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Optimized System for Cerebral Perfusion Monitoring in the Rat Stroke Model of Intraluminal Middle Cerebral Artery Occlusion
Published on: February 17, 2013
Three-dimensional structural changes in cerebral microvessels after transient focal cerebral ischemia in rats:
Minoru Ohtake1, Shinichi Morino, Toshiyuki Kaidoh
1Division of Morphological Analysis, Department of Functional, Morphological and Regulation Science, Faculty of Medicine, Tottori University, Yonago, Japan. ohtake@grape.med.tottori-u.ac.jp
Abstract:
Pathological changes of cerebral microvessels in transient ischemia were investigated by scanning electron microscopy of vascular corrosion casts. Wistar rats were treated with middle cerebral artery (MCA) occlusion for 30 min, 1 h, 3 h, 4 h, 5 h or 7 h and subsequent reperfusion for 2 h. The ultrastructures of the cast were observed and computer-aided montage micrographs were obtained for visualization of the whole microvasculature in the ischemic brain hemisphere. Avascular areas representing ischemic areas were detected in the frontotemporal cortex and caudate putamen in the groups from 30 min to 5 h occlusion. Extravasation of the resin, which probably corresponded to the leakage of plasma or hemorrhage, was seen as spheroidal, conglomerative, large massive and worm-like types. The spheroidal type, which probably indicated a small leakage or minor hemorrhage, began to appear in the 30-min occlusion group. The conglomerative type, which probably indicated a larger leakage or moderate hemorrhage, appeared in the 3- to 5-h occlusion groups. The large massive and worm-like types, which probably indicated a significant hemorrhage, appeared in the 4- and 5-h occlusion groups. The number of these extravasations increased significantly in the 4-h occlusion group. Arterioles near the avascular area frequently showed vasospastic appearances, such as corrugations, fusiform indentations of endothelial nuclei, continuous circulatory constrictions and severe narrowing with interrupted branches. Arteriolar vasospasm possibly caused prolonged hypoperfusion even if reperfusion was achieved. The capillaries had a thin stringy appearance in the 4- and 5-h occlusion groups. These changes seemed to relate closely with increased intracranial pressure by brain edema or hemorrhage. The present study suggested that the risk of brain edema or hemorrhagic infarction increased beyond 3 h of MCA occlusion, and vasospasm of the arterioles might participate in stroke pathophysiology.
Insights
Transient cerebral ischemia in rats shows microvascular damage, including extravasation and arteriolar vasospasm, increasing significantly after 3 hours of middle cerebral artery (MCA) occlusion. These changes suggest a higher risk of hemorrhagic infarction and edema.
Area of Science:
- Neuroscience
- Cerebrovascular Research
- Pathology
Background:
- Transient ischemic attacks can lead to significant brain damage.
- Understanding microvascular changes is crucial for stroke treatment.
Purpose of the Study:
- To investigate pathological changes in cerebral microvessels during transient ischemia.
- To determine the time course of microvascular damage and its relation to stroke severity.
Main Methods:
- Wistar rats underwent middle cerebral artery (MCA) occlusion for varying durations (30 min to 7 h) followed by reperfusion.
- Scanning electron microscopy of vascular corrosion casts was used to visualize microvasculature.
- Computer-aided montage micrographs aided in analyzing ischemic areas and microvascular alterations.
Main Results:
- Avascular areas indicating ischemia were observed from 30 min occlusion.
- Extravasation (hemorrhage/leakage) types varied with occlusion duration, increasing significantly at 4 h.
- Arteriolar vasospasm and capillary thinning were noted, potentially worsening hypoperfusion and relating to edema/hemorrhage.
Conclusions:
- The risk of brain edema or hemorrhagic infarction increases beyond 3 hours of MCA occlusion.
- Arteriolar vasospasm may play a role in the pathophysiology of stroke.
- Microvascular damage is a key feature of transient cerebral ischemia.
