CHANGES IN LCBF, MORPHOLOGY AND RELATED PARAMETERS BY FLUID PERCUSSION INJURY

Citation
L. Qian et al., CHANGES IN LCBF, MORPHOLOGY AND RELATED PARAMETERS BY FLUID PERCUSSION INJURY, Acta neurochirurgica, 138(1), 1996, pp. 90-98
Citations number
19
Categorie Soggetti
Surgery,"Clinical Neurology
Journal title
ISSN journal
00016268
Volume
138
Issue
1
Year of publication
1996
Pages
90 - 98
Database
ISI
SICI code
0001-6268(1996)138:1<90:CILMAR>2.0.ZU;2-N
Abstract
We investigated the pathophysiological and morphological responses of anaesthetized rats to fluid percussion brain injury generated by an or iginal midline fluid percussion injury device. Following different gra des of trauma, 1CBF was measured continuously in the right parietal co rtex through a burr hole using laser Doppler flowmeter, and physiologi cal parameters were monitored. Pathological changes also were evaluate d microscopically. During the first 2 hours following trauma, we found four patterns of cerebral circulatory responses. Little measurable pa thophysiological response occurred after percussion pulses of less tha n 1.33 atmospheres (atm). In animals subjected to pulses of greater th an 4.30 atm, 1CBF increased synchronously with blood pressure, and the n both parameters decreased continuously until death. In animals subje cted to pulses of 1.53 to 2.33 atm, trauma produced a transient increa se in 1CBF with no synchronous rise in blood pressure. In animals subj ected to pulses of 2.70 to 3.87 atm, 1CBF increased synchronously with blood pressure immediately following the injury, but had decreased ma rkedly by 60 seconds and remained below the pre-injury baseline. Blood pressure recovered to baseline within 4 minutes of the injury. The tr ansient increase in 1CBF occurred within 5 seconds following percussio n pulses of greater than 1.53 atm and appeared to be independent of th e rise in systemic blood pressure. Apnoea occurred in animals subjecte d to pulses of greater than 1.53 atm, and the duration of apnoea and m ortality rate correlated with the magnitude of the applied injury. A p ower decrease in the electroencephalogram post-injury and a delay in i ts recovery, both depended on the magnitude of the injury with few reg ional differences in the beta-2 band power. The distribution and exten t of blood-brain barrier disruption and small haemorrhages also correl ated with the magnitude of the injury. The number of neurons decreased significantly in both hippocampi by 2 weeks following moderate trauma . The four patterns of 1CBF changes demonstrated in the present study, as well as the other responses to injury, may be useful for studying graded models of various diffuse brain injuries.