Acidic foci within the ischemic penumbra of the new zealand white rabbit

Francis H. Tomlinson, Robert E. Anderson, Fredric B. Meyer

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Background and Purpose: In vivo panoramic imaging of reduced nicotinamide adenine dinucleotide (NADH), intracellular brain pH (pHi), and cortical blood flow was used to characterize the ischemic penumbra during focal ischemia. During global ischemia, hypoxia, and status epilepticus, the development of cortical acidic foci has been observed. The hypothesis tested was that during focal ischemia, acidic foci develop, which may lead to recruitment of the ischemic penumbra into infarction. Methods: Five fasted New Zealand White rabbits underwent middle cerebral artery (MCA) occlusion under 1.5% halothane anesthesia through a retro-orbital approach, and five animals served as controls. Brain pHi and cerebral blood flow were measured with in vivo umbelliferone fluorescence. Results: Baseline brain pHi was 6.98 ± 0.05, whereas cortical blood flow and NADH fluorescence measured 52.2 ± 8.7 mL/100 g per minute and 35.5 ± 3.7 gray-scale units, respectively. Fifteen minutes after MCA occlusion, overall brain pHi and cortical blood flow of the ischemic penumbra measured 6.61 ± 0.06 and 31.9 ± 9.2 mL/100 g per minute. Over 3 hours there was normalization of pHi in the majority of the penumbra due to increases in cortical blood flow. Within the ischemic penumbra acidic foci developed with an initial pHi of 6.35 ± 0.09 and cortical blood flow of 18.0 ± 5.7 mL/100 g per minute. These foci remained acidic with increased NADH fluorescence despite being surrounded by cortex that was recovering from ischemia. On light microscopy, these acidic foci had a mixed pattern of neuronal injury. Conclusions: Within the ischemic penumbra, acidic foci develop that do not follow a vascular distribution and have microscopic evidence of ischemic neuronal injury. This suggests that there is a cortical selective vulnerability regarding pHi regulation and these acidic foci may lead to recruitment of the ischemic penumbra into infarction.

Original languageEnglish (US)
Pages (from-to)2030-2039
Number of pages10
JournalStroke
Volume24
Issue number12
StatePublished - 1993
Externally publishedYes

Fingerprint

NAD
Rabbits
Ischemia
7-hydroxycoumarin
Fluorescence
Middle Cerebral Artery Infarction
Brain
Infarction
Cerebrovascular Circulation
Radiation Dosage
Status Epilepticus
Wounds and Injuries
Halothane
Blood Vessels
Microscopy
Anesthesia
Light

Keywords

  • Cerebral blood flow
  • Cerebral ischemia
  • Neuronal damage
  • Rabbits

ASJC Scopus subject areas

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

Cite this

Tomlinson, F. H., Anderson, R. E., & Meyer, F. B. (1993). Acidic foci within the ischemic penumbra of the new zealand white rabbit. Stroke, 24(12), 2030-2039.

Acidic foci within the ischemic penumbra of the new zealand white rabbit. / Tomlinson, Francis H.; Anderson, Robert E.; Meyer, Fredric B.

In: Stroke, Vol. 24, No. 12, 1993, p. 2030-2039.

Research output: Contribution to journalArticle

Tomlinson, FH, Anderson, RE & Meyer, FB 1993, 'Acidic foci within the ischemic penumbra of the new zealand white rabbit', Stroke, vol. 24, no. 12, pp. 2030-2039.
Tomlinson FH, Anderson RE, Meyer FB. Acidic foci within the ischemic penumbra of the new zealand white rabbit. Stroke. 1993;24(12):2030-2039.
Tomlinson, Francis H. ; Anderson, Robert E. ; Meyer, Fredric B. / Acidic foci within the ischemic penumbra of the new zealand white rabbit. In: Stroke. 1993 ; Vol. 24, No. 12. pp. 2030-2039.
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AU - Meyer, Fredric B.

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AB - Background and Purpose: In vivo panoramic imaging of reduced nicotinamide adenine dinucleotide (NADH), intracellular brain pH (pHi), and cortical blood flow was used to characterize the ischemic penumbra during focal ischemia. During global ischemia, hypoxia, and status epilepticus, the development of cortical acidic foci has been observed. The hypothesis tested was that during focal ischemia, acidic foci develop, which may lead to recruitment of the ischemic penumbra into infarction. Methods: Five fasted New Zealand White rabbits underwent middle cerebral artery (MCA) occlusion under 1.5% halothane anesthesia through a retro-orbital approach, and five animals served as controls. Brain pHi and cerebral blood flow were measured with in vivo umbelliferone fluorescence. Results: Baseline brain pHi was 6.98 ± 0.05, whereas cortical blood flow and NADH fluorescence measured 52.2 ± 8.7 mL/100 g per minute and 35.5 ± 3.7 gray-scale units, respectively. Fifteen minutes after MCA occlusion, overall brain pHi and cortical blood flow of the ischemic penumbra measured 6.61 ± 0.06 and 31.9 ± 9.2 mL/100 g per minute. Over 3 hours there was normalization of pHi in the majority of the penumbra due to increases in cortical blood flow. Within the ischemic penumbra acidic foci developed with an initial pHi of 6.35 ± 0.09 and cortical blood flow of 18.0 ± 5.7 mL/100 g per minute. These foci remained acidic with increased NADH fluorescence despite being surrounded by cortex that was recovering from ischemia. On light microscopy, these acidic foci had a mixed pattern of neuronal injury. Conclusions: Within the ischemic penumbra, acidic foci develop that do not follow a vascular distribution and have microscopic evidence of ischemic neuronal injury. This suggests that there is a cortical selective vulnerability regarding pHi regulation and these acidic foci may lead to recruitment of the ischemic penumbra into infarction.

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