Rabbit ears were frozen to ‐10°C and thawed in vivo , uniform freezing being secured by vascular occlusion during the freezing procedure. Following thawing and re‐establishment of blood flow the ears showed circulatory changes. Hyperemia, edema formation and stasis with subsequent recovery were observed. Studies were performed to test the functional qualities of the small blood vessels of the affected area. The vascular endothelium, the smooth muscles and the sympathetic vasoconstrictor nerve fibres were examined. The endothelial regenerative power appeared unaltered as revealed by the in growth of new capillaries into transparent ear chambers inserted in the injured ears. Intradermal injections of histamine and bradykinin caused a local increase in the exudation of Evan's blue from the frostbitten blood vessels whereas intradermally injected acetylcholine did not. Stimulation of vasoconstrictor nerve fibres or intravascular injections of adrenaline produced vasoconstriction measured as a decrease in blood flow through the previously frozen ear. It is concluded that the blood vessel walls have retained their functional qualities and that the observed circulatory changes can be induced by endogenous substances liberated or activated consequent to injury.
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Ola B. Reite (1965) studied this question.
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