Mechanical brain injury: the sympathoadrenal response.
Catecholamine release was studied in cats as a function of injury severity in the fluid-percussion model of brain injury. Hyperglycemia was also studied as a function of catecholamine response and injury severity. Epinephrine (E) and norepinephrine (NE) increased as a function of injury. This increase was maximal at about a 3.0-atmosphere (atm) injury level and amounted to a 500-fold increase for E and 100-fold increase for NE. Both catecholamines increased maximally by 10 seconds postinjury. Glucose increased to about 350% of baseline at 500 seconds postinjury and also increased as a function of injury severity. Results suggested that the sympathoadrenal discharge was capable of a graded response which was maximal at about 3.0 atm. Associated with this increase were hypertensin, bradyarrhythmias, tachyarrhythmias, and hyperglycemia.
D000311:Adrenal Glands / Q000378:metabolism; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000378:metabolism; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D001930:Brain Injuries / Q000378:metabolism*; D002415:Cats; D004837:Epinephrine / Q000378:metabolism*; D005260:Female; D007022:Hypotension / Q000378:metabolism; D008297:Male; D008959:Models, Neurological; D009638:Norepinephrine / Q000378:metabolism*; D013564:Sympathetic Nervous System / Q000378:metabolism
D001786:Blood Glucose; D009638:Norepinephrine; D004837:Epinephrine