Experimental Hemorrhage and Blunt Trauma Do Not Increase Circulating Tumor Necrosis Factor

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Abstract
Tumor necrosis factor (TNF) is a potent cytokine mediator of the shock states associated with sepsis and burn injury. This experimental study was done to determine whether circulating TNF plays a major role in the vasomotor collapse seen following experimental hemorrhage and blunt injury. Twenty anesthetized pigs were divided into two groups. Ten animals were bled 60% of their calculated blood volume in 15 minutes. Animals in Group IA (n = 5) had no treatment, and Group IB animals (n = 5) were given twice the shed volume as crystalloid 30 minutes after hemorrhage. The other animals, groups IIa and IIb (n = 5 each), were first subjected to a blunt injury to the thigh sufficient to cause a midshaft femur fracture, then bled and similarly treated. In both groups, mean arterial pressure (MAP), cardiac output (CO), and serum TNF activity by L929 bioassay were measured at 15-minute intervals for 120 minutes after hemorrhage or hemorrhage and blunt injury. An additional three animals were infused with 4 × 108/kg heat-killedE. colito validate the TNF assay. All bled animals sustained a fall in MAP and CO to a mean of 33% of baseline values, with or without fracture. Group IB and IIB animals responded to fluid resuscitation by restoration of MAP and CO to 85%-97% of the baseline values. Tumor necrosis factor was not detectable before injury and remained undetectable in all these animals during the 120 minutes of the experiment despite hemorrhage alone or combined hemorrhage and blunt trauma, with or without fluid resuscitation. The test animals receiving theE. coliresponded with markedly elevated TNF levels, which peaked at 90 minutes after injection. We conclude that hemorrhage alone causes no detectable elevation in serum TNF levels, and the combination of blunt injury and hemorrhage is also without effect on circulating TNF levels during the experimental period. Tumor necrosis factor presumably plays no role in the pathogenesis of shock in this model. This negative finding should help direct future studies and potential pharmacologic manipulation of traumatic shock.

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