Pathological aspects of brain transport phenomena.
The aim of this paper has been to review and discuss the past and the recent investigations concerned with the study of cerebral transport phenomena in pathological conditions which have been divided into two main parts: (1) the effects of experimentally induced blood brain barrier (BBB) injury by (a) HgCl2 or (b) hyper-osmolar intracarotic perfusate; and (2) the effects of ischemia or of an altered oxygen saturation and pCO2 tension on glucose and/or amino acids and/or protein transport across the BBB, in the syanptosomes and cerebral capillaries. The most important observations were as follows: (1) HgCl2 or hyperosmolar perfusates produced an increased BBB permeability to protein tracers but the brain uptake of glucose analogues was found decreased following the former, and increased (except for lactamide) after the latter treatment. (2) (a) In ischemia, the noted increased vesicular transport of peroxidase, as well as the increased saturable and non-saturable passage of glucose analogues across the BBB depended on the duration of cerebral deprivation of blood supply which never resulted in degeneration of endothelial cells of the brain vessels. (b) The progressively decreased specific 2-deoxy-D-glucose uptake in the synaptosomes seen during cerebral ischemia of 30-180 minutes returned to the level of controls 1 hour after reestablishment of cerebral circulation. (c) A decrease in brain uptake of glucose analogues and amino acids (with few exceptions) was observed in severe hypoxia and hypercapnia while an increase or no change in the brain uptakes was seen in hypocapnia. (d) Preliminary investigations of the 2-DG uptake by the cerebral capillaries obtained by fractionation of the brain from animals subjected to normal or altered oxygen saturation and pCO2 tension suggested that cerebral glucose uptake may be directly related to its capillary function.
D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D001812:Blood-Brain Barrier / Q000187:drug effects*; D001921:Brain / Q000378:metabolism*; D002245:Carbon Dioxide / Q000494:pharmacology; D002463:Cell Membrane Permeability / Q000187:drug effects; D003847:Deoxyglucose / Q000378:metabolism; D004727:Endothelium / Q000187:drug effects / Q000378:metabolism; D005070:Evans Blue; D005947:Glucose / Q000378:metabolism; D006601:Hexoses / Q000378:metabolism; D006935:Hypercapnia / Q000378:metabolism; D006982:Hypertonic Solutions / Q000494:pharmacology*; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D008628:Mercury / Q000494:pharmacology*; D010100:Oxygen / Q000494:pharmacology; D010544:Peroxidases / Q000378:metabolism; D013574:Synaptosomes / Q000187:drug effects / Q000378:metabolism
D000596:Amino Acids; D006601:Hexoses; D006982:Hypertonic Solutions; D002245:Carbon Dioxide; D005070:Evans Blue; D003847:Deoxyglucose; D010544:Peroxidases; D008628:Mercury; D005947:Glucose; D010100:Oxygen