Abstract 17352: Effects of Inhibition of p38 Mitogen-Activated Protein Kinase on Post-Resuscitation Myocardial Function in a Rat Model of Cardiopulmonary Resuscitation

    loading  Checking for direct PDF access through Ovid

Abstract

Introduction: The p38 mitogen-activated protein kinase (MAPK) is an intracellular kinase in the cardiovascular system. Activation of p38 MAPK contributes to endothelial dysfunction, increases infarct size, and contributes to cardiac dilatation and heart failure. In the present study, we investigate the effects of inhibition of p38 MAPK on post-resuscitation myocardial function.

Hypothesis: Inhibition of p38 mitogen-activated protein kinase reduces the severity of post-resuscitation myocardial dysfunction in a rat model of cardiopulmonary resuscitation.

Methods: Sixteen male Sprague-Dawley rats weighing between 450-550g were randomized into 2 groups: 1) placebo group; 2) p38 mitogen-activated protein kinase inhibitor group. Ventricular fibrillation (VF) was electrically induced. CPR was initiated after 6 min of untreated VF and continued for 8 min. Defibrillation was then attempted. Mean Arterial Pressure (MAP), Ejection Fraction (EF), Cardiac Output (CO) and myocardial performance index (MPI) were measured at baseline and at hourly intervals for 6 hrs after resuscitation.

Results: p38 mitogen-activated protein kinase inhibitor significantly reduced the severity of post-resuscitation myocardial dysfunction. MAP, EF, CO and MPI in the p38 mitogen-activated protein kinase inhibitor treated animals were significantly better than the placebo group at PR 6hrs (Table 1).

Conclusion: The administration of a p38 mitogen-activated protein kinase inhibitor reduced the severity of post-resuscitation myocardial dysfunction in a rat model of cardiopulmonary resuscitation.

Table 1. EF=ejection fraction; CO=cardiac output; MPI=myocardial performance index.

Values are presented as mean ± SD

*p < 0.05 versus placebo

Related Topics

    loading  Loading Related Articles