Abstract
No simple hypothesis was advanced to explain the relationship between CBF [cerebral blood flow] and cerebral metabolism [in the human and bovine]. The pH hypothesis cannot explain all the experimental observations. The problems remaining are those of methodology. Much of the experimental work quoted depends on results obtained on pial vessels, vessels from tissues other than brain, or from large arteries such as the carotid or the middle cerebral. There are very few results of measurements of parenchymal flow, as methods for measuring local flow and simultaneous chemical changes will cause tissue damage. The value of observations made in transient states is emerging, and also of the potential of small-ion specific micro-electrodes in brain tissue. It seems unlikely at present that any unified hypothesis to explain the chemical control of CBF will depend upon a single stimulus.

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