Late Remote Ischemic Preconditioning in Rat Muscle and Adipocutaneous Flap Models

Abstract

In Brief The purpose of this study was to determine whether remote ischemic preconditioning can be induced by a late mechanism. The rat cremaster flap model was used for assessment of ischemia–reperfusion injury. In the control group (N = 9), 2 hours of flap ischemia was induced after preparation of the cremaster muscle. Ten minutes of ischemia of the contralateral hind limb was induced 24 hours before flap ischemia in the late remote ischemic preconditioning group (LRIP) (N = 8). In vivo microscopy was performed after 1 hour of flap reperfusion in each animal. The epigastric adipocutaneous flap model was used for the second part of the experiment. Three hours of flap ischemia was induced in the control group (N = 8). A similar late remote ischemic preconditioning protocol as in the LRIP group was used for the second late remote ischemic preconditioning group (N = 8). A significantly higher muscle red blood cell velocity in the capillaries, first-order arterioles, and venules, and a higher capillary flow as well as a decreased number of “stickers” were observed in the late remote ischemic preconditioning group compared with the first control group (p < 0.05). Average flap necrotic area was not significantly different within the second control group and the second late remote ischemic preconditioning group in the adipocutaneous flaps. These data show that late remote ischemic preconditioning attenuates ischemia–reperfusion injury in muscle flaps, whereas it is ineffective in adipocutaneous flaps. In rat cremaster and epigastric adipo-cutaneous flap models, a 10-minute ischemic period of the contralateral hindlimb 24 hours before a flap challenge of two to three hours of ischemia resulted in higher red cell velocity and decreased numbers of “stickers” in the muscle flaps. However, there was no difference in adipo-cutaneous flap surviving area.