Proceedings of The Physiological Society

University of Oxford (2011) Proc Physiol Soc 23, PC136

Poster Communications

Effects of exercise training in intraplatelet L-arginine-NO pathway and platelet aggregation in rats with myocardial infarction

C. Matsuura1,2, A. Mendes Ribeiro1,3, W. M. Vianna1, I. K. Mendes1, R. Louzada4, J. P. Werneck-de-Castro4, T. M. Brunini1

1. Departmento de Farmacologia, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil. 2. Escola de Educa


  • Platelet aggregation, L-arginine transport and nitric oxide synthase (NOS) activity<\#13>

Introduction: Myocardial infarction (MI) is one of the major causes of heart failure and is associated with endothelium dysfunction and alterations in platelet activity in humans1. Nitric oxide (NO) is a potent vasodilator that also inhibits platelet activation and aggregation2. The purpose of this study was to assess the effect of exercise training on platelet aggregation and the L-arginine-NO pathway in an experimental model of MI. Methods: 40 male Wistar rats (200-250 g) underwent anterior descending coronary artery ligation or sham surgery, previously anesthetized with tribromoethanol injected intraperitoneally (300mg/kg), resulting in four groups (n=10, each): MI/sedentary (MISed), MI/exercise (MIEx), Sham/sedentary (SSed), and Sham/exercise (SEx). The experimental procedures were approved by the Institutional Animal Care and Use Committee (CEA/051/2009) and were conducted in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals. After 8 weeks with 30 min of daily treadmill training (60% of maximum velocity), the animals were anesthetized with sodium thiopental (40 mg.kg-1, intraperitoneally) and the platelets were isolated from centrifugation of the blood collected from the abdominal aorta. Platelet L-arginine transport was assessed by incubation with L-[3H]-arginine (100 µM), and NOS activity, by the conversion of L-[3H]-arginine into L-[3H]-citrulline. Platelet aggregation induced by ADP (20 µM) was measured in whole blood by electrical impedance (560CA, Chronolog Corporation, PA, USA). Data were compared with a one-way ANOVA, and significance level was set at 5%. Results: Exercise tolerance significantly improved (P < 0.05) in both MIEx and SEx after long-term physical training, as expected. However, no significant differences among the groups were noted in platelet aggregation, platelet L-arginine transport and NOS activity (Table 1). Table 1. Platelet aggregation and L-arginine transport and nitric oxide synthase (NOS) activity. Conclusion: Platelet function and the L-arginine-NO pathway were not affected by either MI or exercise training. It is plausible to assume that the experimental model of MI used in this study does not mimic the vascular alterations observed in human MI.

Where applicable, experiments conform with Society ethical requirements