Experimental study on the effect of antegrade cerebral perfusion on brainswith old cerebral infarction

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
Citations number
27
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
ISSN journal
00225223 → ACNP
Volume
122
Issue
4
Year of publication
2001
Pages
734 - 740
Database
ISI
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.