Sodium, atp, and intracellular ph transients during reversible complete ischemia of dog cerebrum

Scott M. Eleff, Yuichi Maruki, Lee H. Monsein, Richard J. Traystman, R. Nick Bryan, Raymond C Koehler

Research output: Contribution to journalArticle

Abstract

We tested the hypotheses that with the onset of cerebral ischemia, massive cellular sodium influx does not occur until adenosine triphosphate is fully depleted and that on reperfusion, neuronal sodium efflux does not occur until adenosine triphosphate is fully restored. We examined the temporal relationships among transcellular sodium, energy metabolism, and intracellular pH with sodium and phosphorus magnetic resonance spectroscopy in a new, hemodynamically stable, brain stem-sparing model of reversible, complete cerebral ischemia in eight anesthetized dogs. Inflation of a neck tourniquet after placement of glue at the tip of the basilar artery resulted in decreased blood flow to the cerebrum from 29±5 to 0-3±0.5 ml/min/100 g. Medullary blood flow was not significantly affected, and arterial blood pressure was unchanged. Sodium signal intensity decreased and did not lag behind the fall in adenosine triphosphate. After 12 minutes of ischemia, reperfusion resulted in a more rapid recovery of sodium intensity (12.4 ±4.8 minutes) than either adenosine triphosphate (16.5 ±3.7 minutes) or intracellular pH (38.9±1.8 minutes). Because intracellular sodium has a weaker signal than extracellular sodium, the decreased sodium intensity is interpreted as sodium influx and indicates that sodium influx does not require full depletion of adenosine triphosphate. Rapid recovery of sodium intensity during early reperfusion may represent sodium efflux, although increased plasma volume and sodium uptake from plasma may also contribute. If our interpretation of the sodium signal is correct, delayed recovery of adenosine triphosphate may be due to the utilization of adenosine triphosphate for the restoration of transcellular sodium gradient.

Original languageEnglish (US)
Pages (from-to)233-241
Number of pages9
JournalStroke
Volume22
Issue number2
StatePublished - 1991

Fingerprint

Cerebrum
Ischemia
Sodium
Dogs
Adenosine Triphosphate
Reperfusion
Brain Ischemia
Tourniquets
Basilar Artery
Plasma Volume
Economic Inflation
Adhesives
Phosphorus
Energy Metabolism
Brain Stem

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Clinical Neurology
  • Advanced and Specialized Nursing
  • Neuroscience(all)

Cite this

Eleff, S. M., Maruki, Y., Monsein, L. H., Traystman, R. J., Bryan, R. N., & Koehler, R. C. (1991). Sodium, atp, and intracellular ph transients during reversible complete ischemia of dog cerebrum. Stroke, 22(2), 233-241.

Sodium, atp, and intracellular ph transients during reversible complete ischemia of dog cerebrum. / Eleff, Scott M.; Maruki, Yuichi; Monsein, Lee H.; Traystman, Richard J.; Bryan, R. Nick; Koehler, Raymond C.

In: Stroke, Vol. 22, No. 2, 1991, p. 233-241.

Research output: Contribution to journalArticle

Eleff, SM, Maruki, Y, Monsein, LH, Traystman, RJ, Bryan, RN & Koehler, RC 1991, 'Sodium, atp, and intracellular ph transients during reversible complete ischemia of dog cerebrum', Stroke, vol. 22, no. 2, pp. 233-241.
Eleff SM, Maruki Y, Monsein LH, Traystman RJ, Bryan RN, Koehler RC. Sodium, atp, and intracellular ph transients during reversible complete ischemia of dog cerebrum. Stroke. 1991;22(2):233-241.
Eleff, Scott M. ; Maruki, Yuichi ; Monsein, Lee H. ; Traystman, Richard J. ; Bryan, R. Nick ; Koehler, Raymond C. / Sodium, atp, and intracellular ph transients during reversible complete ischemia of dog cerebrum. In: Stroke. 1991 ; Vol. 22, No. 2. pp. 233-241.
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