Magnetic resonance imaging temporarily alters blood-brain barrier permeability in the rat.
Exposure to a short (23.2 min) standard clinical magnetic resonance imaging (MRI) procedure elicits a temporary dysfunction of the blood-brain barrier in rats. Monitoring of the increased permeability of rat brain frontal cortex microvessels with the protein tracer horseradish peroxidase and freeze-fracture electron microscopy, revealed an amplified vesicle-mediated transport of tracer across the microvessel endothelium to the albuminal basal lamina and extracellular compartment of the brain parenchyma. Recovery of normal blood-brain function, as evidenced by exclusion of protein tracer from subendothelial basal lamina and neuropil extracellular milieu, was complete 15-30 min following cessation of the MRI exposure. These findings raise the possibility that exposure to clinical MRI procedures may also temporarily alter central blood-brain permeability in human subjects.
D000818:Animals; D001812:Blood-Brain Barrier; D001921:Brain / Q000098:blood supply; D001927:Brain Diseases / Q000209:etiology*; D002196:Capillaries / Q000648:ultrastructure; D004727:Endothelium / Q000648:ultrastructure; D007365:Intercellular Junctions / Q000648:ultrastructure; D009682:Magnetic Resonance Spectroscopy / Q000009:adverse effects*; D008297:Male; D008854:Microscopy, Electron; D051381:Rats; D011919:Rats, Inbred Strains