BACKGROUND/AIMS: Data from studies in experimental models have suggested that the impairment of mitochondrial function and altered redox state that occur in cirrhosis may be due to impaired hepatic oxygenation. Since interventions that improve oxygen delivery to hepatocytes may improve mitochondrial functions, we studied the effects of oxygen supplementation on the arterial ketone body ratio (AKBR) in normal volunteers and patients with cirrhosis. METHODS: After a 2-hour fast, ketone bodies were measured in arterial blood taken from patients and controls while breathing room air and then after breathing oxygen via a face mask at 12 liters/min for 60 min. RESULTS: The AKBR was reduced in cirrhotic patients compared with controls, 0.74 +/- 0.23 and 1.51 +/- 0.4, respectively (p = 0.002). Oxygen supplementation significantly improved the AKBR in cirrhotic patients, from 0.74 +/- 0.23 to 1.04 +/- 0.28 (p = 0.001) but did not affect the AKBR in controls. CONCLUSION: These findings suggest that reduced hepatocyte oxygenation contributes to impaired hepatic mitochondrial function in cirrhosis. Strategies at increasing hepatic oxygen delivery may improve hepatic mitochondrial function in patients with chronic liver disease. Copyright 2002 S. Karger AG, Basel
BACKGROUND/AIMS: Data from studies in experimental models have suggested that the impairment of mitochondrial function and altered redox state that occur in cirrhosis may be due to impaired hepatic oxygenation. Since interventions that improve oxygen delivery to hepatocytes may improve mitochondrial functions, we studied the effects of oxygen supplementation on the arterial ketone body ratio (AKBR) in normal volunteers and patients with cirrhosis. METHODS: After a 2-hour fast, ketone bodies were measured in arterial blood taken from patients and controls while breathing room air and then after breathing oxygen via a face mask at 12 liters/min for 60 min. RESULTS: The AKBR was reduced in cirrhotic patients compared with controls, 0.74 +/- 0.23 and 1.51 +/- 0.4, respectively (p = 0.002). Oxygen supplementation significantly improved the AKBR in cirrhotic patients, from 0.74 +/- 0.23 to 1.04 +/- 0.28 (p = 0.001) but did not affect the AKBR in controls. CONCLUSION: These findings suggest that reduced hepatocyte oxygenation contributes to impaired hepatic mitochondrial function in cirrhosis. Strategies at increasing hepatic oxygen delivery may improve hepatic mitochondrial function in patients with chronic liver disease. Copyright 2002 S. Karger AG, Basel