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In vivo longitudinal (T1) and transverse (T2) relaxation times of hepatic intracellular and extracellular sodium were studied in rats with sham burn or burn injury with 23Na NMR spectroscopy and shift reagent. Burn injury decreases hepatic extracellular sodium content by 17% compared with sham burn, whereas it increases the percent of the fast T2 component of extracellular sodium, suggesting an increase in the fraction of bound Na+/- sites in the extracellular space. It is interesting that the relaxation characteristics of intracellular sodium remained unchanged despite a 57% increase in intracellular sodium content, suggesting the increase in intracellular free sodium is matched by either a proportional increase in intracellular bound sodium or an uncovering of ordered domain sites that can preferentially orient rapidly exchanging sodium ions. This study also demonstrated that spin lattice (T1) relaxation rates or the percent contribution of the fast/slow T2 components of the combined intracellular/extracellular 23Na signal (before the infusion of shift reagent) may also be sensitive to changes in intracellular sodium levels during pathologic changes.

Delayed fluid resuscitation during burn shock is thought to compromise the integrity of gut mucosa and allow enteric bacteria to cross the luminal wall and infect other sterile organ systems. Superoxide dismutase, a free-oxygen radical scavenger; leupeptin, a protease inhibitor; and verapamil, a calcium channel blocker, were studied to evaluate their efficacy in maintaining cellular integrity in the gut of thermally burned rats whose fluid resuscitation had been delayed. Fifty male rats weighting 280 to 320 gm were given a full-thickness scald burn covering 50% total body surface area. Ten received early fluid resuscitation beginning half an hour after burn, and 40 received fluid resuscitation delayed by 6 hours. Those receiving delayed resuscitation were given superoxide dismutase (n = 10), leupeptin (n = 10), verapamil (n = 10), or a placebo of normal saline solution (n = 10) at the time of fluid resuscitation. Ileal mucosa samples were harvested, and adenosine triphosphate, diphosphate, and monophosphate were measured. Adenosine triphosphate, total nucleotides, and energy charge potential were significantly lower in the placebo group without therapy compared with those of the early resuscitation group. Superoxide dismutase and leupeptin therapy prevented this drop in cellular energy. Total water content was significantly increased in the placebo group compared with that of the early resuscitation group; superoxide dismutase was able to prevent this increase. Data indicate that intestinal reperfusion injury in burned rats can be effectively modulated with superoxide dismutase or leupeptin therapy.