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Effect of Fluoroquinolone on the Enhanced Nitric Oxide-Induced Peripheral Vasodilation Seen in Cirrhosis

Jaye P.F. Chin-Dusting, PhD; Brindi Rasaratnam, MBBS; Garry L.R. Jennings, MD, FRACP; and Francis J. Dudley, FRACP
[+] Article and Author Information

From Baker Medical Research Institute and Alfred Hospital, Prahran, Australia. Acknowledgments: The authors thank Leonie Johnston for nursing care and Pam Arnold for technical expertise. Grant Support: By a grant from the Alfred Healthcare Trusts and a Baker Medical Research Institute grant from the Australian National Health and Medical Research Council. Requests for Reprints: Jaye P.F. Chin-Dusting, PhD, Alfred and Baker Medical Unit, Baker Medical Research Institute, Commercial Road, Prahran 3181, Victoria, Australia. Current Author Addresses: Drs. Chin-Dusting and Jennings: Alfred and Baker Medical Unit, Baker Medical Research Institute, Commercial Road, Prahran 3181, Victoria, Australia.


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1997;127(11):985-988. doi:10.7326/0003-4819-127-11-199712010-00007
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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.

Figures

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Figure 1.
Effect of NG -monomethyl-L-arginine. Top.GBottom.GPP

Response of forearm blood flow to N -monomethyl-L-arginine in controls (circles), cirrhotic patients who received placebo (squares), and cirrhotic patients who received norfloxacin (triangles). The constricting effect of N ( ) -monomethyl-L-arginine, expressed as a percentage of basal forearm vascular resistance in controls (circles), cirrhotic patients who received placebo (squares), and cirrhotic patients who received norfloxacin (triangles). * < 0.05 for cirrhotic patients who received placebo compared with controls. † < 0.05 for cirrhotic patients who received norfloxacin compared with cirrhotic patients who received placebo. Error bars represent SEs.

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Grahic Jump Location
Figure 2.
Effect of acetylcholine. Top.Bottom.P

Responses of forearm blood flow to acetylcholine in controls (circles), cirrhotic patients who received placebo (squares), and cirrhotic patients who received norfloxacin (triangles). The dilatory effect of acetylcholine, expressed as a percentage of basal forearm vascular resistance in controls (circles), cirrhotic patients who received placebo (squares), and cirrhotic patients who received norfloxacin (triangles). * < 0.05 for cirrhotic patients who received placebo compared with controls.

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