L-arginine improves resting cardiac transmembrane potential after burn injury

Previous studies from our laboratory have suggested that burn injury disrupts nitric oxide production and promotes a loss of cell membrane integrity. We hypothesized that administration of L-arginine, a precursor of nitric oxide (NO), would prevent postburn depolarization of the cardiac cell membrane and preserve cell membrane integrity. Third degree scald burn comprising 43% of the total body surface area was produced in rats (n = 22); sham burn controls (n = 11) were included. Burn rats were either untreated (N = 11) or given 300 mg/kg L-arginine immediately, 3, 6, and 23 h postburn. Untreated burn injury caused depolarization of the cardiac cell membrane (cardiac Em fell from 79.0 +/- 1.4 mV in shams to 67.0 +/- 1.5 mV 24 h after untreated burn, p < .05) and an increase in myocardial tissue lactate. Urine nitrate levels (assessed to provide a measure of NO production) fell after untreated burn (0.49 +/- 0.10 microM/24 h) compared with levels measured in sham burns (7.99 +/- 0.64 microM/24 h, p < .05), indicating that burn injury reduced NO production. Postburn administration of L-arginine improved cardiac Em (81.5 +/- 2.1 mV), reduced myocardial tissue lactate levels, and increased urinary nitrate levels above values measured for untreated burns. Our data indicate that L-arginine, in the absence of fluid resuscitation, provides postburn cardiac cell membrane protection, possibly due to enhanced nitric oxide production.