R. Hartl et al., EARLY WHITE BLOOD-CELL DYNAMICS AFTER TRAUMATIC BRAIN INJURY - EFFECTS ON THE CEREBRAL MICROCIRCULATION, Journal of cerebral blood flow and metabolism, 17(11), 1997, pp. 1210-1220
Increasing clinical and experimental evidence suggests that traumatic
brain injury (TBI) elicits an acute inflammatory response. In the pres
ent study we investigated whether white blood cells (WBC) are activate
d in the cerebral microcirculation early after TBI and whether WBC acc
umulation affects the posttraumatic cerebrovascular response. Twenty-f
our anesthetized rabbits had chronic cranial windows implanted 3 weeks
before experimentation. Animals were divided into four experimental g
roups and were studied for 7 hours (groups I, IIa, and III) or 2 hours
(group IIb). Intravital fluorescence videomicroscopy was used to visu
alize WBC (rhodamine 6G, intravenously), pial vessel diameters, and bl
ood-brain barrier (BBB) integrity (Na+-fluorescein) at 6 hours (groups
I, IIa, and III) or 1 hour (group IIb) after TBI. Group I (n = 5) con
sisted of sham-operated animals. Groups IIa (n = 7) and IIb (n = 5) re
ceived fluid-percussion injury at 1 hour. Group III (n = 7) received f
luid-percussion injury and 1 mg/kg anti-adhesion monoclonal antibody (
MoAb) ''IB4'' 5 minutes before injury. Venular WBC sticking, intracran
ial pressure (ICP), and arterial vessel diameters increased significan
tly for 6 hours after trauma. IB4 reduced WBC margination and prevente
d vasodilation. Intracranial pressure was not reduced by treatment wit
h IB4. Blood-brain barrier damage occurred at 1 hour but not at 6 hour
s after TBI and was independent of WBC activation. This first report u
sing intravital videomicroscopy to study the inflammatory response aft
er TBI reveals upregulated interaction between WBC and cerebral endoth
elium that can be manipulated pharmacologically. White blood cell acti
vation is associated with pial arteriolar vasodilation. White blood ce
lls do not induce BBB breakdown less than 6 hours after TBI and do not
contribute to posttraumatic ICP elevation. The role of WBC more than
6 hours after TBI should be investigated further.