Effects of cigarette smoke in mice wound healing is strain dependent.

It has been clinically and experimentally shown that cigarette smokers suffer from impaired wound healing, but the mechanisms that lead to the alterations are not well understood. The aim of this study was to investigate if the effects of cigarette smoke exposure on excisional cutaneous wound healing are different depending on the strain (Swiss, BALB/c and C57BL/6 mice) studied. Male mice were exposed to smoke of nine whole cigarettes per day, 3 times/day, daily, for 10 days. In the 11th day a full-thickness excisional wound was performed. Control group was sham-exposed and also had a full-thickness excisional wound. The cigarette smoke exposure protocol was performed until euthanasia. Animals were euthanatized 14 days after wounding. Wound contraction was evaluated 7 and 14 days after lesion. Sections were stained with hematoxylin-eosin, Sirius red or toluidine blue and immunostained for alpha-smooth muscle actin. Smoke exposed animals presented delay in wound contraction, in fibroblastic and inflammatory cells recruitment and in myofibroblastic differentiation; those alterations were strain dependent. Cigarette smoke exposure also affected mast cells recruitment and neoepidermis thickness. In conclusion, the present study demonstrated that the effects of cigarette smoke in mice cutaneous wound healing are related to mice strain studied.

Sympathetic denervation accelerates wound contraction but delays reepithelialization in rats.

Participation of the peripheral nervous system in wound healing is not well understood. The aim of this study was to investigate the effects of sympathetic denervation on rat excisional cutaneous wound healing. Male rats were chemically denervated with intraperitoneal administration of 6-hydroxydopamine (6-OHDA) in 1% ascorbic acid. 6-OHDA or vehicle was administered twice a week until euthanasia, beginning 7 days before wounding. A full-thickness excisional lesion was performed and the lesion area measured to evaluate wound contraction. After euthanasia, the lesion and adjacent normal skin were formalin-fixed and paraffin-embedded. Sections were stained with hematoxylin and eosin or toluidine blue, or immunostained for alpha-smooth muscle actin. Animals treated with 6-OHDA showed acceleration in wound contraction, increase in myofibroblastic differentiation, reduction in mast cell migration, and a delay in reepithelialization. To investigate the effects of neurogenic inflammation, a group of animals was treated with 6-OHDA only after the acute inflammatory phase, and these animals showed delayed wound contraction 3 and 7 days after wounding when compared to those treated before the lesion. In conclusion, the present study shows that sympathetic denervation affects cutaneous wound healing, probably by a decrease in neurogenic inflammation during the initial phase of healing and the absence of catecholamines throughout the final phase.