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 language | English (US) |
|---|---|
| Journal | American Journal of Physiology - Heart and Circulatory Physiology |
| Volume | 267 |
| Issue number | 5 36-5 |
| State | Published - 1994 |
| Externally published | Yes |
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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 journal › Article
}
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
C2 - 7977818
AN - SCOPUS:0028019474
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 -