesis in tumor progression.

Blood Vessels↗

Hepatocyte growth factor promotes lymphatic vessel formation and function.

The lymphatic vascular system plays a pivotal role in mediating tissue fluid homeostasis and cancer metastasis, but the molecular mechanisms that regulate its formation and function remain poorly characterized. A comparative analysis of the gene expression of purified lymphatic endothelial cells (LEC) versus blood vascular endothelial cells (BVEC) revealed that LEC express significantly higher levels of hepatocyte growth factor receptor (HGF-R). Whereas little or no HGF-R expression was detected by lymphatic vessels of normal tissues, HGF-R was strongly expressed by regenerating lymphatic endothelium during tissue repair and by activated lymphatic vessels in inflamed skin. Treatment of cultured LEC with HGF promoted LEC proliferation, migration and tube formation. HGF-induced proliferation of LEC did not require vascular endothelial growth factor receptor-3 activation, and HGF-induced cell migration was partially mediated via integrin alpha-9. Transgenic or subcutaneous delivery of HGF promoted lymphatic vessel formation in mice, whereas systemic blockade of HGF-R inhibited lymphatic function. These results identify HGF as a novel, potent lymphangiogenesis factor, and also indicate that HGF-R might serve as a new target for inhibiting pathological lymphangiogenesis.

Blood Vessels↗