Pancreatitis-induced ascitic fluid and hepatocellular dysfunction in severe acute pancreatitis

Takashi Ueda, Hung S Ho, Steven E. Anderson, Yoshifumi Takeyama

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Background. Multiple organ failure (MOF) is the most serious complication in severe acute pancreatitis, contributing to its high mortality. It has been suggested that changes of high-energy phosphates, intracellular pH, and intracellular cation homeostasis are closely related to hepatocellular injury associated with MOF. Methods. Phosphorus metabolites, intracellular pH (pH(i)), and intracellular Na+ concentration ([Na+](i)) were measured in rat livers in vivo using 31P and 23Na NMR spectroscopy after deoxycholic acid (DCA)induced pancreatitis or intraperitoneal injection (ip) of pancreatitis-induced ascitic fluid (PAF). Results. Two hours after induction of DCA-pancreatitis, the liver experienced significant intracellular acidosis (pH(i) = 6.99 ± 0.16) and sodium loading (75 ± 9 mM) and a reduction in its energy state (β-ATP/P(i) = 0.2 ± 0.03 and P(i) = 164 ± 12). Although ip injection of PAF into healthy rats did not induce systemic hypotension, the livers under these conditions also developed severe disturbances in hepatocellular ion homeostasis and depletion of its bioenergetics. The longer the abdomen was exposed to the PAF, the worse the changes were. At 3 h after ip injection of PAF, hepatic [Na+](i) significantly increased (42 ± 3 mM) along with a significant decrease in pH(i) (7.30 ± 0.03). At 6 h after ip injection of PAF, the hepatic β- ATP/P(i) ratio decreased to 0.34 ± 0.05 and P(i) increased to 97 ± 27. Conclusions. PAF induced severe hepatocellular acidosis, rapid accumulation of hepatic intracellular sodium, impaired hepatic cytosolic phosphorylation potential, and increased hepatic utilization of ATP. These effects may account for the eventual development of liver dysfunction associated with necrotizing pancreatitis.

Original languageEnglish (US)
Pages (from-to)305-311
Number of pages7
JournalJournal of Surgical Research
Volume82
Issue number2
DOIs
StatePublished - Apr 1999

Fingerprint

Ascitic Fluid
Pancreatitis
Liver
Deoxycholic Acid
Multiple Organ Failure
Adenosine Triphosphate
Acidosis
Injections
Homeostasis
Sodium
Intraperitoneal Injections
Abdomen
Hypotension
Phosphorus
Energy Metabolism
Cations
Liver Diseases
Magnetic Resonance Spectroscopy
Phosphates
Phosphorylation

Keywords

  • Acute pancreatitis
  • Ascitic fluid
  • Hepatocellular injury
  • Intracellular Na
  • Intracellular pH
  • NMR spectroscopy

ASJC Scopus subject areas

  • Surgery

Cite this

Pancreatitis-induced ascitic fluid and hepatocellular dysfunction in severe acute pancreatitis. / Ueda, Takashi; Ho, Hung S; Anderson, Steven E.; Takeyama, Yoshifumi.

In: Journal of Surgical Research, Vol. 82, No. 2, 04.1999, p. 305-311.

Research output: Contribution to journalArticle

Ueda, Takashi ; Ho, Hung S ; Anderson, Steven E. ; Takeyama, Yoshifumi. / Pancreatitis-induced ascitic fluid and hepatocellular dysfunction in severe acute pancreatitis. In: Journal of Surgical Research. 1999 ; Vol. 82, No. 2. pp. 305-311.
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abstract = "Background. Multiple organ failure (MOF) is the most serious complication in severe acute pancreatitis, contributing to its high mortality. It has been suggested that changes of high-energy phosphates, intracellular pH, and intracellular cation homeostasis are closely related to hepatocellular injury associated with MOF. Methods. Phosphorus metabolites, intracellular pH (pH(i)), and intracellular Na+ concentration ([Na+](i)) were measured in rat livers in vivo using 31P and 23Na NMR spectroscopy after deoxycholic acid (DCA)induced pancreatitis or intraperitoneal injection (ip) of pancreatitis-induced ascitic fluid (PAF). Results. Two hours after induction of DCA-pancreatitis, the liver experienced significant intracellular acidosis (pH(i) = 6.99 ± 0.16) and sodium loading (75 ± 9 mM) and a reduction in its energy state (β-ATP/P(i) = 0.2 ± 0.03 and P(i) = 164 ± 12). Although ip injection of PAF into healthy rats did not induce systemic hypotension, the livers under these conditions also developed severe disturbances in hepatocellular ion homeostasis and depletion of its bioenergetics. The longer the abdomen was exposed to the PAF, the worse the changes were. At 3 h after ip injection of PAF, hepatic [Na+](i) significantly increased (42 ± 3 mM) along with a significant decrease in pH(i) (7.30 ± 0.03). At 6 h after ip injection of PAF, the hepatic β- ATP/P(i) ratio decreased to 0.34 ± 0.05 and P(i) increased to 97 ± 27. Conclusions. PAF induced severe hepatocellular acidosis, rapid accumulation of hepatic intracellular sodium, impaired hepatic cytosolic phosphorylation potential, and increased hepatic utilization of ATP. These effects may account for the eventual development of liver dysfunction associated with necrotizing pancreatitis.",
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AB - Background. Multiple organ failure (MOF) is the most serious complication in severe acute pancreatitis, contributing to its high mortality. It has been suggested that changes of high-energy phosphates, intracellular pH, and intracellular cation homeostasis are closely related to hepatocellular injury associated with MOF. Methods. Phosphorus metabolites, intracellular pH (pH(i)), and intracellular Na+ concentration ([Na+](i)) were measured in rat livers in vivo using 31P and 23Na NMR spectroscopy after deoxycholic acid (DCA)induced pancreatitis or intraperitoneal injection (ip) of pancreatitis-induced ascitic fluid (PAF). Results. Two hours after induction of DCA-pancreatitis, the liver experienced significant intracellular acidosis (pH(i) = 6.99 ± 0.16) and sodium loading (75 ± 9 mM) and a reduction in its energy state (β-ATP/P(i) = 0.2 ± 0.03 and P(i) = 164 ± 12). Although ip injection of PAF into healthy rats did not induce systemic hypotension, the livers under these conditions also developed severe disturbances in hepatocellular ion homeostasis and depletion of its bioenergetics. The longer the abdomen was exposed to the PAF, the worse the changes were. At 3 h after ip injection of PAF, hepatic [Na+](i) significantly increased (42 ± 3 mM) along with a significant decrease in pH(i) (7.30 ± 0.03). At 6 h after ip injection of PAF, the hepatic β- ATP/P(i) ratio decreased to 0.34 ± 0.05 and P(i) increased to 97 ± 27. Conclusions. PAF induced severe hepatocellular acidosis, rapid accumulation of hepatic intracellular sodium, impaired hepatic cytosolic phosphorylation potential, and increased hepatic utilization of ATP. These effects may account for the eventual development of liver dysfunction associated with necrotizing pancreatitis.

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KW - Intracellular pH

KW - NMR spectroscopy

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