Effects of acetyl salicylic acid and cilostazol administration on serum thrombomodulin concentration in diabetic patients

Physical training decreases plasma thrombomodulin in Type I and Type II diabetic patients

“…However, some indirect evidence exists. Pharmacological vasodilation through cilostazol has been associated with a decrease in TM concentrations in Type II diabetic patients [40] and treatment with the angiotensin-converting enzyme inhibitor enalaprilat, with a known protective effect on endothelium, reduced the release of TM and other soluble endothelial-derived substances in critically-ill patients [40]. These findings support the hypothesis that the reduction in TM concentrations observed in our study after the exercise programme could reflect an improvement in endothelial function.…”

Macro‐ and microvascular endothelial dysfunction in diabetes

“…Cilostazol, a selective inhibitor of phosphodiesterase‐3, possesses vasodilator properties and has anti‐inflammatory effects. In diabetic patients, cilostazol reduces soluble CD40 ligand and thrombomodulin levels in the serum, leading to a reduction of restenosis after percutaneous transluminal coronary angioplasty . Cilostazol also improves the function of circulating endothelial progenitor cells in diabetic patients with ischemic cerebrovascular disease .…”

Dysfunction of the endothelial nitric oxide signalling pathway in diabetes and hyperglycaemia

“…In human retinal endothelial cells, modulation of plasminogen activator (PA) synthesis by insulin-like growth factor-I (IGF-1), epidermal growth factor (EGF) or acidic fibroblast growth factor (aFGF) is influenced by diabetes and the state of cell confluency (Grant & Guay, 1991). Vascular complications in diabetic subjects are also associated with elevated basal concentrations of serum thrombomodulin (Tanni, Hada, Kitami, Nakano, Takahashi, Ito, Sato & Shibata, 1993), a higher rate of receptor-mediated degradation of very low density lipoprotein (VLDL) by endothelial cells (Klein & Lopes-Virella, 1993), an abnormal metabolism of methylamine and formation of atherosclerotic plaques in the vascular wall (Yu & Zou, 1993).…”