Abstract
Introduction. During reperfusion after ischemic arrest, endothelial dysfunction and inhibition of nitric oxide synthase (NOS) are observed, due to increased oxidative stress, with subsequent decrease in NO bioavailability. This plays important effects in tissue perfusion regulation and function, i.e. postresuscitation myocardial dysfunction. Asymmetric dimethylarginine (ADMA) is an endogenous competitive inhibitor of NOS and thereby modulates NO production. We therefore hypothesized that plasmatic ADMA level would be altered following resuscitation from cardiac arrest. Methods. Ventricular fibrillation was induced in 17 rats and was untreated for 6 min. CPR, including mechanical chest compression, ventilation, and epinephrine, was then initiated and continued for additional 6 min prior to defibrillations. Two hrs (n=6), 4 hrs (n=6) and 72 hrs (n=6) following resuscitation, left ventricle ejection fraction (LVEF) was echocardiographically assessed. Animals were then sacrificed, plasma collected and ADMA levels were measured using an enzyme-linked immunosorbent assay method. Additional 5 rats were not subjected to cardiac arrest and served as controls. Results. Severe postresuscitation myocardial dysfunction, represented by depressed LVEF, was observed at 2 and 4 hr postresuscitation (p<0.01, Table). However, LVEF recovered 72 hr after resuscitation. Similarly to myocardial dysfunction, plasmatic ADMA significantly decreased following resuscitation, while its level was restored 72 hr later. However, ADMA reductions were significantly evident only 4 hr after resuscitation (p<0.05, Fig) and therefore occurred slower than LVEF impairment. Conclusions. Plasmatic ADMA levels were temporary altered following resuscitation, similarly to postresuscitation myocardial dysfunction. Decreases in plasmatic ADMA may reflect adaptative changes aimed to enhance NO release and thereby preservation of myocardium endothelial function.
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