DEHYDROEPIANDROSTERONE PROTECTS MUSCLE FLAP MICROCIRCULATORY HEMODYNAMICS FROM ISCHEMIA REPERFUSION INJURY - AN EXPERIMENTAL IN-VIVO STUDY/

This study evaluated the potential for dehydroepiandrosterone (DHEA) t o protect skeletal muscle from reperfusion injury using intravital mic roscopic observations of isolated rat cremaster muscle flaps. The flap s were subjected to warm ischemia followed by reperfusion in three gro ups of rats. In group 1 (control, n = 14), muscle flaps were subjected to 6 hours of ischemia and then evaluated after either 90 minutes (n = 8) or 24 hours (n = 6) of reperfusion, Group 2 animals (propylene gl ycol pretreatment, n 8) were pretreated with a propylene glycol vehicl e, then underwent 6 hours of ischemia and were evaluated after 90 minu tes reperfusion, Group 3 animals (DHEA pretreatment, n = 12) were pret reated with DHEA dissolved in propylene glycol, subjected to 6 hours o f ischemia, and then evaluated after either 90 minutes (n = 6) or 24 h ours (n = 6) of reperfusion. Red blood cell velocity in the flap's mai n arteriole, functional capillary density, venular constriction index (the ratio of internal to external diameter of postcapillary venules), and micro emboli formation were measured, Muscle samples were evaluat ed by electron microscopy. Control animals showed a 61% reduction in r ed blood cell velocity (p < 0.05) accompanied by a 69% reduction in fu nctional capillary density (p < .05) acutely and total cessation of fl ow by 24 hours, No differences between control and propylene glycol tr eated animals were noted, In DHEA-pretreated animals, reflow occurred in 100% of the flaps, there was a temporary 39% reduction (p < 0.05) i n functional capillary density, and all flaps remained viable at 24 ho urs. In this study, DHEA pretreatment markedly improved muscle flap mi crocirculatory hemodynamics and protected flaps against ischemia/reper fusion injury.