Inhibition of ion transport in septic rat heart: 133cs+ as an nmr
active k+ analog.
Schornack, Paul A., Sheng-Kwei Song, Richard Hotchkiss, and Joseph J.
H. Ackerman.
Department of Chemistry, Washington University, One Brookings
Drive, St. Louis, MO 63130-4899, and Departments of Anesthesiology,
Medicine,and Radiology, Washington University School of Medicine, 660
South Euclid Avenue, St. Louis, MO 63110-1093
APStracts 3:0411C, 1996.
Sepsis, the systemic response to severe infection, and the resulting
multiorgan failure it induces are major contributors to intensive
care unit morbidity and mortality. A number of abnormalities in ion
transport processes and intracellular free sodium, [Na+]i, and
potassium, [K+]i, concentrations have been reported to occur during
sepsis/endotoxemia. An effect of sepsis on the Na+/K+ ATPase may be
an important contribution to changes in intracellular ion balance and
the resultant pathophysiology of the disorder. The purpose of this
study was to examine the effect of sepsis on the Na+/K+ ATPase in the
isolated perfused rat heart using 133Cs nuclear magnetic resonance,
NMR. Cs+ is a K+ analog and 133Cs NMR offers the opportunity of
examining Na+/K+ ATPase activity in the intact organ via tracer
kinetics. Sepsis was induced in halothane anesthetized male Sprague
-Dawley rats using the cecal-ligation and perforation, CLP, model.
Twenty-four to thirty-six hours after surgery, hearts from CLP or
sham-operated rats were perfused with Krebs-Henseleit buffer
containing 1.25 mM Cs+. The influx rate constant for Cs+ was
decreased by 24% in septic rat hearts, i.e., 0.25 +/- 0.08 SD min-1
for controls and 0.19 +/- 0.04 SD min-1 for septic, p = 0.003. There
was no difference for Cs+ efflux (0.005 +/- 0.001 SD min-1 for
controls and 0.005 +/- 0.002 SD min-1 for septic, p = 0.8). These
results are consistent with an inhibition of the Na+/K+ ATPase pump
during sepsis/endotoxemia. A decrease in the activity of the Na+/K+
ATPase pump may be responsible for or contribute to the changes in
[Na+]i and [K+]i during the disorder.
Received 2 November 1994; accepted in final form 15 November
1996.
APS Manuscript Number C654-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996