To evaluate our experience with fungal burn wound infection, we performed a 10-year review for comparison with our experience with bacterial burn wound infection. During the study period, a marked decline occurred in bacterial wound infection but not in fungal wound infection. Patients with either bacterial or fungal burn wound infection had massive injury, with burn size averaging greater than 50% of the total body surface area. Factors that appear to have markedly reduced bacterial burn wound infection, including patient isolation, topical chemotherapeutic agents, and burn wound excision, do not appear to have had a similar effect on fungal wound infection. The mechanism of spread and colonization of fungi, and the lack of effective topical chemotherapeutic antifungal agents, may explain in part our findings.

The potentiation of LPS-induced pulmonary hypertension following NAME infusion suggests that inhibition of nitric oxide synthase may have a limited role in the treatment of septic shock.

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Nitric oxide is biosynthesized from the amino acid L-arginine by the enzyme nitric Qm1 oxide synthase. Nitric oxide is a vasodilator, a neurotransmitter, and may modulate Q (414 immune function. The experiments presented here were performed to determine M whether the synthesis of nitric oxide is Increased following experimental bum injury 00 AN___ in rats. After a 30% total body surface area bum in 300-g Lewis rats, the urinary output of nitrate, a stable metabolite of nitric oxide, was significantly Increased for 8 __ days postburn compared with that In sham-bumed control rats. The origin of the V win urinary nitrate from L-arginine was demonstrated by administering the stable Isotope ' 5 N 2 -guanido-arginine to burned and sham-burned rats and observing an immediate <1% of the administered arginine isotope in both the burned and unburned rats; the recovery of the Isotope increased tenfold over baseline recovery in burned rats. The arginine analog N-monomethyl-arginine, an Inhibitor of the enzyme nitric oxide synthase, blocked the postbum rise in urinary NO 3 output In burned rats, but did not completely Inhibit the output of NO 3 in bum wound-infected rats. Experimental bum injury In rats results In an Increase in L-arginine-dependent nitric oxide production and urinary nitrate output.BURN INJURY is associated with a hypermetabolic ucts of nitric oxide. The major route of elimination of response; the degree of hypermetabolism that follows these end products is by urinary excretion.' Experimental burn injury is related to burn size. 1 The hemodynamic studies in animals have demonstrated an increase in both component of the hypermetabolic response is character-arginine-dependent NO synthesis and the urinary excreized by an elevation of cardiac output and a depression tion of N0 2 /NO 3 following the administration of endoof peripheral vascular resistance. Althour:: -he precise toxin. 9 Also, increases in plasma levels of N0 2 /NO 3 have CL mechanisms that induce postburn hypermetabolism are been observed in humans with sepsis, and in patients 94, not fully understood, catecholamines are considered to with advanced malignancies following the administration be one of the principal mediators of postburn hyperme-of interleukin-2. 10 ' 1 1 Blockade of NO synthesis, by steretabolism.2 When burn injury is complicated by the de-ospecific inhibitors Gf the enzyme NOS, has been studied : !• velopment of a burn wound infection, there is often an in multiple species of experimental animals and results ,~ ':' associated increase in the magnitude of the hypermeta-in an acute increase in blood pressure and peripheral bolic response.' vascular resistance, suggesting that the synthesis and r", Nitric oxide (NO), biosynthesi7eJ in mammalian spe-release of NO may regulate, in part, both blood pressure cies by the enzyme nitric oxide synthase (NOS, EC and vascular tone. 12 , 1 3 "1.14.14.39) from the amino acid L-arginine and molecular Nitric oxide is also produced by macrophages, and the oxygen, is a vasodilator, a neurotransmitte...