Key result
Fluid-percussion brain injury induced a maximal 500-fold increase in epinephrine and 100-fold increase in norepinephrine at a 3.0-atmosphere injury level.
Effect estimate: 500-fold increase for E, 100-fold increase for NE
No immediate clinical implications from feline TBI model; leaves open human mechanistic and interventional studies.
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.
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Rosner et al. (1984) studied Mechanical brain injury (n=16). Fluid-percussion brain injury vs. Baseline was evaluated on Catecholamine release (epinephrine and norepinephrine) (500-fold increase for E, 100-fold increase for NE). Fluid-percussion brain injury induced a maximal 500-fold increase in epinephrine and 100-fold increase in norepinephrine at a 3.0-atmosphere injury level.
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