Intradermal Anti-Prostaglandin Agents and Sunburn

Inhibitors of prostaglandin (PG) biosynthesis, indomethacin and aspirin, decrease and delay ultraviolet light-induced erythema when injected intradermally in humans and guinea pigs. Increasing amounts of inhibitor cause a more intense blanch with a longer duration demonstrating a dose response. Indomethacin was approximately 45 times more effective than aspirin. Indomethacin can cause blanching of UV redness if injected at any time from the period of irradiation to 18 hr after UV exposure. Triamcinolone acetonide was effective in preventing erythema in humans, but not in guinea pigs. The ability of anti-PG agents to decrease and delay UV-induced redness lends further support to a role for PG in the mediation of sunburn

Dichotomy In Response To Indomethacin In Uv-C And Uv-B Induced Ultraviolet Light Inflammation

In subjects irradiated with both UV-C and UV-B ultraviolet light (UVL), 10 μg of intradermal indomethacin decreased the redness in all 13 of the UV-B irradiated areas but in only 2 of 13 of the UV-C irradiated areas. Higher doses of intradermal indomethacin (50 μg and 100 μg) decreased the redness produced by UV-C irradiation in 6 subjects. It is suggested that the failure of 10 μg of indomethacin to decrease the redness of the UV-C induced inflammation, while decreasing the redness in the UV-R induced inflammation, is consistent with the possibility that prostaglandins participate in UV-R but not UV-C induced inflammation

Prostaglandin and Dna Synthesis in Human Skin: Possible Relationship to ultraviolet light effects

The effect of prostaglandin E2 (PGE2) on DNA synthesis in human skin was evaluated. PGE2 (1μg) was injected intradermally into normal buttock skin of 15 volunteers followed by tritiated thymidine for autoradiographic quanitation of DNA sythesizing cells. Controls of normal saline, histamine (50μg), and lower doses of PGE2 were also injected into 8 of the volunteers. Forty-eight hours after injection of 1μg and 0.1μg PGE2 there was a 264% and 62% increase, respectively, in the number of DNA synthesizing epidermal cells/high-power field as compared to saline controls. These differences were statistically significant (p<0.01). Histamine (50μg) produced a statistically significant 36% higher labeling index compared to its saline controls (p<0.05). Many types of skin injury, including ultraviolet light (UVL) irradiation, produce an increase in the number of DNA synthesizing cells about 48 hr after the stimulus. Our findings suggest the PGE, a putative mediator of UVL-induced inflammation, may be one of the chemical mediators for the UVL-induced increase in DNA sythesizing cells. Histamine may also contribute to the increase in DNA synthesizing cells following UVL-induced inflammation

The Biology of Skin Grafts: Skin Grafts as Pharmacologic Agents

† BACKGROUND.— Skin grafting is commonly used to treat nonhealing wounds. However, how skin grafts help to heal wounds is not entirely known. Why epithelium from grafted skin is able to migrate and cover these wounds, while epithelium at the edge of nonhealing wounds is unable to, is a long unanswered biologic question. OBSERVATIONS.— The recent use of cultured epithelial allografts has rekindled interest in the biology of skin grafts. Replaced, even in chronic wounds, by recipient epithelium, cultured epithelial allografts appear to work by providing a potent stimulus to healing imparted by the graft itself. Based on this, we have reassessed how skin autografts help to heal wounds and hypothesize that, in a similar fashion, autografts may work not only by replacing tissue but also by providing a stimulus for healing. CONCLUSIONS.— We suggest that skin grafts may work not only as tissue replacement but as pharmacologic agents that provide a stimulus for healing. We believe that, someday, it may be possible to augment the stimulatory properties of donor skin to speed healing of the recipient wound.(Arch Dermatol. 1993;129:481-483

The development of bioengineered skin

Driven by the need for donor tissue for patients suffering from extensive burns, alternatives to autologous and cadaver-derived tissue have been under development for the past 20 years. Unilayered and bilayered models representing the skin's epidermal and/or dermal components have been developed using both cells and matrix materials. In addition to their use in patients with extensive burns, trials using these products on refractory and challenging patients with both acute and chronic wounds have led to the commercial availability of some of these products

Electrical Stimulation and Wound Healing

• Living tissues possess direct current surface electropotentials that regulate, at least in part, the healing process. Following tissue damage, a current of injury is generated that is thought to trigger biological repair. In addition, exogenous electrical stimuli have been shown to enhance the healing of wounds in both human subjects and animal models. Intractable ulcers have demonstrated accelerated healing and skin wounds have resurfaced faster and with better tensile properties following exposure to electrical currents. This article examines the bioelectric properties of living systems and reviews the existing literature on electrical stimulation and wound healing.(Arch Dermatol. 1990;126:222-225