P. Mathew et al., A NEW EXPERIMENTAL-MODEL OF CONTUSION IN THE RAT - HISTOPATHOLOGICAL ANALYSIS AND TEMPORAL PATTERNS OF CEREBRAL BLOOD-FLOW DISTURBANCES, Journal of neurosurgery, 85(5), 1996, pp. 860-870
The authors have derived a simple reproducible rodent of focal injury
that uses a mechanical suction force applied through intact dura. The
time course and pattern of changes in neurons, glia, and microvasculat
ure were investigated using this model. Early traumatic disruption of
the blood-brain barrier and hemorrhage do not occur in this model; how
ever, many of the features of human contusion seen with light and elec
tron microscopy are closely reproduced. At the site of injury, early s
welling adn lucency of neural dendritic processes have been shown to p
recede an astrocyte response. In the absence of perivascular hemorrhag
e, delayed perivascular protein leakage and polymorphonuclear infiltra
tion of the damaged cortex occurs, which is suggestive of an acute inf
lammatory response. Cerebral blood flow (CBF) has been measured using
C-14-iodoantipyrine autoradiography at 30 minutes, 4 hours, and 24 hou
rs after induction of negative-pressure injury in rats anesthetized wi
th halothane and in time-matched sham-operated controls. A significant
reduction in blood flow in the sensorimotor cortex at the site of the
injury was present at 30 minutes, 4 hours, and 24 hours after inducti
on of the lesion, compared to the contralateral cortex (superficial la
mina, ipsilateral 50 +/- 7 ml/100 g/minute, contralateral 112 +/- 26 m
l/100 g/minute). The CBF was significantly reduced at the ipsilateral
entorhinal cortex at 30 minutes postinjury but no significant reductio
n was demonstrated at later time points. Although marked alternations
in CBF occurred in this cortical injury model, the magnitude and durat
ion of the reduction in CBF are not consistent with those necessary fo
r production of ischemic cell damage. These data indicate that this mo
del of cortical injury can be used to examine biomechanical aspects of
confusion without domination by ischemic pathophysiology.