|
|
The founder of Vascular Therapeutics, Inc. was president of a small biomedical company in the mid-90's. During that time he observed significant therapeutic results from the use of an electronic device which the biomedical company marketed. That company had little or no scientific or medical knowledge as to the mechanism of action whereby the results were achieved. After leaving that company, he dedicated six years to study, reaching the conclusion that the results were derived from an improvement in vascular function: more specifically, from a reduction in endothelial dysfunction. Enhanced Vascular Flow, accomplished through a special version of neuromuscular stimulation, causes laminar shear stress and endothelial mechanotransduction leading to the production or upregulation of many vasoactive substances, including: |
Nitric oxide Prostacycline Superoxide dismutase Glutathion Krupple-like Factor 2 Adenosine Endothelial progenitor cells Thioredoxin Angiotensin II Adrenomedullin Lactic acid Carbon monoxide Bradykinin Heme oxygenase-1 Granulocyte-macrophage colony __stimulating factor |
Thousand of research articles are available at PubMed elucidating the beneficial effects of shear stress, endothelial mechanotransduction and the substances upregulated or downregulated. Here are a few suggestions: |
Davies PF, Flow mediated endothelial mechanotransduction, Physiol Rev. 1995 Jul;75(3):519-60 Traub O, Berk BC; Mechanisms by Which Endothelial Cells Transduce an Atheroprotective Force, Arteriosclerosis Thrombosis and Vascular Biology, 1998;18:677-685. Yamawaki H, Pan S, Lee RT, Berk BC. Fluid shear stress inhibits vascular inflammation by decreasing thioredoxin-interacting protein in endothelial cells., J Clin Invest. 2005 Mar;115(3):733-8 Ramana KV, Chandra D, Sirvastava S, Bhatnagar A and Sirvastava SK, Nitric oxide regulates the polyol pathway of glucose metabolism in vascular smooth muscle cells, The FASEB Journal. 2003;17:417-425 |