Tumor necrosis factor-alpha is associated with early postresuscitation myocardial dysfunction.
OBJECTIVE
Left ventricular dysfunction after successful cardiopulmonary resuscitation contributes to early death following resuscitation. The stress-induced proinflammatory cytokines, particularly tumor necrosis factor-alpha and interleukin-1beta, are known to depress myocardial function. We hypothesized that tumor necrosis factor-alpha and interleukin-1beta, synthesized and released in response to the stress of global ischemia accompanying cardiac arrest, play a role in development of postresuscitation left ventricular dysfunction.


METHODS
Hemodynamic variables, tumor necrosis factor-alpha , interleukin-1beta, interleukin-6 (enzyme-linked immunosorbent assay method), and ionized calcium were measured in ten anesthetized swine before and after 7 mins of cardiac arrest and during the early postresuscitation period (60-90 mins).


RESULTS
Tumor necrosis factor-alpha increased three-fold within 15 mins of restoration of circulation and remained elevated throughout the observation period. A significant negative correlation was observed between tumor necrosis factor-alpha and left ventricular systolic change in pressure over time (r = -.54, p <.001). Interleukin-1beta was undetectable before and after resuscitation, and interleukin-6 was detectable in only two animals after resuscitation. Although a significant decline in ionized calcium was observed and correlated with left ventricular systolic change in pressure over time, an independent role for ionized calcium in postresuscitation left ventricular dysfunction was not demonstrated.


CONCLUSIONS
Tumor necrosis factor-alpha increases during the early postresuscitation period and may play a role in postresuscitation myocardial dysfunction.
Department of Emergency Medicine, Research and Education Institute at Harbor-UCLA Medical Center, 1000 West Carson Street, Torrance, CA 90509, USA. jniemann@emedharbor.edu
James T
JT
Niemann
Daniel
D
Garner
Roger J
RJ
Lewis
D000818:Animals; D002118:Calcium / Q000378:metabolism; D016887:Cardiopulmonary Resuscitation / Q000009:adverse effects*; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D006439:Hemodynamics / Q000276:immunology; D007511:Ischemia / Q000276:immunology / Q000378:metabolism; D008297:Male; D034421:Sus scrofa; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D018487:Ventricular Dysfunction, Left / Q000276:immunology* / Q000378:metabolism* / Q000503:physiopathology
D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha; D002118:Calcium