Bicarbonate conservation during incomplete cerebral ischemia with superimposed hypercapnia

P. D. Hurn, Raymond C Koehler, S. E. Norris, A. E. Schwentker, R. J. Traystman

Research output: Contribution to journalArticle

Abstract

We superimposed extreme hypercapnia (arterial PCO2 400-450 mmHg) immediately before and during incomplete cerebral ischemia to distinguish the role of intracellular pH (pH(i)) and bicarbonate ([HCO3-](i)) in postischemic metabolic and electrophysiological recovery. Incomplete global ischemia was produced in seven anesthetized dogs by 30 min of intracranial hypertension followed by 4 h of reperfusion. ATP, phosphocreatine (PCr), and pH(i) were measured with 31P magnetic resonance spectroscopy, and [HCO3-](i) was calculated from the Henderson-Hasselbalch equation using the measured pH(i) and sagittal sinus PCO2. Cerebral blood flow was reduced to 7 ± 1 ml·min-1·100 g-1 (± SE) during ischemia with extreme hypercapnia, and pH(i) decreased to 5.72 ± 0.09. During normocapnic reperfusion, pH(i) rapidly returned to near baseline values by 14 min. [HCO3-](i) fell from 12.1 ± 0.9 to 6.0 ± 1.2 mM by the midpoint of ischemia and recovered by 30 min of reperfusion. ATP, PCr, and O2 consumption also recovered rapidly and completely. Somatosensory-evoked potentials (SEP) recovered to 43 ± 10% of control amplitude. These results are in marked contrast to the poor metabolic and SEP recovery previously observed in hyperglycemic dogs in which pH(i) decreased to the same range as with hypercapnic ischemia, but in which [HCO3-](i) was much lower (1.1 ± 0.5 mM). Therefore, [HCO3-](i) depletion during hyperglycemic ischemia may be a more important factor in recovery than end-ischemic pH(i) per se. We speculate that higher [HCO3-](i) may improve glial cell buffering capacity or decrease iron availability for hydroxyl radical production.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume261
Issue number3 30-3
StatePublished - 1991

Fingerprint

Hypercapnia
Bicarbonates
Brain Ischemia
Ischemia
Reperfusion
Somatosensory Evoked Potentials
Phosphocreatine
Cerebrovascular Circulation
Adenosine Triphosphate
Dogs
Intracranial Hypertension
Neuroglia
Hydroxyl Radical
Magnetic Resonance Spectroscopy
Iron

Keywords

  • Adenosine triphosphate
  • Bicarbonate ion
  • Cerebral blood flow
  • Intracellular pH
  • Magnetic resonance spectroscopy
  • Somatosensory- evoked potential

ASJC Scopus subject areas

  • Physiology

Cite this

Bicarbonate conservation during incomplete cerebral ischemia with superimposed hypercapnia. / Hurn, P. D.; Koehler, Raymond C; Norris, S. E.; Schwentker, A. E.; Traystman, R. J.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 261, No. 3 30-3, 1991.

Research output: Contribution to journalArticle

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AB - We superimposed extreme hypercapnia (arterial PCO2 400-450 mmHg) immediately before and during incomplete cerebral ischemia to distinguish the role of intracellular pH (pH(i)) and bicarbonate ([HCO3-](i)) in postischemic metabolic and electrophysiological recovery. Incomplete global ischemia was produced in seven anesthetized dogs by 30 min of intracranial hypertension followed by 4 h of reperfusion. ATP, phosphocreatine (PCr), and pH(i) were measured with 31P magnetic resonance spectroscopy, and [HCO3-](i) was calculated from the Henderson-Hasselbalch equation using the measured pH(i) and sagittal sinus PCO2. Cerebral blood flow was reduced to 7 ± 1 ml·min-1·100 g-1 (± SE) during ischemia with extreme hypercapnia, and pH(i) decreased to 5.72 ± 0.09. During normocapnic reperfusion, pH(i) rapidly returned to near baseline values by 14 min. [HCO3-](i) fell from 12.1 ± 0.9 to 6.0 ± 1.2 mM by the midpoint of ischemia and recovered by 30 min of reperfusion. ATP, PCr, and O2 consumption also recovered rapidly and completely. Somatosensory-evoked potentials (SEP) recovered to 43 ± 10% of control amplitude. These results are in marked contrast to the poor metabolic and SEP recovery previously observed in hyperglycemic dogs in which pH(i) decreased to the same range as with hypercapnic ischemia, but in which [HCO3-](i) was much lower (1.1 ± 0.5 mM). Therefore, [HCO3-](i) depletion during hyperglycemic ischemia may be a more important factor in recovery than end-ischemic pH(i) per se. We speculate that higher [HCO3-](i) may improve glial cell buffering capacity or decrease iron availability for hydroxyl radical production.

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