The blood-brain barrier in hypoxia: ultrastructural aspects and adenylate cyclase activity of brain capillaries.
The ultrastructure of brain microvessels, their permeability to serum albumin, the activities of some endothelial enzymes and the effect of histamine were investigated in rats after a prolonged hypobaric-hypoxic treatment. After prolonged hypoxia, the permeation of serum albumin into endothelial cells increased together with the number of pinocytotic vesicles of the endothelium. Intracarotid histamine stimulated this process even further, and its effect was mediated by H2-histamine receptors. After hypoxia the specific activity of capillary alkaline phosphatase and gamma-glutamyl transpeptidase remained unchanged, while that of adenylate cyclase was greatly increased. Histamine did not modify the structure of tight junctions of isolated capillaries of normoxic animals. Both hypoxia- and histamine-induced modification of the brain microvessels were accompanied by an increase of pinocytosis, which may be stimulated by the activation of capillary adenylate cyclase.
D000818:Animals; D001812:Blood-Brain Barrier; D001921:Brain / Q000098:blood supply*; D002196:Capillaries / Q000648:ultrastructure; D002534:Hypoxia, Brain / Q000473:pathology* / Q000503:physiopathology; D007365:Intercellular Junctions / Q000648:ultrastructure; D008297:Male; D008854:Microscopy, Electron; D010873:Pinocytosis; D051381:Rats; D011919:Rats, Inbred Strains; D011970:Receptors, Histamine H2 / Q000502:physiology; D012709:Serum Albumin / Q000378:metabolism
D011970:Receptors, Histamine H2; D012709:Serum Albumin