Oxidative stress and endothelial damage in patients with asymptomatic carotid atherosclerosis.

It is known that oxidative stress can be able to induce cytotoxicity of blood cells, stimulate release of inflammatory cytokines, and induce the production of growth factors. The aim of this study was to investigate oxidative stress and endothelial dysfunction in patients with asymptomatic carotid artery disease and healthy controls. Native low-density lipoproteins, oxidised low-density lipoproteins, malondialdehyde, nitrates, glutathione peroxidase activity and endothelin-1 were determined in patients without severe (range between 30% and 50%) carotid artery stenosis. Native low-density lipoproteins, oxidized low-density lipoproteins, malondialdehyde, glutathione peroxydase, and endothelin-1 concentrations were higher in patients than in health controls (P<0.001). No difference was observed in nitrate values (P<0.8). Our results revealed oxidative stress in patients without severe carotid artery stenosis and clinical symptoms. This was shown by the elevated malondialdehyde and oxidized low-density lipoprotein levels.

Effects of ischaemic stress on leukocyte activation processes in patients with chronic peripheral occlusive arterial disease: role of L-propionyl carnitine administration.

An open study was carried out to assess whether, in patients with occlusive peripheral arterial disease (PAD), ischaemic stress induced by maximal physical exercise is associated with leukocyte activation processes, and to evaluate the effects of L-propionyl carnitine (LPC) administration on such processes. Fifteen patients with occlusive PAD (stage II-A), with a mean pain-free walking distance (PWD) of 199 +/- 70.66 m were orally treated with 2000 mg/day LPC for 2 months. Serum levels of E-selectin, P-selectin, L-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-I (VCAM-1) were measured at rest and after the performance of a treadmill walking test (treadmill speed 3.5 km h(-1), inclination 12%) in the untreated condition, and again after treatment with LPC. Significant increases of these factors were observed after maximal exercise compared with resting values. Such increase was significantly reduced after LPC treatment compared with the untreated condition. This study shows that ischaemia induced by maximal stress is associated with leukocyte activation processes, and that LPC is capable of modulating these processes. LPC, therefore, may have a protecting role during ischaemia.