Abstract
We previously showed that the progression of burn-induced injury was inhibited by exposing the peripheral area of injured skin to sublethal hyperthermia following the burn. We called this phenomenon post-heat shock tolerance. Here we suggest a mechanism for this phenomenon. Exposure of the peripheral primary hyperalgesic/allodynic area of burned skin to local hyperthermia (45°C, 30 seconds), which is a non-painful stimulus for normal skin, results in a painful sensation transmitted by nociceptors. This hyperthermia is too mild to induce any tissue injury, but it does result in pain due to burn-induced hyperalgesia/allodynia. This mild painful stimulus can result in the induction of descending anti-nociceptive mechanisms, especially in the adjacent burned area. Some of these inhibitory mechanisms, such as alterations of sympathetic outflow and the production of endogenous opioids, can modify peripheral tissue inflammation. This decrease in burn-induced inflammation can diminish the progression of burn injury.
Highlights
We previously showed that it was possible to inhibit the progression of burn-induced skin injury by exposing the peripheral area of injured skin to sublethal hyperthermia following the burn [1]
Second-degree burn injury was induced in mice, some of which had been injected with the opioid receptor blocker Naloxone 30 minutes prior to burn, and some of which were subjected to mild local hyperthermia (45°C, 1 and 3 minutes after burn)
Since there is hyperalgesia/allodynia in the peripheral zone of burn injury, it is likely that exposure of this area to local hyperthermia (45°C, 30 seconds), a non-painful stimulus for normal skin, results in a painful sensation transmitted by nociceptors (Figure 1)
Summary
We previously showed that it was possible to inhibit the progression of burn-induced skin injury by exposing the peripheral area of injured skin to sublethal hyperthermia following the burn [1]. Sympathetic preganglionic nuclei of the thoracolumbar spinal cord receive an intense innervation from several classes of descending pathway, especially, In normal skin, heat resulting in painful sensation by nociceptors, carries a risk of tissue damage [6]; the hyperthermia used in post-heat shock tolerance is too mild to induce any tissue injury, but causes pain in the presence of burn-induced hyperalgesia/allodynia. This mild painful stimulus can result in the induction of descending anti-nociceptive mechanisms, especially in the adjacent burned area. 2 – If activation of the noradrenergic system is a mechanism by which post-burn local hyperthermia decreases the progression of burn injury, administration of adrenergic receptor antagonists before the application of post-burn local hyperthermia should inhibit the effects of post-burn local hyperthermia on the progression of burn injury
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