This study investigated the effects of the anti-inflammatory agent D-myo-inositol-1,2,6-trisphosphate (IP3) on burn edema. Two sets of experiments were performed. In the first set, a full-thickness burn injury was induced in the abdominal skin of anesthetized rats. Postburn intravenous treatment was given with IP3, indomethacin or saline solution. Extravasation of Evans blue albumin in the burned tissue was quantified by a spectrophotometric technique. Results showed significant inhibition of albumin extravasation by IP3 in three of five different doses compared to saline-treated animals. In the second set of experiments, a deep full-thickness burn through the abdominal skin and rectus muscle was induced. The therapeutic window of IP3 could be more well-defined. Resulted showed a significant reduction of albumin extravasation in the skin at all four dose levels and in the abdominal muscle at three of four doses. Indomethacin had no significant effect on postburn edema formation. The mechanisms responsible for the inhibition of albumin leakage by IP3 could be secondary to reduced formation of edema-promoting inflammatory mediators by the agent, resulting in improved vascular patency.

Albumins↗

PubMedDate not supplied

Local anesthetics improve dermal perfusion after burn injury.

Deep partial-thickness burn injury was induced in the abdominal skin of anesthetized rats. Dermal perfusion was assessed by laser Doppler flowmetry. In the first set of experiments, one group of rats (n = 15) was topically treated with a lidocaine-prilocaine cream 5% (25 mg of each in 1 g) for 6 hours, starting 5 minutes after inducing the burn injury. In one control group (n = 14), the thermal injury was treated with placebo cream. Results showed a markedly reduced perfusion in the skin of the control animals within the first hour after burn injury, with further decrease during the following 5 hours of observation. In animals treated with the lidocaine-prilocaine cream, skin perfusion in the burned area was significantly increased during the first 30 minutes after the burn injury compared to before the burn (p < 0.01), followed by a decrease to a level below the preburn stage but significantly higher than that of control animals during the first hour after burn injury (p < 0.05). As opposed to burned control animals, skin perfusion gradually recovered toward preburn levels at the end of the experiment in local anesthetic-treated animals. In the second experimental set, four groups of animals were burned and subsequently treated with a bolus dose of lidocaine intravenously (2 mg/kg), followed by continuous intravenous lidocaine infusions at a rate of 50 (n = 10), 100 (n = 11), or 150 (n = 10) micrograms.kg-1.min-1. The infusions were started 5 minutes after the burn injury and lasted for 6 hours. Corresponding volumes of saline solution were given to burned control animals (n = 10). Results showed a significantly improved skin perfusion in the lidocaine-treated group in a dose-response fashion as compared to control animals. A maximum improvement of dermal perfusion in the burned area was induced by intravenous lidocaine at an infusion rate of 150 micrograms.kg-1.min-1 as compared to burned controls treated with isotonic saline solution infusions (p < 0.01). Results showed that topical or systemic administration of local anesthetics can prevent progressive dermal ischemia after thermal injury.

Administration, Topical↗