Baker, Charla L.
Nquyen, Anh Q.
Cherry, Brandon H.
Olivencia-Yurvati, Albert H.
Mallet, Robert T.


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Ischemia-reperfusion injury sustained following cardiac arrest initiates an injury cascade that leads to inflammatory changes in multiple organs. The inflammatory response is characterized by an increase in cytokines and infiltrative neutrophils. In a study focused on the myocardial and systemic effects of an induced hemorrhagic shock in goats, pyruvate administration blunted inflammation in cardiac tissue. Further, pyruvate-fortified Ringer’s has been shown to suppress inflammation during reperfusion by decreasing the amount of reactive oxygen species and improving the glucose metabolism, providing multi-organ protection. These findings suggest a pyruvate-fortified resuscitation fluid infusion following cardiac arrest may attenuate the inflammatory response to ischemia-reperfusion. Of particular interest, pulmonary tissue has been shown to be affected by ischemia-reperfusion. Therefore, we hypothesized that intravenous administration of pyruvate during cardiac arrest and early recovery would exert anti-inflammatory effects to protect the lungs from ischemia-reperfusion injury. To test this hypothesis, Yorkshire swine were subjected to cardiac arrest and infused with either NaCl (n=3) or Na-pyruvate (n=3) during cardiopulmonary resuscitation (CPR). Lung biopsies collected after 4 hours recovery were embedded in paraffin, sectioned, and stained for haematoxylin and eosin (H&E), and compared to biopsies from sham (non-arrest; n=3) animals using brightfield microscopy. Sections were examined for the histological marker of acute lung injury—i.e., neutrophils in the alveolar or interstitial space. The CPR NaCl showed appreciable neutrophil infiltration in the alveoli in contrast to the CPR Na-pyruvate. These early results suggest that the Na-pyruvate may suppress pulmonary inflammation following cardiac arrest. Purpose (a): To identify a new pharmacological strategy to protect the lungs from ischemia-reperfusion injury due to cardiac arrest. Methods (b): Yorkshire swine (30-40 kg) were subjected to cardiac arrest-resuscitation or non-arrest sham protocols. Ventricular fibrillation was induced by a train of electric impulses transmitted to the right ventricle via a pacing wire. Precordial compressions (100/min) were given from 6-10 min arrest, and then sinus rhythm was restored with defibrillatory transthoracic countershocks. NaCl or Na-pyruvate was infused iv at 0.1 mmol/kg/min during chest compressions and the first 60 min post-defibrillation. After 4 h recovery, lung tissue was excised, fixed in 4% paraformaldehyde and embedded in paraffin wax. Sections were cut and stained with H&E. Twenty random high power fields independently were scored in a blinded fashion. Scoring: No neutrophils in the alveolar space= 0; 1-5 neutrophils= 1; >5 neutrophils= 2. Interstitial neutrophils were counted, averaged, and compared among the three experimental groups. Results (c): H&E staining showed no statistically significant difference of interstitial (P=0.49) and alveolar (P=0.65) neutrophil infiltrate among the sham, CPR and CPR + Pyruvate. Conclusions (d): There was no statically significant difference in pulmonary neutrophil infiltration at 4 hour post cardiac arrest and resuscitation in CPR and pyruvate treated CPR compared to sham. Further analysis of longer post-arrest recoveries are necessary to better understand the anti-inflammatory effect of pyruvate in lung tissue in this experiment model.