Effects of ischemia on intracellular sodium and phosphates in the
in vivo rat liver.
Xia, Zhao-Fan, Jureta W. Horton, Pi-Yu Zhao, Evelyn E. Babcock, A.
Dean Sherry, Craig R. Malloy.
Department of Surgery, Mary Nell and Ralph B. Rogers Magnetic
Resonance Center (Department of Radiology), Department of Internal
Medicine (Cardiology Division), Department of Veterans Affairs
Medical Center, Dallas, Texas, University of Texas Southwestern
Medical Centers, Dallas, Texas, Department of Chemistry, University
of Texas at Dallas, Richardson, Texas and the: Research Institute of
Burn and Trauma, Changhai Hospital, Shanghai, China
APStracts 3:0246A, 1996.
Metabolic factors which influence the transition from reversible to
irre versible ischemic injury were studied in the rat liver in vivo
using 31P NMR spectroscopy. Hepatic ischemia for 15, 35 or 65 minutes
was produced by oc clusion of the hepatic artery and portal vein in
rats. Ischemia caused a rapid decrease in [ATP]/[Pi] and pH within 5
minutes, but there was little change in these variables detectable by
31P NMR with longer periods of ischemia. After reperfusion, the [ATP]
and [Pi] returned towards normal in livers exposed to 15 or 35
minutes of ischemia, but 65 min of ischemia was associated with only
modest recovery in [ATP], and the [ATP] later decreased. Since the
31P NMR spectrum was similar after brief compared to prolonged
ischemia, it appears that neither ATP depletion, Pi accumulation nor
acidosis predict metabolic recovery. Hepatic intracellular sodium was
also measured in separate groups of animals by 23Na NMR in the
presence of a shift agent, thulium (III) 1,4,7,10
-tetraazacyclododecane- N',N'',N'''tetramethylenephosphonate (TmDOTP5
-), and by atomic absorption spectroscopy (AAS). Under baseline
conditions, the concentration of intra cellular sodium [Na+]i was
15.2 mM by AAS and 16.5 mM by 23Na NMR. Although the 31P NMR spectrum
responded very rapidly to the onset of ischemia, [Na+]i measured by
23Na NMR increased gradually but steadily at about 1.0 mM/min during
early (up to 15 minutes) ischemia. These observations demonstrate
that a rise in intracellular sodium does occur during early ischemia,
that TmDOTP5- can be applied in vivo for analysis of intracellular
sodium in the ischemic liver, and that 31P NMR spectroscopy is very
sensitive to early ischemic injury.
Received 9 June 1995; accepted in final form 24 April 1996.
APS Manuscript Number A614-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 28 May 96