Hypoxic reperfusion after ischemia in swine does not improve acute brain recovery

J. A. Ulatowski, Jeffrey Kirsch, R. J. Traystman

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

We tested the hypothesis that transient hypoxic reperfusion after 15 min of global cerebral ischemia would improve acute recovery of electrical function. We also determined the changes in cerebral blood flow (CBF) and cerebral oxygen consumption (CMR(O2)) during transient hypoxic reperfusion. Pentobarbital-anesthetized pigs were exposed to cerebral ischemia by raising intracranial pressure to 100 mmHg above arterial pressure with rapid infusion of artificial cerebral spinal fluid into a lateral ventricle. During the reperfusion period, normoxia was maintained at an arterial oxygen partial pressure (Pa(O2)) of 80-120 mmHg for 120 min of reperfusion and hypoxia at a Pa(O2) of 35-45 mmHg for the first 30 min of reperfusion in another group. The postischemic hypoxia group showed persistent elevation in microsphere- determined CBF at 30 min of reperfusion in all brain regions and lack of delayed hypoperfusion through 120 min of reperfusion. The normoxic group demonstrated transient postischemic hyperemia and hypoperfusion. CMR(O2) was not significantly different between groups at any time point. In both groups, the somatosensory-evoked potential amplitude reached only 10% recovery by the end of 120 min of reperfusion. We conclude that hypoxemia during reperfusion after cerebral ischemia in this model does not improve acute brain electrical function and prolongs postischemic hyperemia.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume267
Issue number5 36-5
StatePublished - 1994
Externally publishedYes

Fingerprint

ischemia
Reperfusion
hypoxia
Swine
Ischemia
brain
blood flow
swine
Brain
pentobarbital
evoked potentials
normoxia
Cerebrovascular Circulation
Brain Ischemia
oxygen consumption
Hyperemia
oxygen
Somatosensory Evoked Potentials
Partial Pressure
Lateral Ventricles

Keywords

  • cerebral blood flow
  • cerebral oxygen consumption
  • elevated intracranial pressure
  • hypoxia
  • ischemia-reperfusion
  • somatosensory-evoked potentials

ASJC Scopus subject areas

  • Physiology
  • Agricultural and Biological Sciences(all)

Cite this

Hypoxic reperfusion after ischemia in swine does not improve acute brain recovery. / Ulatowski, J. A.; Kirsch, Jeffrey; Traystman, R. J.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 267, No. 5 36-5, 1994.

Research output: Contribution to journalArticle

@article{789bd197ea2b4332870bc21240c6d103,
title = "Hypoxic reperfusion after ischemia in swine does not improve acute brain recovery",
abstract = "We tested the hypothesis that transient hypoxic reperfusion after 15 min of global cerebral ischemia would improve acute recovery of electrical function. We also determined the changes in cerebral blood flow (CBF) and cerebral oxygen consumption (CMR(O2)) during transient hypoxic reperfusion. Pentobarbital-anesthetized pigs were exposed to cerebral ischemia by raising intracranial pressure to 100 mmHg above arterial pressure with rapid infusion of artificial cerebral spinal fluid into a lateral ventricle. During the reperfusion period, normoxia was maintained at an arterial oxygen partial pressure (Pa(O2)) of 80-120 mmHg for 120 min of reperfusion and hypoxia at a Pa(O2) of 35-45 mmHg for the first 30 min of reperfusion in another group. The postischemic hypoxia group showed persistent elevation in microsphere- determined CBF at 30 min of reperfusion in all brain regions and lack of delayed hypoperfusion through 120 min of reperfusion. The normoxic group demonstrated transient postischemic hyperemia and hypoperfusion. CMR(O2) was not significantly different between groups at any time point. In both groups, the somatosensory-evoked potential amplitude reached only 10{\%} recovery by the end of 120 min of reperfusion. We conclude that hypoxemia during reperfusion after cerebral ischemia in this model does not improve acute brain electrical function and prolongs postischemic hyperemia.",
keywords = "cerebral blood flow, cerebral oxygen consumption, elevated intracranial pressure, hypoxia, ischemia-reperfusion, somatosensory-evoked potentials",
author = "Ulatowski, {J. A.} and Jeffrey Kirsch and Traystman, {R. J.}",
year = "1994",
language = "English (US)",
volume = "267",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "5 36-5",

}

TY - JOUR

T1 - Hypoxic reperfusion after ischemia in swine does not improve acute brain recovery

AU - Ulatowski, J. A.

AU - Kirsch, Jeffrey

AU - Traystman, R. J.

PY - 1994

Y1 - 1994

N2 - We tested the hypothesis that transient hypoxic reperfusion after 15 min of global cerebral ischemia would improve acute recovery of electrical function. We also determined the changes in cerebral blood flow (CBF) and cerebral oxygen consumption (CMR(O2)) during transient hypoxic reperfusion. Pentobarbital-anesthetized pigs were exposed to cerebral ischemia by raising intracranial pressure to 100 mmHg above arterial pressure with rapid infusion of artificial cerebral spinal fluid into a lateral ventricle. During the reperfusion period, normoxia was maintained at an arterial oxygen partial pressure (Pa(O2)) of 80-120 mmHg for 120 min of reperfusion and hypoxia at a Pa(O2) of 35-45 mmHg for the first 30 min of reperfusion in another group. The postischemic hypoxia group showed persistent elevation in microsphere- determined CBF at 30 min of reperfusion in all brain regions and lack of delayed hypoperfusion through 120 min of reperfusion. The normoxic group demonstrated transient postischemic hyperemia and hypoperfusion. CMR(O2) was not significantly different between groups at any time point. In both groups, the somatosensory-evoked potential amplitude reached only 10% recovery by the end of 120 min of reperfusion. We conclude that hypoxemia during reperfusion after cerebral ischemia in this model does not improve acute brain electrical function and prolongs postischemic hyperemia.

AB - We tested the hypothesis that transient hypoxic reperfusion after 15 min of global cerebral ischemia would improve acute recovery of electrical function. We also determined the changes in cerebral blood flow (CBF) and cerebral oxygen consumption (CMR(O2)) during transient hypoxic reperfusion. Pentobarbital-anesthetized pigs were exposed to cerebral ischemia by raising intracranial pressure to 100 mmHg above arterial pressure with rapid infusion of artificial cerebral spinal fluid into a lateral ventricle. During the reperfusion period, normoxia was maintained at an arterial oxygen partial pressure (Pa(O2)) of 80-120 mmHg for 120 min of reperfusion and hypoxia at a Pa(O2) of 35-45 mmHg for the first 30 min of reperfusion in another group. The postischemic hypoxia group showed persistent elevation in microsphere- determined CBF at 30 min of reperfusion in all brain regions and lack of delayed hypoperfusion through 120 min of reperfusion. The normoxic group demonstrated transient postischemic hyperemia and hypoperfusion. CMR(O2) was not significantly different between groups at any time point. In both groups, the somatosensory-evoked potential amplitude reached only 10% recovery by the end of 120 min of reperfusion. We conclude that hypoxemia during reperfusion after cerebral ischemia in this model does not improve acute brain electrical function and prolongs postischemic hyperemia.

KW - cerebral blood flow

KW - cerebral oxygen consumption

KW - elevated intracranial pressure

KW - hypoxia

KW - ischemia-reperfusion

KW - somatosensory-evoked potentials

UR - http://www.scopus.com/inward/record.url?scp=0028019474&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028019474&partnerID=8YFLogxK

M3 - Article

VL - 267

JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

SN - 1931-857X

IS - 5 36-5

ER -