Background: In patients with cirrhosis, portosystemic shunts allow intestinal bacteria and endotoxin to enter the systemic circulation. Endotoxemia may induce increased synthesis of nitric oxide, thereby contributing to arterial vasodilation.
Objective: To test the hypothesis that the antibiotic norfloxacin blocks the effects of nitric oxide.
Design: Placebo-controlled, double-blind, crossover study.
Setting: Alfred Hospital, Melbourne, Australia.
Patients: 9 patients with alcohol-related cirrhosis and 10 healthy controls.
Intervention: Norfloxacin, 400 mg twice daily, for 4 weeks.
Measurements: Peripheral blood flow was measured by using forearm venous occlusion plethysmography.
Results: Basal forearm blood flow was higher in patients with cirrhosis than in controls (3.69 ± 0.27 mL/100mL per minute and 2.47 ± 0.40 mL/100mL per minute; P = 0.014) but returned toward normal after norfloxacin was given (2.64 ± 0.31 mL/100 mL of tissue per minute in patients with cirrhosis). Responses to NG -monomethyl-L-arginine were greater in patients with cirrhosis but returned to normal after norfloxacin was given.
Conclusion: Bacterial endotoxemia in patients with cirrhosis induces increased synthesis of nitric oxide that can be corrected with norfloxacin.