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[Changes of regional cerebral blood flow after total cerebral ischemia (author's transl)].

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Abstract

In normothermic 53 mongrel dogs complete cerebral circulatory arrest for 8 to 10 min was produced with Aortic occlusion balloon catheter and followed by blood recirculation of the brain for 2 hrs. Local cerebral blood flow in 11 different regions were measured before and after ischemia using radioactive labelled microspheres (15 +/- 3 micrometers). Before ischemia, regional blood flow rates within the brain varied between 26.1 +/- 5.8 and 61.3 +/- 7.9 ml/100 g/min (mean +/- SD). Reactive hyperemia was present in the brain 8 to 15 min after the beginning of the recirculation. Local cerebral blood flow rates increased two to ten times above the control flow, more increased in brain stem, cerebellum, thalamus and basal ganglia. Regional cerebral blood flow returned to or slightly below normal 30 min after ischemia, and subsequently decreased 60 to 120 min after ischemia. At 120 min after ischemia local cerebral blood flow rates decreased 40 to 60% of the control flow in cerebral cortices and basal ganglia, 70 to 90% of control flow in subcortical white matter and brain stem. With these result: 1) There is considerable redistribution and inhomogeneity of of flow rates within the brain after total cerebral ischemia for 8 to 10 min. 2) It is indicated that low flow rates of the brain 60 to 120 min after ischemia can not maintain the nutritive blood flow in some cerebral regions, especially in cerebral cortices and basal ganglia. Farther more it may be resulted in secondary brain tissue damage. 3) It is suggested that post-ischemic recirculation may be a factor in the genesis of "selective vulnerability." 4) The inhomogeneity of regional cerebral blood flow rates can be associated with the animal species of the dog.

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In normothermic 53 mongrel dogs complete cerebral circulatory arrest for 8 to 10 min was produced with Aortic occlusion balloon catheter and followed by blood recirculation of the brain for 2 hrs. Local cerebral blood flow in 11 different regions were measured before and after ischemia using radioactive labelled microspheres (15 +/- 3 micrometers). Before ischemia, regional blood flow rates within the brain varied between 26.1 +/- 5.8 and 61.3 +/- 7.9 ml/100 g/min (mean +/- SD). Reactive hyperemia was present in the brain 8 to 15 min after the beginning of the recirculation. Local cerebral blood flow rates increased two to ten times above the control flow, more increased in brain stem, cerebellum, thalamus and basal ganglia. Regional cerebral blood flow returned to or slightly below normal 30 min after ischemia, and subsequently decreased 60 to 120 min after ischemia. At 120 min after ischemia local cerebral blood flow rates decreased 40 to 60% of the control flow in cerebral cortices and basal ganglia, 70 to 90% of control flow in subcortical white matter and brain stem. With these result: 1) There is considerable redistribution and inhomogeneity of of flow rates within the brain after total cerebral ischemia for 8 to 10 min. 2) It is indicated that low flow rates of the brain 60 to 120 min after ischemia can not maintain the nutritive blood flow in some cerebral regions, especially in cerebral cortices and basal ganglia. Farther more it may be resulted in secondary brain tissue damage. 3) It is suggested that post-ischemic recirculation may be a factor in the genesis of "selective vulnerability." 4) The inhomogeneity of regional cerebral blood flow rates can be associated with the animal species of the dog.

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Available abstract

In normothermic 53 mongrel dogs complete cerebral circulatory arrest for 8 to 10 min was produced with Aortic occlusion balloon catheter and followed by blood recirculation of the brain for 2 hrs. Local cerebral blood flow in 11 different regions were measured before and after ischemia using radioactive labelled microspheres (15 +/- 3 micrometers). Before ischemia, regional blood flow rates within the brain varied between 26.1 +/- 5.8 and 61.3 +/- 7.9 ml/100 g/min (mean +/- SD). Reactive hyperemia was present in the brain 8 to 15 min after the beginning of the recirculation. Local cerebral blood flow rates increased two to ten times above the control flow, more increased in brain stem, cerebellum, thalamus and basal ganglia. Regional cerebral blood flow returned to or slightly below normal 30 min after ischemia, and subsequently decreased 60 to 120 min after ischemia. At 120 min after ischemia local cerebral blood flow rates decreased 40 to 60% of the control flow in cerebral cortices and basal ganglia, 70 to 90% of control flow in subcortical white matter and brain stem. With these result: 1) There is considerable redistribution and inhomogeneity of of flow rates within the brain after total cerebral ischemia for 8 to 10 min. 2) It is indicated that low flow rates of the brain 60 to 120 min after ischemia can not maintain the nutritive blood flow in some cerebral regions, especially in cerebral cortices and basal ganglia. Farther more it may be resulted in secondary brain tissue damage. 3) It is suggested that post-ischemic recirculation may be a factor in the genesis of "selective vulnerability." 4) The inhomogeneity of regional cerebral blood flow rates can be associated with the animal species of the dog.

Key concepts: Cerebral blood flow, Ischemia, Thalamus, Blood flow, Reactive hyperemia, Medicine, Basal ganglia, Anesthesia

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