Experimental study on the effect of antegrade cerebral perfusion on brainswith old cerebral infarction
Authors
Washiyama, N
Kazui, T
Takinami, M
Yamashita, K
Fujita, S
Terada, H
Suzuki, K
Muhammad, BAH
Fujie, M
Yamamoto, S
Citation
N. Washiyama et al., Experimental study on the effect of antegrade cerebral perfusion on brainswith old cerebral infarction, J THOR SURG, 122(4), 2001, pp. 734-740
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
SICI code
0022-5223(200110)122:4<734:ESOTEO>2.0.ZU;2-W
Abstract
Objective: Patients with old cerebral infarction who undergo aortic arch op
erations are susceptible to postoperative neurologic dysfunction. To verify
such susceptibility, we performed this experimental study.
Methods: A cerebral infarct model was created in mongrel dogs by means of i
njection of cylindrical silicone embolus through the internal carotid arter
y. The dogs that had obvious neurologic deficits 1 day later and survived f
or 4 weeks or more were included in the cerebral infarct model. One month a
fter cerebral infarction was induced, deep hypothermia and selective cerebr
al perfusion were used in 14 mongrel dogs (infarct group, n = 7; control gr
oup, n = 7). During this procedure, serum glutamate concentration and venou
s-arterial lactate difference were measured. Histopathologic study of the b
rain was also performed.
Results: Changes in venous-arterial lactate difference in both groups were
almost similar, except in the rewarming phase. At 32 degreesC during rewarm
ing, the venous-arterial lactate difference in the infarct group was signif
icantly higher than that in the control group (P =.006). Although precoolin
g concentrations of serum glutamate were similar in both groups, the values
in the infarct group at the end of rewarming were significantly higher tha
n those in the control group (P =.046). Oil histologic examination, the pre
sence of old cerebral infarction with gliosis was confirmed in the infarct
group, but neither new cerebral infarction nor destruction of the blood-bra
in barrier was found.
Conclusion: We observed an accelerated anaerobic metabolism and an increase
d extracellular glutamate release in the infarct group. The brain with old
cerebral infarction is more susceptible to ischemia during arch operation t
han noninfarcted brain.