ALPHA-TRINOSITOL INHIBITS EDEMA GENERATION AND ALBUMIN EXTRAVASATION IN THERMALLY INJURED SKIN

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Abstract
Pharmacologic attempts to reduce edema generation and albumin extravasation into thermally injured skin have until recently been disappointing unless the drugs (usually antiphlogistic or anti-inflammatory drugs) were given before injury. We have studied the effect of α-trinositol (PP56, i.e., 1d-myo-inositol-1,2,6-trisphosphate) given after the injury in an experimental full-thickness 10% TBSA scald burn in anesthetized rats. Total tissue water content (TTW) and albumin extravasation (Ealb) were determined in injured and noninjured skin (series I, n = 12). Interstitial fluid hydrostatic pressure (Pif) was measured in injured skin (series II, n = 14). α-Trinositol was administered (α-trinositol groups) as an IV bolus (40 mg/kg) at 5 minutes after injury followed by an IV infusion (1.3 mg/kg/min). In both series a placebo group received burn injury and normal saline in equal volumes instead of α-trinositol. Compared with placebo, α-trinositol reduced TTW and Ealb as well as the increased negativity of Pif in injured tissue significantly. The effect on Ealb was most prominent, with a reduction from 153.9 ± 35.6 (SEM) μL/g in the NaCl group to 23.1 ± 6.3 after α-trinositol (p < 0.005). Total tissue water was reduced from 2.51 ± 0.13 to 2.17 ± 0.06 mL/g (p < 0.05) and Pif (measured between 21 and 40 minutes postinjury) from −24.7 ± 4.1 to −3.2 ±1.1 mm Hg (p < 0.005). We conclude that α-trinositol markedly attenuates postburn edema formation by ameliorating both the burn-induced albumin leakage and the increased negativity in tissue pressure, the latter being a main driving force to explain the rapid formation of edema.

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