Acute effects of calvarial damage on dural mast cells, pial vascular permeability, and cerebral cortical histamine levels in rats and mice.
Neurological complications after mild head injury can include vasogenic edema and/or subsequent development of epilepsy, conditions associated with elevated histamine. In the present study we assessed the potential of mast cells located in the dura mater to contribute to elevated cortical histamine and breakdown of the blood-brain barrier after minor head injury, modeled by either a parietal craniectomy or producing a groove in (scoring) the parietal bone surface to model a grazing head injury. We measured the following effects at 5-20 min after a unilateral parietal craniectomy (rats) or unilateral scoring of the parietal bone (mice): (1) mast cell integrity in subjacent dura mater; (2) subjacent vs. contralateral histamine in dura mater and cerebral cortex; (3) vascular permeability of cerebral cortical blood vessels subjacent to the injury, and; (4) the effects of an H(2)-receptor antagonist on cerebral cortical vascular permeability.


RESULTS
Dural mast cells subjacent to the craniectomy became activated (degranulated) concomitant with (1) decreased histamine in dura mater subjacent to the craniectomy; (2) increased histamine in the subjacent cerebral cortex; and (3) extravasation of Evans blue-albumin which stained the subjacent cerebral cortex, indicating a localized breakdown of the blood-brain barrier. Similar results were observed in mice after scoring the parietal bone surface and, additionally, pretreatment with the histamine H(2)-receptor antagonist zolantadine (1 h before injury) dose-dependently inhibited extravasation of Evans blue-albumin. We conclude that even a minor grazing injury of the skull, in the absence of penetrating brain injury or concussion, can activate dural mast cells and elevate cortical histamine, a novel mechanism with potential contributions to neurotraumatic complications arising from a relatively minor or grazing head wound.
Stokely
Martha E
ME
Department of Pharmacology and Neuroscience, and North Texas Eye Research Institute, University of North Texas Health Science Center at Fort Worth, Fort Worth, Texas, USA.
Orr
Edward L
EL
D000418:Albumins / Q000493:pharmacokinetics; D000818:Animals; D001812:Blood-Brain Barrier / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D002536:Cerebral Arteries / Q000378:metabolism / Q000503:physiopathology; D002540:Cerebral Cortex / Q000098:blood supply / Q000378:metabolism* / Q000503:physiopathology; D002633:Chemotaxis / Q000502:physiology; D006259:Craniocerebral Trauma / Q000378:metabolism / Q000503:physiopathology; D003399:Craniotomy; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004388:Dura Mater / Q000166:cytology / Q000293:injuries* / Q000503:physiopathology*; D005070:Evans Blue / Q000493:pharmacokinetics; D005260:Female; D016489:Head Injuries, Closed / Q000378:metabolism / Q000503:physiopathology; D006632:Histamine / Q000378:metabolism*; D006635:Histamine H2 Antagonists / Q000494:pharmacology; D008407:Mast Cells / Q000378:metabolism*; D051379:Mice; D008833:Microcirculation / Q000378:metabolism / Q000503:physiopathology; D010841:Pia Mater / Q000098:blood supply; D051381:Rats; D011917:Rats, Inbred Lew; D022142:Secretory Vesicles / Q000378:metabolism; D012886:Skull / Q000293:injuries*; D015854:Up-Regulation / Q000502:physiology
D000418:Albumins; D006635:Histamine H2 Antagonists; D005070:Evans Blue; D006632:Histamine