Dehydroepiandrosterone protects muscle flap microcirculatory hemodynamics from ischemia/reperfusion injury: an experimental in vivo study.

Abstract

This study evaluated the potential for dehydroepiandrosterone (DHEA) to protect skeletal muscle from reperfusion injury using intravital microscopic observations of isolated rat cremaster muscle flaps. The flaps were subjected to warm ischemia followed by reperfusion in three groups 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 glycol pretreatment, n = 8) were pretreated with a propylene glycol vehicle, then underwent 6 hours of ischemia and were evaluated after 90 minutes reperfusion. Group 3 animals (DHEA pretreatment, n = 12) were pretreated with DHEA dissolved in propylene glycol, subjected to 6 hours of ischemia, and then evaluated after either 90 minutes (n = 6) or 24 hours (n = 6) of reperfusion. Red blood cell velocity in the flap's main arteriole, functional capillary density, venular constriction index (the ratio of internal to external diameter of postcapillary venules), and microemboli formation were measured. Muscle samples were evaluated by electron microscopy. Control animals showed a 61% reduction in red blood cell velocity (p < 0.05) accompanied by a 69% reduction in functional capillary density (p < .05) acutely and total cessation of flow by 24 hours. No differences between control and propylene glycol treated animals were noted. In DHEA-pretreated animals, reflow occurred in 100% of the flaps, there was a temporary 39% reduction (p < 0.05) in functional capillary density, and all flaps remained viable at 24 hours. In this study, DHEA pretreatment markedly improved muscle flap microcirculatory hemodynamics and protected flaps against ischemia/reperfusion injury.