Jaye P.F. Chin-Dusting, PhD; Brindi Rasaratnam, MBBS; Garry L.R. Jennings, MD, FRACP; Francis J. Dudley, FRACP
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.
To test the hypothesis that the antibiotic norfloxacin blocks the effects of nitric oxide.
Placebo-controlled, double-blind, crossover study.
Alfred Hospital, Melbourne, Australia.
9 patients with alcohol-related cirrhosis and 10 healthy controls.
Norfloxacin, 400 mg twice daily, for 4 weeks.
Peripheral blood flow was measured by using forearm venous occlusion plethysmography.
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.
Bacterial endotoxemia in patients with cirrhosis induces increased synthesis of nitric oxide that can be corrected with norfloxacin.
Chin-Dusting JP, Rasaratnam B, Jennings GL, et al. Effect of Fluoroquinolone on the Enhanced Nitric Oxide-Induced Peripheral Vasodilation Seen in Cirrhosis. Ann Intern Med. 1997;127:985–988. doi: 10.7326/0003-4819-127-11-199712010-00007
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Published: Ann Intern Med. 1997;127(11):985-988.
Gastroenterology/Hepatology, Liver Disease.
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