Pyrrolidine dithiocarbamate as an effector and trigger in ischemia-reperfusion injury in adipocutaneous flaps in rats.

Immune and inflammatory responses and the regulation of cellular events seem to be major factors in ischemia-reperfusion (I/R) injury. The inhibition of nuclear transcription factor κB (NF-κB) by pyrrolidine dithiocarbamate (PDTC) shows beneficial effects in animal models in various diseases and tissues with respect to I/R injury. If these results from other tissues could be transferred to adipocutaneous flaps in rats, a new approach to pharmacologic preconditioning could be defined for tissue transfer, and PDTC could be a solution as a trigger and effector to ameliorate the aftermath of the I/R injury. Fifty-six male WISTAR rats were divided into four experimental groups. An epigastric adipocutaneous flap was raised, and the average flap necrosis was assessed for all groups on the fifth postoperative day using planimetric software. The control group had a significantly lower flap necrosis than the ischemic control group (p < .05). The PDTC nonischemic group had a significantly lower flap necrosis than the ischemic control group (p  =  .005). The ischemic PDTC group had a 10% reduction in flap necrosis that was not significant. Our data show that a significant reduction in flap necrosis can be achieved by intravenous application of PDTC.