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Alterations in cortical oxygen tension during the development of ischemic cerebral edema in primates (Macaca mulatta)
Abstract:
With a closed head primate stroke model, acute cerebral ischemia limited to the middle cerebral artery (MCA) territory was produced by macrosphere embolization of the internal carotid artery bifurcation. Measurements of the oxygen tension (PO2) at the cerebral cortical surface were obtained by continuous on-line mass spectrometry. Percentage of dry weight and tissue sodium, potassium, and chloride concentrations from ischemic and nonischemic hemispheres were determined at various times. With this preparation, we registered the precise onset of cortical surface PO2 depletion, which showed an exponential downward trend (fast component from 0 to 5 minutes, t 1/2 = 0.8 minute, rate of change = 89% per minute; slow component from 5 to 240 minutes, t 1/2 = 285 minutes, rate of change = 0.3% per minute). After the onset of cerebral ischemia, there was an immediate fall of the cortical surface PO2 with reductions of more than 45% at 5 minutes before definite hemiparesis and electroencephalographic abnormalities were recognized. During the secondary phase from 5 to 240 minutes the cortical surface PO2 fell by only an additional 23% of the steady state. Even so, when cortical surface PO2 was maintained at this critically low level, the earliest cerebral cortical edema was evident 180 minutes after MCA occlusion. Thereafter, progressive accumulation of edema fluid in the cortex (90 to 170.8 microliters per g of tissue) and in the white matter (19 to 46.2 microliter per g of tissue) was detected by the end of 240 minutes of cerebral ischemia.
Insights
Acute cerebral ischemia in primates rapidly depletes cortical oxygen. Edema formation begins within 180 minutes of middle cerebral artery occlusion, even with slow oxygen decline.
Area of Science:
- Neuroscience
- Cerebrovascular Research
- Ischemic Stroke Models
Background:
- Cerebral ischemia, particularly middle cerebral artery (MCA) occlusion, is a leading cause of stroke.
- Understanding the temporal dynamics of oxygen depletion and edema formation is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the real-time changes in cortical surface oxygen tension (PO2) following acute cerebral ischemia in a primate model.
- To determine the onset and progression of cerebral edema in relation to PO2 depletion after MCA occlusion.
Main Methods:
- A closed head primate stroke model was utilized, inducing ischemia via embolization of the internal carotid artery bifurcation to target the MCA territory.
- Continuous on-line mass spectrometry was employed to measure cortical surface PO2.
- Tissue samples were analyzed for dry weight and electrolyte concentrations (sodium, potassium, chloride) at various time points.
Main Results:
- Cortical surface PO2 depletion exhibited a biphasic exponential decay following MCA occlusion.
- A rapid initial drop of over 45% in PO2 occurred within 5 minutes, preceding clinical signs of stroke.
- Cerebral edema became evident at 180 minutes and progressively increased in both cortical and white matter by 240 minutes.
Conclusions:
- Acute cerebral ischemia leads to rapid and significant cortical oxygen depletion.
- Cerebral edema formation is a delayed but progressive consequence of ischemia, occurring even when oxygen levels stabilize at a critically low state.