Publications by authors named "B Schwippert"

Platelet activation and hyperreactivity are known to be associated with a rapid development and progression of diabetic angiopathy. The present study attempts to clarify whether IDDM patients without diabetic complications have an increased platelet activation and whether in vivo platelet activation is altered in the presence of diabetic microangiopathy. Platelet activation was assessed by flow cytometry analysis in 50 healthy controls (c) and in 41 patients with insulin-dependent diabetes mellitus (IDDM type 1) who were screened for diabetic complications.

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Aims: To study the recovery of platelet function after discontinuation of clopidogrel treatment in healthy volunteers.

Methods: Ten healthy volunteers were treated with clopidogrel (75 mg day(-1)) for 7 days. CD62P expression and PAC-1 binding were measured by flow cytometry.

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Background: Diabetes mellitus is associated with increased generation of free oxygen radicals and depleted scavenging potential (oxidative stress), leading to increased LDL oxidation and platelet hyperreactivity, the major components of atherothrombotic vascular lesions. A main goal of antioxidant therapy is to protect the LDL particle from atherogenic oxidation and to reduce the activated cellular hemostasis.

Methods: We evaluated the influence of a high dose supplementation with 800 IU of the natural antioxidant RRR-alpha-tocopherol (vitamin E) per day for six months on serum levels, vitamin E load of LDL particles (HPLC), lag phase of LDL oxidation (Esterbauer's assay), platelet adhesion molecules, leukocyte-platelet coaggregation (flow cytometry, D-III protocol) and coagulation (INR/PTT) in a group of 36 patients with type 2 diabetes (f/m 22/14; age 58+/-8.

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Aims: Platelet activation is known to be associated with arrhythmic effects in myocardial ischaemia. The present study attempts to clarify whether diabetic cardiovascular autonomic neuropathy (CAN) is associated with intravascular platelet activation.

Methods: Platelet activation was assessed by flow cytometry analysis in 30 patients with Type 1 diabetes mellitus screened for diabetic complications.

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There is much evidence that diabetes and hyperglycaemia contribute to the impairment of endothelial function and induce severe changes in the proliferation, the adhesive and synthetic properties of endothelial cells. Induction of apoptosis could represent one mechanism to prevent the new accumulation of those vascular defects and to allow generation of vascular endothelium. In this study, we demonstrate that high concentrations of glucose or proinsulin induce apoptosis in human umbilical endothelial cells by three independent methods (DNA fragmentation, fluorescence activated cell sorting analysis, and morphology).

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