ABSTRACT
BACKGROUND: Capillary flowmotion protects pedicled flaps during critical perfusion conditions. However, free tissue transfer, causing ischemia-reperfusion and surgical trauma, have been shown to blunt these protective blood flow fluctuations. Because heat shock priming protects tissue after transfer, we herein studied whether heat shock protein expression is capable to preserve critical perfusion-induced capillary flowmotion in transferred composite flaps. METHODS: In Sprague Dawley rats (n = 16), osteomyocutaneous flaps were subjected to critical perfusion after harvest and 1 h and 4 h after free transfer. In eight animals additional heat shock priming was induced 24 h before flap harvest. Microcirculation including capillary flowmotion was analyzed using intravital fluorescence microscopy. RESULTS: After harvest, critical perfusion induced capillary flowmotion in skeletal muscle tissue of all flaps. By this, functional capillary density (FCD), an indicator of nutritive perfusion, was maintained not only in muscle but also in periosteum, subcutis, and skin. In contrast, 1 h after flap transfer muscle capillary flowmotion was completely abrogated, resulting in a significant decrease of FCD in all tissues. Heat shock-priming completely restored capillary flowmotion, and, by this, maintained tissue FCD. CONCLUSIONS: The loss of muscle capillary flowmotion after free tissue transfer-associated ischemia-reperfusion can be prevented by heat shock-priming. This may represent the mechanism of protection by local heat application.
