These experiments tested the role of cholinergic mechanisms in the cha
nges of cerebral cortical blood flow (CBF) induced by brain trauma. CB
F was measured with Iodo-C-14-antipyrine autoradiography, in 128 cereb
ral cortex regions of both hemispheres, distributed in eight coronal s
lices. The effects of a 6.3-mm diameter craniotomy over the left motor
-sensory cortex with no weight drop, and of trauma (drop weight of 20
g from 30 cm height on left motor-sensory cortex through a 6.3 mm circ
ular craniotomy) on CBF were studied at 2 and 24 h after the intervent
ions. A group of control animals that received no intervention was als
o set up. Animals were treated with the cholinesterase inhibitor physo
stigmine salicylate (3.3 mu g/kg/min i.v. infusion started 60 min befo
re CBF measurements), the cholinergic blocker scopolamine hydrobromide
(1 mg/kg i.v. pulse, 18 min before CBF measurements), or with the dru
gs vehicle (saline). A focus of decreased CBF at the site of impact wa
s observed 2 h after trauma, extending caudally as far as the occipita
l cortex. CBF on the contralateral cerebral cortex was also decreased.
Both phenomena reversed partially at 24 h. This spontaneous recovery
of CBF was blocked by scopolamine. Physostigmine reversed the decrease
in CBF of the traumatized cortex, partially around the contused area
and completely in more distant regions. The cerebral cortex contralate
ral to the trauma showed significantly higher CBF 24 h after trauma wh
en compared to intact controls or craniotomy that peaked at the area s
ymmetrical to the center of trauma. This phenomenon was also enhanced
by physostigmine and completely blocked by scopolamine. These results
suggest a prominent role of cholinergic mechanisms in the vascular adj
ustments that accompany cerebral trauma.