Recovery of the Cortical Evoked Response Following Temporary Middle Cerebral Artery Occlusion in Baboons: Relation to Local Blood Flow and Po2

The degree of recovery of the somatosensory cortical evoked response following a period (15 to 65 minutes) of partial ischemia, produced by temporary occlusion of the middle cerebral artery (MCA), was assessed in baboons and related to the local tissue blood flow and Pth before, during and after the occlusion. Flow was measured using the technique of two-minute hydrogen clearance. Failure of complete recovery of the evoked response was associated with significantly greater depths of ischemia and tissue hypoxia during occlusion, and with significantly greater and persisting tissue hypoxia after occlusion, than complete recovery. Complete recovery of the eioked response also was associated with tissue hyperoxia after occlusion. The reduced postocclusive Po2 levels associated with incomplete recovery of the evoked response suggest that reduced perfusion during ischemia was sufficiently severe to cause some degree of irreversible anoxic damage. The effect of a brief (three to ten minutes) period of ventilation with air (instead of oxygen) under such low-now conditions was to depress the evoked response significantly further; normally perfused brain, however, was unaffected by this procedure. This finding has clinical implications in regard to normobaric oxygen therapy.

[1]  K. Hossmann,et al.  The role of cerebral blood flow for the recovery of the brain after prolonged ischemia , 2004, Zeitschrift für Neurologie.

[2]  L. Symon,et al.  Measurements of oxygen tension in the cerebral cortex of baboons , 1976, Journal of the Neurological Sciences.

[3]  L. Symon,et al.  Changes in regional cortical tissue oxygen tension and cerebral blood flow during temporary middle cerebral artery occlusion in baboons , 1976, Journal of the Neurological Sciences.

[4]  L. Symon,et al.  Relationship between the cortical evoked potential and local cortical blood flow following acute middle cerebral artery occlusion in the baboon. , 1974, Experimental neurology.

[5]  L. Salford,et al.  The influence of arterial hypoxia and unilateral carotid artery occlusion upon regional blood flow and metabolism in the rat brain. , 1974, Acta physiologica Scandinavica.

[6]  R. Ratcheson,et al.  Cerebral metabolic state following complete compression ischemia. , 1974, Brain research.

[7]  B. Siesjö,et al.  Effect of ischemia on monoamine metabolism in the brain. , 1974, Acta physiologica Scandinavica.

[8]  F. Plum The clinical problem: how much anoxia-ischemia damages the brain? , 1973, Archives of neurology.

[9]  J. Hartmann,et al.  Disaggregation of Polyribosomes in Intact Gerbils Following Ischemia. An Ultrastructural Study , 1973, Stroke.

[10]  L. Symon,et al.  The Hydrogen Clearance Method in Assessment of Blood Flow in Cortex, White Matter and Deep Nuclei of Baboons , 1973, Stroke.

[11]  F. Plum,et al.  Pathophysiology of Anoxic Brain Damage , 1973 .

[12]  G. Boysen,et al.  Relation between EEG, regional cerebral blood flow and internal carotid artery pressure during carotid endarterectomy. , 1973, Electroencephalography and clinical neurophysiology.

[13]  U. Müller,et al.  Metabolism and function of dog's brain recovering from longtime ischemia. , 1972, The American journal of physiology.

[14]  J. Ganz,et al.  Experimental studies of hyperaemic phenomena in the cerebral circulation of primates. , 1972, Brain : a journal of neurology.

[15]  F. Regli,et al.  Effects of Inhalation of Oxygen on Blood Flow and Microvasculature of Ischemic and Nonischemic Cerebral Cortex , 1970, Stroke.

[16]  K. Hossmann,et al.  Recovery of Neuronal Function after Prolonged Cerebral Ischemia , 1970, Science.

[17]  N. Zwetnow Effects of increased cerebrospinal fluid pressure on the blood flow and on the energy metabolism of the brain. An experimental study. , 1970, Acta physiologica Scandinavica. Supplementum.

[18]  A. G. Waltz Red venous blood: occurrence and significance in ischemic and nonischemic cerebral cortex. , 1969, Journal of neurosurgery.

[19]  O. L. Davies,et al.  Statistical Methods. 6th Edition. , 1968 .

[20]  N. Lassen,et al.  The luxury-perfusion syndrome and its possible relation to acute metabolic acidosis localised within the brain. , 1966, Lancet.

[21]  C F SCHMIDT,et al.  Oxygen toxicity; effects in man of oxygen inhalation at 1 and 3.5 atmospheres upon blood gas transport, cerebral circulation and cerebral metabolism. , 1953, Journal of applied physiology.

[22]  S. Kety,et al.  THE EFFECTS OF ALTERED ARTERIAL TENSIONS OF CARBON DIOXIDE AND OXYGEN ON CEREBRAL BLOOD FLOW AND CEREBRAL OXYGEN CONSUMPTION OF NORMAL YOUNG MEN. , 1948, The Journal of clinical investigation.

[23]  R. Grenell Central nervous system resistance; the effects of temporary arrest of cerebral circulation for periods of two to ten minutes. , 1946, Journal of neuropathology and experimental neurology.

[24]  R. Grenell Central Nervous System ResistanceI. The Effects of Temporary Arrest of Cerebral Circulation for Periods of Two to Ten Minutes , 1946 .

[25]  H. Kabat,et al.  RECOVERY OF FUNCTION FOLLOWING ARREST OF THE BRAIN CIRCULATION , 1941 .

[26]  J. H. Gibbon,et al.  TEMPORARY ARREST OF THE CIRCULATION TO THE CENTRAL NERVOUS SYSTEM: II. PATHOLOGIC EFFECTS , 1940 .