Mj. Souter et al., EFFECTS OF ALFENTANIL ON CEREBRAL HEMODYNAMICS IN AN EXPERIMENTAL-MODEL OF TRAUMATIC BRAIN INJURY, British Journal of Anaesthesia, 79(1), 1997, pp. 97-102
Alfentanil is reported to increase intracranial pressure (ICP) after n
eurotrauma. A direct cerebral vasodilator effect has been postulated.
We studied 17 Sprague-Dawley rats allocated to one of three groups. An
imals were anaesthetized and their lungs ventilated, and arterial pres
sure, ICP and/or regional cerebral blood flow (CBF) measurements were
undertaken. Group 1 (n=6) received a severe closed head injury while g
roup 2 (n=5) received no injury. ICP and mean arterial pressure (MAP)
were measured before, during and after rapid infusion of alfentanil 25
0, 500 and 750 mu g kg(-1). CBF was measured by hydrogen clearance bef
ore rapid infusions and at 30-min intervals after starting a subsequen
t slow infusion of alfentanil 500 mu g kg(-1) h(-1). Group 3 (n=6) und
erwent CBF measurement only, for comparison with those of groups 1 and
2. They received an injury but no alfentanil. ICP or MAP values did n
ot differ significantly between groups 1 and 2. Rapid i.v. doses of al
fentanil produced increases in ICP and reductions in MAP. ICP changes
were consistent with a drug effect (P<0.001) but were small. Reduction
s in MAP were significant (P<0.05) and preceded changes in ICP. CBF va
lues were similar and unaffected by slow alfentanil infusion in groups
1 and 2, and did not differ significantly between groups 1 and 3. We
conclude that alfentanil did not appear to exert a direct effect on th
e cerebral circulation. Changes in ICP after rapid infusion were secon
dary to reductions in SAP. Slow infusion did not cause such changes.