Background: The role of mitochondrial dysfunction has not been thoroughly clarified in the pathogenesis of critically ill patients. The objective of this study was to investigate mitochondrial membrane potential (ΔΨm) and apoptosis in circulating platelets in patients with systemic inflammatory response syndrome (SIRS).
Methods: This prospective observational study was conducted from May 2011 to February 2012. Criteria for inclusion were adult patients with SIRS. We used mitochondrial indicator JC-1 in conjunction with flow cytometry to measure ΔΨm and annexin V to evaluate apoptosis in peripheral blood platelets. ΔΨm was expressed as the percentage of platelets with altered ΔΨm. Severity of illness was assessed by SIRS score, Acute Physiology and Chronic Health Evaluation II score, and Sequential Organ Failure Assessment score.
Results: This study was composed of 36 patients who met the inclusion criteria and 12 healthy controls. Causes of SIRS were sepsis in 13, trauma in 13, and others in 10 patients. Platelet ΔΨm depolarization was significantly enhanced in patients with SIRS versus that in controls (median [interquartile range], 10.6% [8.1-12.6%] vs. 7.1% [6.1-8.0%]; p < 0.001). The percentage of apoptotic platelets was significantly higher in patients with SIRS than in controls (8.7% [5.5-13.5%] vs. 5.4% [3.9-7.0%]; p = 0.006). Interestingly, ΔΨm depolarization increased significantly with the increase in SIRS scores (p < 0.001). There was a significant correlation between ΔΨm depolarization and severity of illness, as indicated by Acute Physiology and Chronic Health Evaluation II score, Sequential Organ Failure Assessment score, and serum lactate levels (all, p < 0.05).
Conclusion: We demonstrated that ΔΨm depolarization and apoptosis were enhanced in circulating platelets in patients with SIRS. Our findings suggest that ΔΨm depolarization may be associated with the progression of SIRS.
Level of evidence: Diagnostic study, level III.