title: Cardiac function and the proinflammatory cytokine response after recovery from cardiac arrest in swine.
abstract: 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)-alpha, interleukin (IL)-1beta, 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-alpha abruptly increased after resuscitation, peaking at 15 min following return of spontaneous circulation, and declined to baseline levels after 3 h. IL-1beta 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-alpha and IL-1beta 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-alpha values. The anti-TNF-alpha antibody infliximab attenuated the decrease in myocardial function observed 30 min after reperfusion. TNF-alpha increases during recovery from cardiac arrest are associated with depression of left ventricle (LV) function. The effect of TNF-alpha can be attenuated by anti-TNF-alpha antibodies.
authors: The David Geffen School of Medicine at UCLA, University of California-Los Angeles, CA, USA. jniemann@emedharbor.edu
authors: James T
authors: JT
authors: Niemann
authors: John P
authors: JP
authors: Rosborough
authors: Scott
authors: S
authors: Youngquist
authors: Atman P
authors: AP
authors: Shah
authors: Roger J
authors: RJ
authors: Lewis
authors: Quynh T
authors: QT
authors: Phan
authors: Scott G
authors: SG
authors: Filler
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage; D000911:Antibodies, Monoclonal / Q000008:administration & dosage; D016207:Cytokines / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects / Q000276:immunology; D006323:Heart Arrest / Q000188:drug therapy / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism; D000069285:Infliximab; D008297:Male; D023421:Models, Animal; D015427:Reperfusion Injury / Q000188:drug therapy / Q000276:immunology*; D012151:Resuscitation; D012737:Sex Factors; D013552:Swine; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D016207:Cytokines; D018836:Inflammation Mediators; D000069285:Infliximab