Search

Adam J BiaÅ‚as,1 Karolina Siewiera,2 Cezary WataÅ‚a,2 Anna Rybicka,3 BartÅ‚omiej Grobelski,3 Leon KoÅ›mider,4,5 Jolanta Kurek,6 Joanna MiÅ‚kowska-Dymanowska,1 Wojciech J Piotrowski,1 PaweÅ‚ Górski1 1Department of Pneumology and Allergy, Medical University of Lodz, Lodz, Poland; 2Department of Hemostasis and Hemostatic Disorders, Medical University of Lodz, Lodz, Poland; 3The animal house, Pharmaceutical Faculty, Medical University of Lodz, Lodz, Poland; 4Department of Pharmaceutics, School of Pharmacy, Virginia Commonwealth University, Richmond, VA, USA; 5Center for the Study of Tobacco Products, Virginia Commonwealth University, Richmond, VA, USA; 6Institute of Occupational Medicine and Environmental Health, Sosnowiec, Poland Background: COPD represents a major global health issue, which is often accompanied by cardiovascular diseases. A considerable body of evidence suggests that cardiovascular risk is elevated by the activation of blood platelets, which in turn is exacerbated by inflammation. As reactive oxygen species are believed to be an important factor in platelet metabolism and functioning, the aim of our study was to perform a complex assessment of mitochondrial function in platelets in chronic smoke exposed animals with COPD-like lung lesions. Materials and methods: Eight-week-old, male Dunkin Hartley guinea pigs (the study group) were exposed to the cigarette smoke from commercial unfiltered cigarettes (0.9 mg/cig of nicotine content) or to the air without cigarette smoke (control group), using the Candela Constructions® exposure system. The animals were exposed for 4 hours daily, 5 days a week, with 2×70 mL puff/minute, until signs of dyspnea were observed. The animals were bled, and isolated platelets were used to monitor blood platelet respiration. The mitochondrial respiratory parameters of the platelets were monitored in vitro based on continuous recording of oxygen consumption by high-resolution respirometry. Results: A