Characterizing the Potential for Neutrophils to Mediate the Inflammation Response Associated with Cardiac Arrest and Resuscitation

Abstract

Post-Resuscitation Injury (PRI) may contribute to poor recovery after cardiac arrest and resuscitation, and this complication may be due to a dramatic inflammatory response suspected to occur in the early hours following successful resuscitation. The purpose of this study was to evaluate whether blood neutrophils, a known source of oxidants under other acute inflammatory conditions, mediate an inflammatory response soon after resuscitation. Using a laboratory model of cardiac arrest and resuscitation (A/R), adult Sprague Dawley rats were anesthetized and subjected to a cardiac arrest and resuscitation protocol. During the experiments, blood samples were taken at specific time points to monitor blood glucose and mean arterial blood pressure. Sham experiments were performed as a control. Tissues from animals receiving no surgical procedures were also obtained as a further control. After two hours of resuscitation, heart, lung, liver, and brain tissues were collected and quick-frozen. Later, samples were thawed, homogenized, and analyzed for neutrophilspecific myeloperoxidase (MPO) accumulation using the Hycult Biotech ELISA kit. MPO accumulation is used as an indicator of neutrophil sequestration in the organ. We found a marked increase in tissue MPO in the lung, indicative of neutrophil accumulation. There was a statistically significant difference (t-Test) between sham vs. resuscitation groups for both hepatic and cardiac tissues. These findings indicate that neutrophils do sequester in the heart and liver in the early hours following successful resuscitation. Because of their potential for oxidative injury, neutrophils likely contribute to the inflammatory response and cardiac stunning observed in the early hours of resuscitation. Efforts to limit neutrophil-mediated microvascular and oxidative injury may reduce PRI and improve recovery.