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Cardiac Function and the Proinflammatory Cytokine Response After Recovery From Cardiac Arrest in Swine

2009; Mary Ann Liebert, Inc.; Volume: 29; Issue: 11 Linguagem: Inglês

10.1089/jir.2009.0035

1557-7465

James T. Niemann, John P. Rosborough, Scott T. Youngquist, Atman P. Shah, Roger J. Lewis, Quynh T. Phan, Scott G. Filler,

Cardiac Ischemia and Reperfusion

Increased levels of cytokines have been reported after resuscitation from cardiac arrest. We hypothesized that proinflammatory cytokines, released in response to ischemia/reperfusion, increase following resuscitation and play a role in post–cardiac arrest myocardial dysfunction. Ventricular fibrillation (VF) was induced by coronary occlusion in 20 swine. After 7 min of VF, resuscitation was performed as per guidelines. Plasma levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 were measured 15 min after the start of resuscitation in all animals and at intervals of 6 h in resuscitated animals. Intravascular pressures and cardiac output (CO) were also recorded. TNF-α abruptly increased after resuscitation, peaking at 15 min following return of spontaneous circulation, and declined to baseline levels after 3 h. IL-1β increased more slowly, reaching a maximum 2 h after reperfusion. IL-6 concentrations were not significantly different from control values at any time point. Males demonstrated greater elevations of TNF-α and IL-1β than females. Stroke work was significantly depressed at all time points with a nadir at 15–30 min after reperfusion, corresponding to the peak TNF-α values. The anti-TNF-α antibody infliximab attenuated the decrease in myocardial function observed 30 min after reperfusion. TNF-α increases during recovery from cardiac arrest are associated with depression of left ventricle (LV) function. The effect of TNF-α can be attenuated by anti-TNF-α antibodies.