Hyperglycemia-Induced Platelet Activation in Type 2 Diabetes Is Resistant to Aspirin but Not to a Nitric Oxide–Donating Agent
| العنوان: | Hyperglycemia-Induced Platelet Activation in Type 2 Diabetes Is Resistant to Aspirin but Not to a Nitric Oxide–Donating Agent |
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| المؤلفون: | Stefania Momi, Paolo Gresele, Paola Lucidi, Geremia B. Bolli, Stefania Marzotti, Silvia Giannini, Pietro Minuz, Giuseppe Guglielmini |
| المصدر: | Diabetes Care |
| بيانات النشر: | American Diabetes Association, 2010. |
| سنة النشر: | 2010 |
| مصطلحات موضوعية: | Adult, Male, medicine.medical_specialty, Adolescent, Platelet Aggregation, type 2 diabetes mellitus, platelets, nitric oxide, Emerging Treatments and Technologies, Endocrinology, Diabetes and Metabolism, Type 2 diabetes, Nitric oxide, Young Adult, chemistry.chemical_compound, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Humans, Nitric Oxide Donors, Platelet, Antipyretic, Platelet activation, Original Research, Aged, Advanced and Specialized Nursing, Aspirin, business.industry, Middle Aged, Flow Cytometry, Platelet Activation, medicine.disease, Endocrinology, chemistry, Hyperglycemia, Platelet aggregation inhibitor, Female, business, Platelet Aggregation Inhibitors, medicine.drug |
| الوصف: | OBJECTIVE Acute, short-term hyperglycemia enhances high shear stress–induced platelet activation in type 2 diabetes. Several observations suggest that platelets in type 2 diabetes are resistant to inhibition by aspirin. Our aim was to assess comparatively the effect of aspirin, a nitric oxide–donating agent (NCX 4016), their combination, or placebo on platelet activation induced by acute hyperglycemia in type 2 diabetes. RESEARCH DESIGN AND METHODS In a double-blind, placebo-controlled, randomized trial, 40 type 2 diabetic patients were allocated to 100 mg aspirin once daily, 800 mg NCX 4016 b.i.d., both of them, or placebo for 15 days. On day 15, 1 h after the morning dose, a 4-h hyperglycemic clamp (plasma glucose 13.9 mmol/l) was performed, and blood samples were collected before and immediately after it for platelet activation and cyclooxygenase-1 (COX-1) inhibition studies. RESULTS Acute hyperglycemia enhanced shear stress–induced platelet activation in placebo-treated patients (basal closure time 63 ± 7.1 s, after hyperglycemia 49.5 ± 1.4 s, −13.5 ± 6.3 s, P < 0.048). Pretreatment with aspirin, despite full inhibition of platelet COX-1, did not prevent it (−12.7 ± 6.9 s, NS vs. placebo). On the contrary, pretreatment with the NO donor NCX 4016, alone or in combination with aspirin, suppressed platelet activation induced by acute hyperglycemia (NCX 4016 +10.5 ± 8.3 s; NCX 4016 plus aspirin: +12.0 ± 10.7 s, P < 0.05 vs. placebo for both). Other parameters of shear stress–dependent platelet activation were also more inhibited by NCX 4016 than by aspirin, despite lesser inhibition of COX-1. CONCLUSIONS Acute hyperglycemia-induced enhancement of platelet activation is resistant to aspirin; a NO-donating agent suppresses it. Therapeutic approaches aiming at a wider platelet inhibitory action than that exerted by aspirin may prove useful in patients with type 2 diabetes. |
| تدمد: | 1935-5548 0149-5992 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::57e07b2d031d8964b164c6c984c6367bTest https://doi.org/10.2337/dc09-2013Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....57e07b2d031d8964b164c6c984c6367b |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 19355548 01495992 |
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