Journal of Applied Physiology, Vol 49, Issue 5 856-862, Copyright © 1980 by American Physiological Society
Physiological effects of controlled concussive brain trauma
J. E. Millen, F. L. Glauser and M. Zimmerman
Utilizing a fluid percussion device, we measured the physiological effects
of brain trauma in cats exposed to controlled levels of injury. Concussive
brain injury at 3-4 atm of intensity led to profound elevations of the mean
systemic arterial blood pressure from 128 +/- 26 to 229 +/- 33 mmHg, left
ventricular end-diastolic pressure from 4 +/- 2 to 24 +/- 15 mmHg, and
pulmonary wedge pressures (PWP) from 5 +/- 3 to 27 +/- 17 mmHg and a
relatively moderate increase in intracranial pressure (ICP) from 6 +/- 3 to
38 +/- 31 mmHg (all P < 0.001). Pulmonary edema was evidenced by a
significant increase in lung tissue wet-to-dry weight ratios to 3.74 +/-
0.81 as compared with a control group of 2.29 +/- 0.23 (P < 0.001).
There was poor correlation between wet-to-dry weight ratios and PWP.
Approximately 60% of all spontaneously breathing animals become permanently
apneic within 6 min after injury, while the remaining 40% developed
transient apnea. Arterial O2 or CO2 pressure alterations, in contrast to
pretreatment with phentolamine did not affect the hemodynamic or edemogenic
response to trauma. Phentolamine did not block the apneic response or
increase in ICP. Comparative studies using intravenous levarterenol without
trauma produced responses similar to trauma. Concussive brain injury of 3-4
atm results in pulmonary edema, apnea, sympathetically mediated peripheral
vasoconstriction and left ventricular failure effect.
