Cardiac Arrest Induces Lung Inflammation 3 days after Cardiac Arrest in Domestic Pigs

Introduction: Cardiac arrest, a leading cause of death in the United States, is associated with detrimental damages, which includes the lungs. Reperfusion of ischemic tissue following cardiac arrest leads to systemic inflammation inflicted by free radical production. Pyruvate , a cellular metabolite and an antioxidant, has a demonstrated protective anti-oxidative effect on the heart through enhancement of the natural anti-oxidative glutathione system. Purpose: Using Myeloperoxidase activity as a marker for neutrophilic inflammation, we sought to quantify the extent of the inflammation in lung tissue, and to determine pyruvate’s protective effect against ischemia/reperfusion injury in the lung. Methods: Fourteen juvenile male Yorkshire swine were divided into three groups, a sham group(n=3) which underwent no cardiac arrest or CPR protocol, a CPR group(n=5) which received an intravenous infusion of sodium chloride solution, and a CPR + Pyruvate group which instead received an infusion of pyruvate solution(n=6). The CPR groups were placed in cardiac arrest via ventricular fibrillation for six minutes, followed by four minutes of cardiopulmonary compression and subsequent defibrillating counter shocks. The respective infusions were delivered at a rate of 0.1 mmol/kg/min throughout CPR and for 60 minutes following cardioversion. After three days, left lung samples were collected and assayed for protein content and myeloperoxidase activity. Results: Three days following the procedure, Myeloperoxidase (MPO) activity was elevated in animals subjected to cardiac arrest compared to sham, although the result was not statistically significant (P=0.15). Pyruvate did not dampen MPO activity in the left lung.