Protective effect of nitric oxide in an endotoxin-induced septic shock.

BACKGROUND

Calcium ion (Ca++)-independent nitric oxide (NO) synthase activity in animals was markedly induced by treatment with endotoxin, but NO levels in various tissues removed from endotoxin-treated animals have not been reported. The role of NO during an endotoxin-induced septic shock remains controversial.

METHODS

ICR mice, randomly divided into one of six treatment groups, received intraperitoneal injections as follows: phosphate-buffered saline; Escherichia coli LPS (LPS); N(omega)-nitro-L-arginine (L-NNA); N(omega)-nitro-D-arginine (D-NNA); LPS plus L-NNA; and LPS plus D-NNA. The mice were either monitored for mortality or killed for nitrite/nitrate assays and histologic analysis.

RESULTS

NO levels in many tissues were markedly increased by injection of LPS, and administration of L-NNA increased mortality rates of LPS-treated mice, in association with an increase in tissue damage in the lung, liver, and kidney.

CONCLUSIONS

The endogenous NO generated during LPS-mediated septic shock could be protective.