Penumbral microcirculatory changes associated with peri-infarct depolarizations in the rat.
OBJECTIVE
This study was designed to investigate the influence of peri-infarct depolarization elicited by occlusion of the middle cerebral artery on the dynamics of the microcirculation.


METHODS
The microcirculation in the frontoparietal cortex of 9 rats was visualized in real time through a closed cranial window with the use of laser-scanning confocal fluorescence microscopy combined with intravenous fluorescein isothiocyanate (FITC)-dextran and FITC-labeled erythrocytes. The direct current potential/electrocorticogram was continuously monitored. Intraluminal focal ischemia was induced for 2 hours in 6 rats anesthetized with halothane and mechanically ventilated. Reperfusion was monitored for 1 hour. Three rats underwent sham operation. Brains were removed 24 hours after occlusion and processed for histology.


RESULTS
In control conditions, the velocity of fluorescent erythrocytes through capillaries was 0.51+/-0.19 mm/s (mean+/-SD), and the diameter of the arterioles studied was 33+/-12 microm. Under ischemia, erythrocyte velocity through capillaries was significantly decreased to 0.33+/-0.14 mm/s, while arteriole diameter did not change significantly. During spontaneous peri-infarct depolarizations, arteriole diameter was significantly increased (119+/-23% of baseline), while capillary erythrocyte velocity was further decreased by 14+/-34%. The direction of arteriolar blood flow episodically and transiently reversed during approximately half of the peri-infarct depolarizations. The decrease in capillary erythrocyte velocity was more pronounced (23+/-37%) in these cases. After reperfusion, the microcirculatory variables rapidly returned to baseline. All rats in the ischemic group had infarcts 24 hours after occlusion.


CONCLUSIONS
Peri-infarct depolarization has an adverse influence on penumbral microcirculation, reducing capillary perfusion by erythrocytes, despite dilatation of arterioles. These findings suggest that a steal phenomenon contributes to the deleterious effect of these depolarizations.
Pinard
Elisabeth
E
Laboratoire de Recherches Cérébrovasculaires, CNRS UPR 646, Université Paris 7, IFR 6, Paris, France. pinard@ext.jussieu.fr
Nallet
Hélène
H
MacKenzie
Eric T
ET
Seylaz
Jacques
J
Roussel
Simon
S
D000818:Animals; D001160:Arterioles / Q000473:pathology / Q000503:physiopathology; D001783:Blood Flow Velocity; D002540:Cerebral Cortex / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology; D002544:Cerebral Infarction / Q000473:pathology / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D013181:Cortical Spreading Depression; D003911:Dextrans; D004569:Electroencephalography; D004912:Erythrocytes / Q000737:chemistry / Q000166:cytology; D016650:Fluorescein-5-isothiocyanate / Q000031:analogs & derivatives* / Q000737:chemistry; D020244:Infarction, Middle Cerebral Artery / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008564:Membrane Potentials; D008833:Microcirculation / Q000473:pathology / Q000503:physiopathology*; D020678:Microscopic Angioscopy; D018613:Microscopy, Confocal; D008856:Microscopy, Fluorescence; D051381:Rats; D017207:Rats, Sprague-Dawley; D014654:Vascular Patency
D003911:Dextrans; C015219:fluorescein isothiocyanate dextran; D016650:Fluorescein-5-isothiocyanate