2005Zhongguo linchuang yaolixue yu zhiliaoxueRequires access

Quantitative analysis of focal ischemic cerebral infarction in mice

Wei Er-qing

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Abstract

AIM:To confirm the action of the light transmission method in evaluating focal ischemic cerebral infarction on persistent focal cerebral ischemia in mice. METHODS:Persistent focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO). Bederson's neurological scores, climbing board and hanging test were performed 24 h after ischemia, and infarct volume, brain hemisphere area, neuron density of cortex and subcortex were measured with computer-assisted imaging. Pranlukast ( 0.1 mg·kg -1) or nimodipine ( 0.4 mg·kg -1) were injected ip once daily for 3 days and to 1 h before MCAO assess the neuroprotective effect. RESULTS:The infarct volumes measured by light transmission closely correlated with that measured by TTC staining and neuron densities. The infarct volumes measured by light transmission well correlated with the neurological scores measured by integrated graded approach, too. Both pranlukast and nimodipine significantly attenuated infarct volumes and the ratio of ischemic/non-ischemic hemispheres, and reduced neurological deficits and neuron death. CONCLUSION:Light transmission and integrated graded approach can be used not only for qualitative analysis of focal cerebral ischemia, but also for evaluating the neuroprotective effect of drugs.

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AIM:To confirm the action of the light transmission method in evaluating focal ischemic cerebral infarction on persistent focal cerebral ischemia in mice. METHODS:Persistent focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO). Bederson's neurological scores, climbing board and hanging test were performed 24 h after ischemia, and infarct volume, brain hemisphere area, neuron density of cortex and subcortex were measured with computer-assisted imaging. Pranlukast ( 0.1 mg·kg -1) or nimodipine ( 0.4 mg·kg -1) were injected ip once daily for 3 days and to 1 h before MCAO assess the neuroprotective effect. RESULTS:The infarct volumes measured by light transmission closely correlated with that measured by TTC staining and neuron densities. The infarct volumes measured by light transmission well correlated with the neurological scores measured by integrated graded approach, too. Both pranlukast and nimodipine significantly attenuated infarct volumes and the ratio of ischemic/non-ischemic hemispheres, and reduced neurological deficits and neuron death. CONCLUSION:Light transmission and integrated graded approach can be used not only for qualitative analysis of focal cerebral ischemia, but also for evaluating the neuroprotective effect of drugs.

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Available abstract

AIM:To confirm the action of the light transmission method in evaluating focal ischemic cerebral infarction on persistent focal cerebral ischemia in mice. METHODS:Persistent focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO). Bederson's neurological scores, climbing board and hanging test were performed 24 h after ischemia, and infarct volume, brain hemisphere area, neuron density of cortex and subcortex were measured with computer-assisted imaging. Pranlukast ( 0.1 mg·kg -1) or nimodipine ( 0.4 mg·kg -1) were injected ip once daily for 3 days and to 1 h before MCAO assess the neuroprotective effect. RESULTS:The infarct volumes measured by light transmission closely correlated with that measured by TTC staining and neuron densities. The infarct volumes measured by light transmission well correlated with the neurological scores measured by integrated graded approach, too. Both pranlukast and nimodipine significantly attenuated infarct volumes and the ratio of ischemic/non-ischemic hemispheres, and reduced neurological deficits and neuron death. CONCLUSION:Light transmission and integrated graded approach can be used not only for qualitative analysis of focal cerebral ischemia, but also for evaluating the neuroprotective effect of drugs.

Key concepts: Nimodipine, Ischemia, Neuroprotection, Medicine, Cerebral infarction, Infarction, Anesthesia, Middle cerebral artery

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