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Tumor necrosis factor-&agr; 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-&agr; and interleukin-1&bgr;, are known to depress myocardial function. We hypothesized that tumor necrosis factor-&agr; and interleukin-1&bgr;, 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-&agr;, interleukin-1&bgr;, 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-&agr; 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-&agr; and left ventricular systolic change in pressure over time (r = −.54, p < .001). Interleukin-1&bgr; 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. Conclusion:Tumor necrosis factor-&agr; increases during the early postresuscitation period and may play a role in postresuscitation myocardial dysfunction.