Delayed postischemic hypoperfusion

Cerebral blood flow (CBF) was assessed with radioactive butanol and antipyrine during and after 1 hour of unilateral carotid artery occlusion in gerbils. Animals with clinical evidence of stroke demonstrated a marked fall in ipsilateral CBF during occlusion “no-reflow” phenomenon did not develop; instead, blood flow returned to normal 5 minutes after the termination of carotid occlusion. Flow subsequently fell to half the control value, however, and remained depressed for several hours despite increased local metabolic demands. This delayed imbalance in energy supply and demand creates a potential for additional brain damage that might be prevented by appropriate therapeutic intervention.

[1]  J. Dougherty,et al.  Experimental cerebral ischemia produces platelet aggregates , 1979, Neurology.

[2]  F. Plum,et al.  Ischaemic brain damage in the gerbil in the absence of 'no-reflow'. , 1975, Journal of neurology, neurosurgery, and psychiatry.

[3]  K. Welch,et al.  Catecholamine and 5‐Hydroxytryptamine Levels in Ischemic Brain: Influence of p‐Chlorophenylalanine , 1977, Stroke.

[4]  K. Hossmann,et al.  Studies on the pathogenesis of ischemic brain damage and the mechanism of its amelioration by thiopental. , 1977, Acta neurologica Scandinavica. Supplementum.

[5]  M. Reivich,et al.  Local glucose utilization in acute focal cerebral ischemia , 1977, Neurology.

[6]  R. Busto,et al.  Energy metabolites and water content in rat brain during the early stage of development of cerebral infarction. , 1974, Brain : a journal of neurology.

[7]  P. Prosenz.  Investigations on the filter capacity of the dog's brain. A contribution to the question of cerebral arteriovenous shunts. , 1972, Archives of neurology.

[8]  P. Safar,et al.  Global Ischemia in Dogs: Intracranial Pressures, Brain Blood Flow and Metabolism , 1975, Stroke.

[9]  J. Brierley,et al.  The nature, distribution and earliest stages of anoxic-ischaemic nerve cell damage in the rat brain as defined by the optical microscope. , 1968, British journal of experimental pathology.

[10]  M. Reivich,et al.  Diaschisis with Cerebral Infarction , 1977, Stroke.

[11]  J. Hallenbeck,et al.  Prevention of postischemic impairment of microvascular perfusion , 1977, Neurology.

[12]  A. Smith.  Barbiturate protection in cerebral hypoxia. , 1977, Anesthesiology.

[13]  K. Welch,et al.  Critical cerebral blood flow for production of hemiparesis after unilateral carotid occlusion in the gerbil. , 1977, Journal of neurology, neurosurgery, and psychiatry.

[14]  R. Osburne,et al.  Cerebral blood flow. A predictor of recovery from ischemia in the gerbil. , 1975, Archives of neurology.

[15]  T. Duffy,et al.  CEREBRAL ENERGY METABOLISM DURING TRANSIENT ISCHEMIA AND RECOVERY IN THE GERBIL 1 , 1977, Journal of neurochemistry.

[16]  J. Brierley,et al.  Delayed pentobarbital administration limits ischemic brain damage in gerbils , 1979, Annals of neurology.

[17]  N. Lassen,et al.  Regional Cerebral Blood Flow in the Rat Measured by the Tissue Sampling Technique; a Critical Evaluation Using Four Indicators C14‐Antipyrine, C14‐Ethanol H3‐Water and Xenon133 , 1974 .

[18]  Vascular and neuronal factors in diaschisis with focal cerebral ischemia. , 1966, Research publications - Association for Research in Nervous and Mental Disease.

[19]  K. Hossmann,et al.  Cerebral Uptake of Glucose and Oxygen in the Cat Brain After Prolonged Ischemia , 1976 .

[20]  M E Raichle,et al.  Correlation Between Regional Cerebral Blood Flow and Oxidative Metabolism: In Vivo Studies in Man , 1976 .

[21]  藤本 司.  Pathophysiologic aspects of ischemic edema , 1977 .

[22]  R. V. Van Uitert,et al.  Regional Brain Blood Flow in the Conscious Gerbil , 1978, Stroke.