Enteral nutrition delivered via a nasojejunal tube is associated with a significant reduction in gastric residual volume, a strong trend toward improved tolerance of enteral nutrition, and an extremely low requirement for parenteral nutrition.

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This simple, rapid, sensitive, reliable, and economical assay for bismuth in plasma, erythrocytes, and urine is based on atomic absorption spectrophotometry with hydride generation. Acid digestion eliminates the problem of foaming, which hitherto has complicated such assay of bismuth in plasma and erythrocytes. The detection limit of the assay has been improved to 0.1 micrograms/L, as compared with a previously documented limit of 2.5 micrograms/L. Average recovery exceeded 95% in all biological fluids. Economy of use derives from elimination of need for electrodeless discharge lamps and atomic absorption grade borohydride. Determination of basal concentrations of bismuth in clinical samples of body fluids gave reference intervals of 0.1-3.5 micrograms/L for plasma, 0.3-4.6 micrograms/L for urine.

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.