No abstract

Angiogenesis is a key process for wound healing. There are few reports of LED phototherapy on angiogenesis, mainly in vivo. The aim of the present investigation was to evaluate histologically the angiogenesis on dorsal cutaneous wounds treated with laser (660 and 790 nm) or LEDs (700, 530, and 460 nm) in a rodent model. Twenty-four young adult male Wistar rats weighting between 200 and 250 g were used on the present study. Under general anesthesia, one excisional wound was created on the dorsum of each animal that were then randomly distributed into six groups with four animals each: G0-control; G1-laser λ660 nm (60 mW, ϕ ∼2 mm, 10 J/cm(2)); G2-laser λ790 nm (50 mW, ϕ ∼2 mm, 10 J/cm(2)); G3-LED λ700 ± 20 nm (15 mW, ϕ ∼16 mm, 10 J/cm(2)); G4-LED λ530 ± 20 nm (8 mW, ϕ ∼16 mm, 10 J/cm(2)); G5-LED λ460 ± 20 nm (22 mW, ϕ ∼16 mm, 10 J/cm(2)). Irradiation started immediately after surgery and was repeated every other day for 7 days. Animal death occurred at the eighth day after surgery. The specimens were removed, routinely processed to wax, cut and stained with HE. Angiogenesis was scored by blood vessel counting in the wounded area. Quantitative results showed that green LED (λ530 ± 20 nm), red LED (λ700 ± 20 nm), λ790 nm laser and λ660 nm laser caused significant increased angiogenesis when compared to the control group. It is concluded that both laser and LED light are capable of stimulating angiogenesis in vivo on cutaneous wounds and that coherence was not decisive on the outcome of the treatment.

The use of green and red LED light is effective in increasing fibroblastic proliferation on rodents.

A study of the effects of insulin-induced hypoglycemia in the obese yellow agouti A^y mouse was initiated to test the hypothesis that the central melanocortin pathways are required for a normal sympathetic response to hypoglycemia. An experimental protocol was performed in which young nonobese male mice were isolated and fasted beginning on day 1, then tested for glucose responses to insulin-induced hypoglycemia on day 2. Normal mice demonstrated the expected glucose rebound to hypoglycemia, exceeding baseline glucose levels by 2–3 times as a consequence of increased gluconeogenesis and glycogenolysis before returning to baseline levels. A^y animals lacked the rebound, exhibiting instead a gradual restoration of baseline glucose levels. The results suggested a defective sympathetic response to hypoglycemia in the A^y mouse. However, a more detailed analysis demonstrated that the lack of a hyperglycemic rebound was due to an acute inhibition of feeding specifically in the A^y mouse, which resulted not from the hypoglycemia stressor, but rather from the stress of isolation. Handling and intraperitoneal administration of saline also specifically inhibited food intake in the A^y but not the wild-type mouse, while restraint stress had an equivalent inhibitory effect on food intake on wild-type and A^y mice. Since the A^y mouse has defective hypothalamic melanocortin-4 receptor (MC4-R) signaling, these data imply that the central melanocortin pathway is necessary for regulating the effects of stress on feeding behavior. Furthermore, these data demonstrate the need for exercising extreme caution in designing experiments to analyze feeding behavior and metabolism in genetic or pharmacological models involving perturbation of the melanocortin system.