Search PubMedSearch

PubMed · 2265658

Decrease in hepatic mitochondrial redox state by massive infusion of citrate-phosphate-dextrose solution in jaundiced rabbits.

Abstract

To clarify the mechanism of metabolic derangement by massive blood transfusion to the damaged liver, the changes in the hepatic mitochondrial redox state, as reflected in arterial ketone body ratio (acetoacetate/3-hydroxybutyrate), were studied in jaundiced rabbits by infusion of massive citrate-phosphate-dextrose (CPD) solution. The jaundiced rabbits received common bile duct ligation (BDL group), and the sham group had a simple exploration of the bile duct. CPD solution was infused for 3 h at a rate of 9 ml/kg/h in each group. As metabolic parameters, blood gas, pyruvate, lactate, citrate and ketone body ratio were analyzed in the arterial blood. During the course, arterial ketone body ratio decreased significantly (p less than 0.01) in the BDL group with severe metabolic acidosis, while it was maintained at high value in the sham group with metabolic alkalosis. Organic acids were more highly accumulated in the BDL group than in the sham group. These results suggested a hepatodepressant effect of massive blood transfusion, especially in the damaged liver.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Y Wada, K Mori, H Egawa, M Noguchi, M Zaima, K Ozawa. 1990. Decrease in hepatic mitochondrial redox state by massive infusion of citrate-phosphate-dextrose solution in jaundiced rabbits.. https://doi.org/10.1159/000129107

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Characterization of a kidney-specific pattern of chromatin structure in the rat phosphoenolpyruvate carboxykinase gene.

The kidney-specific chromatin structure of the phosphoenolpyruvate carboxykinase (PEPCK) gene was examined and compared to that of the liver. Kidney nuclear extracts were found to lack a liver-enriched factor, pepA, that binds to HSS A, a distal enhancer of the PEPCK gene that may be involved in opening the chromatin domain of the PEPCK gene in the liver. To begin the characterization of the kidney-specific chromatin structure of the PEPCK gene, nuclease hypersensitive sites (HSS) were mapped by indirect end-labeling analysis in proximal tubules from control rats, proximal tubules from acidotic rats which express induced levels of PEPCK, and NRK52E cells, a rat kidney epithelial cell line which does not express the PEPCK gene. A subset of HSS, at -400/+1 over the proximal promoter and at +1900 within the coding region, correlate with kidney-specific PEPCK expression. Two other HSS, at -3.1 kb and +6.2 kb, are detected in kidney cells regardless of PEPCK expression. The HSS at -4800, -1240, and +4650, previously identified in PEPCK-expressing liver cells, were not observed in the kidney. As in the liver, the pattern of hypersensitivity in the kidney does not change by altering the rate of transcription.

Acidosis

Treatment of hypernatremia in an acidotic neonatal calf.

A 7-day-old Jersey calf was evaluated because of diarrhea and pneumonia. The calf was hypernatremic, hypoproteinemic, and acidemic, and was treated initially with i.v. administration of fluids with sodium concentration (175 mEq/L) similar to the calf's serum sodium concentration. Sodium concentration of the administered fluids was gradually decreased over the following days, but the calf's serum sodium concentration decreased too rapidly, and the calf developed neurologic signs attributed to cerebral edema. Treatment with mannitol and i.v. administration of fluids with a higher concentration of sodium resulted in abatement of clinical signs. In calves, hypernatremia may develop over several days. Prescribing traditional isotonic or hypotonic fluids in such cases will be harmful, because during chronic hypernatremia, the brain's adaptive mechanisms involve accumulation of organic osmoles that may take several days to equilibrate across cell membranes, and cerebral edema may result. Administration of fluids containing sodium concentration approximately equal to the patient's measured serum sodium concentration is required to decrease serum sodium concentration more slowly than is possible with traditional isotonic fluids.

Acidosis