Attenuation of reperfusion-induced lipoperoxidation by systemic use of oxygen radical scavengers after pedicle occlusion.
Oxygen free radicals are implicated to cause tissue injury during ischemia and reperfusion and may play a central role in the no-reflow phenomena. Modulation of these substances has been suggested as a means of decreasing the amount of tissue loss due to ischemia and subsequent reperfusion. Pretreatment of tissues with a variety of agents has been reported to minimize the production of oxygen radicals and augment tissue survival after an ischemic insult. Ischemic clinical situations, however, usually present unexpectedly and thus pretreatment is not feasible. Our study evaluated the activity and effect of free radical scavengers delivered systemically during the ischemic interval to an ischemia/reperfusion rat intestinal model. Superoxide dismutase and dimethylthiourea were given systemically after occlusion and reperfusion to simulate a clinical sequence of a failing flap, that is, the vascular compromise, the diagnosis, and the successful resolution of the vascular embarrassment. Measurements of malonyldialdehyde (MDA), the end product of lipoperoxidation of cell walls, were compared with controls. Tissue histology was assessed and correlated with the use of these agents. A third group of rats was systemically alkalinized to attempt to shift the Bohr curve and decrease free oxygen substrate in the ischemic tissues on reperfusion. Rats treated with superoxide dismutase and dimethylthiourea showed significant reductions of MDA compared with nontreated rats (p less than 0.05), indicating attenuation of reperfusion lipoperoxidation. Systemic alkalinization of the rats did not significantly change the levels of MDA. Tissue histology showed severe injury in all ischemic groups regardless of the level of MDA.(ABSTRACT TRUNCATED AT 250 WORDS)