Two main mechanisms have been explored in an attempt to explain injury to the cells of tissues due to freezing in vivo. The first is direct cellular injury caused by injurious osmotic changes and ice crystal formation that happens as a result of freezing (Mazur, 1984). The second is host response injury caused by the vascular damage and immunologic response in response to freezing (Gage and Baust, 1998). The amount of injury caused by freezing appears to vary with tissue type and thermal history of the freezing protocol. The hypothesis of this study was that host response injury, specifically vascular injury, causes the majority of tissue necrosis at the edge of a frozen region and therefore determines the size of the lesion seen after in vivo freezing. Many investigations have previously made a qualitative correlation between thermal history, vascular injury, and tissue necrosis (e.g. Greene. 1943 and Rabb et al., 1974). We chose the dorsal skin flap chamber (DSFC) implanted in the Copenhagen rat as the cryosurgical model for this study. This in vivo freezing model appears insensitive to the immunologic phenomenon (Hoffmann et al., 1999) and allows us to monitor thermal history and investigate both vascular and tissue injury in response to cryosurgery.

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