Intracellular pH during reperfusion influences evoked potential recovery after complete cerebral ischemia

Yuichi Maruki, Raymond C. Koehler, Scott M. Eleff, Richard J. Traystman

Research output: Contribution to journalArticle

Abstract

Background and Purpose: Increasing ischemic duration delays recovery of intracellular pH and depresses recovery of somatosensory evoked potentials. We tested whether manipulation of the rate of pH recovery influences evoked potential recovery after complete ischemia. Methods: Four groups of eight anesthetized dogs underwent 12 minutes of complete ischemia followed by 4 hours of reperfusion with either 1) normocapnia, 2) normocapnia and acetazolamide (25 mg/kg at reperfusion plus 12.5 mg/kg per hour, 3) hypocapnia, or 4) hypercapnia. Intracellular pH was measured by phosphorus magnetic resonance spectroscopy, and intracellular bicarbonate was calculated using sagittal sinus partial pressure of CO2 during reperfusion. Results: In the normocapnic control group, intracellular pH decreased from 7.10�±0.04 (�±SEM) to 6.13�±0.08 during ischemia and recovered to 6.90�±0.08 by 30 minutes of reperfusion. Bicarbonate also largely recovered (9.9�±1.6 mM). With acetazolamide pH (6.51�±0.10) and estimated bicarbonate (4.8+1.3 mM) remained depressed at 30 minutes and did not fully recover until 60-75 minutes. However, percent recovery of somatosensory evoked potential amplitude at 4 hours of reperfusion was less with acetazolamide (23�±4%) than in the control group (52�±5%). With hypercapnic reperfusion, which delayed pH recovery but not bicarbonate recovery, evoked potential recovery was also depressed (27�±5%). With hypocapnic reperfusion, which delayed bicarbonate recovery but not pH recovery, evoked potential recovery (52�±6%) was not depressed compared with controls. Recovery of adenosine triphosphate and oxygen consumption was similar among groups. Conclusions: Delayed recovery of intracellular pH with or without delayed recovery of bicarbonate during reperfusion further impairs somatosensory evoked potential recovery independent of recovery of highenergy phosphates. Persistence of acidosis during reperfusion can contribute to postischemic electrophysiological deficit.

Original languageEnglish (US)
Pages (from-to)697-703
Number of pages7
JournalStroke
Volume24
Issue number5
DOIs
StatePublished - May 1993

Keywords

  • Acetazolamide
  • Acidosis
  • Cerebral ischemia
  • Dogs

ASJC Scopus subject areas

  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine
  • Advanced and Specialized Nursing

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