HISTOLOGICAL EVIDENCE FOR CELLULAR ADAPTATION TO NON-FREEZING COLD INJURY

Abstract

The development and the healing of non-freezing cold injury in ears of rats maintained at 6[degree]C for 118 days and followed at different times of exposure revealed histological changes of a different nature at 4-6 mm away from the edge of the ear from the changes at 1-3 mm. In the first 3 mm during the first 21 days of exposure there was a continuous drop in the number of prophases and telophases and a parallel increase in the number of blocked and degenerating metaphases. In the second week, inflammatory reactions appeared; in the third week, the edema and lymphocyte infiltration was quite severe, and at that time 10% of the epithelium was degenerating. At the end of the fourth week, in the non-necrotic part of the epidermis, the number of prophases and telophases had returned to the initial level and the number of blocked metaphases was back to normal. After 56 to 118 days, no signs of edema, necrosis, or blocked metaphases could be found. In summary, the cold injury developed in the first 3 or 4 weeks and healed in the following month. After 2 months, cold temperature had no damaging effect on the epidermal tissue. At 4-6 mm from the edge of the ear, no cold injury developed, but in the first week there was a slight degree of mitotic blocking which disappeared during the second week. Essentially the same picture was observed at the 1-3 mm location in the ears of rats kept at 15[degree] C. On the assumption that mitotic blocking is due to a disturbance of the ionic transfer through the cellular membrane, it is suggested that the primary cause of cold injury is a direct thermal damage to the membrane.