Establishment of microembolic model in rat brains
- Author:
Yang ZHAO
1
Author Information
1. Department of Neurology
- Publication Type:Journal Article
- From:
Chinese Journal of Cerebrovascular Diseases
2006;3(11):508-512
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To establish a well reproducible and highly stable microembolic model in rat brains and to provide a platform for investigating the ischemic neuronal injury of microemboli. Methods: Fifty-four Sprague-Dawley rats were randomly assigned to sham-operation group (n = 10) and atherosclerotic plaque microembolic model group (n = 44). The latter were further redivided into 106-150 μm (n = 20), 75-105 μm (n = 12) and 55-74 μm (n = 12) groups according to the size of microemboli. Under the operating microscope, an indwelling venous catheter was inserted retrogradely from external carotid artery into internal carotid artery. Each rat was injected 100 corresponding microemboli of atherosclerotic plaque. The rats were killed after 24 hours. The severity of neuronal ischemic injury was detected by HE staining, the in situ TUNEL method for detection of apoptosis and immunohistochemistry staining for caspase-3 protein. Results: No infarction was found in the pathological section of brain tissue in the sham-operation group. The proportion of cerebral infarction in the 106-150 υm, 75-105 μm and 55-74 μm groups were 15/17, 11/12 and 5/12, respectively, there was significant difference as compared with the sham-operation group (P < 0.05); The numbers of TUNEL apoptosis were 33.3 ± 10.9, 25.9 ± 9.7 and 18.0 ± 6.9/HP, respectively, and they were significantly higher than those in the sham-operation group (5.7 ± 2.7/HP) (all P < 0.01). The cell numbers of positive expression of caspase-3 protein were 67 ± 11, 59 ± 12 and 46 ± 11/HP, respectively, and they were significantly higher than those in the sham-operation group (7.8 ± 3.1/HP) (all P < 0.01). Conclusion: The microemboli of 55-150 μm atherosclerotic plaque can stably result in microinfarction or neuronal apoptosis in rat brain tissues. The model may be used as an ideal means in the studying of physiopathology of cerebral microembolism.
