Acute alterations in muscle flap microcirculation during tumor necrosis factor alpha-induced inflammation

In reconstructive microsurgery of free tissue transfer, ischemia-reperfusion (IR) injury is an unavoidable component of the procedure, which can affect free flap survival markedly. A notable amount of evidence implicates neutrophils in IR injury. Transforming necrosis factor alpha (TNF-alpha) is known to have a central role as a mediator of neutrophil activation in IR injury. The effect of inflammatory stimuli, TNF-alpha, on flow hemodynamics and leukocyte-endothelial interactions in the muscle flaps submitted to IR injury was investigated. In group 1, 6 rats were administered 1 ml of vehicle solution. In group II rats (N = 6), 1 ml of recombinant human TNF-alpha (10 ng per milliliter) was injected intra-arterially. After an hour of ischemia, the cremaster muscle flaps were monitored at 1-hour intervals during 6 hours of reperfusion. After clamp removal, the number of rolling, adhering, and transmigrating leukocytes in the TNF-alpha group was increased by 4-fold, 3-fold, and 3.5-fold respectively compared with the control group (p < 0.05). The increase in rolling leukocytes continued for as long as 3 more hours, whereas the number of adhering and transmigrating leukocytes remained high throughout the experiment. A significant increase in the diameters of the third- and fourth-order arterioles in the TNF-a group was accompanied by a decrease in the number of flowing capillaries at all intervals (p < 0.05). The effect of TNF-alpha-induced inflammation on leukocyte activation was found to be maximal during the first 3 hours of reperfusion. The vasodilatory effect of TNF-alpha was observed only on the third- and fourth-order arterioles.