Role of hypoxia on platelet function in patients with chronic obstructive pulmonary disease

Aim: Objective of our study is to establish the presence of platelet hyperactivity in hypoxemic patients with COPD.
Methods: Platelet hyperactivity in patients with COPD as compared to age and sex matched controls was determined by following experiments. Thrombin was used on washed human platelets suspension and ADP on platelet rich plasma to show that there was raised light transmittance in the presence of platelet activation. Free intracellular calcium was measured in a fluorescence spectrophotometer after pre-treatment with calcium chloride. Analysis of leukocyte contamination eliminated the role of leukocyte mediated inflammatory processes in platelet activation. The study was approved by the Institutional Ethics Committee and due informed consent was obtained from participants in the study.
Results: 22 hypoxemic patients were selected for the study based on their diagnosis of COPD (from history and spirometry) along with age and sex matched controls. Presence of comorbidities and other factors that cause platelet activation were excluded. Level of platelet aggregation was determined by several experiments. By an aggregometer using platelet agonists (thrombin and ADP) it was found that platelet aggregation was significantly higher in hypoxemic COPD patients than normal healthy controls. Fluorescence spectrophotometer was used to measure intracellular calcium as a marker of platelet activation and it was found that hypoxemic COPD patients had significantly higher platelet aggregation than normal healthy controls. However no significant difference was found in other markers of platelet activation studied namely P-selectin exposure and PAC-1 binding between the two groups.
Conclusion: There is increased platelet aggregation in hypoxemic COPD patients as determined by platelet agonist studies and increased intracellular calcium. Possible role of intracellular calcium as marker of thrombotic risk. In conclusion hypoxemia due to COPD has a direct atherothrombotic effect independent of other prothrombotic factors.