ISSN: 1449-1907International Journal of Medical Sciences
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Int J Med Sci 2016; 13(5):347-356. doi:10.7150/ijms.14393 This issue Cite
Research Paper
The Influence of Acute Hyperglycemia in an Animal Model of Lacunar Stroke That Is Induced by Artificial Particle Embolization
1. Department of Neurology, China Medical University Hospital, Taichung 404, Taiwan
2. School of Medicine, China Medical University, Taichung 404, Taiwan
3. Center for Stem Cell Research, Kaohsiung Medical University, Kaohsiung 807, Taiwan
4. School of Pharmacy, Kaohsiung Medical University, Kaohsiung 807, Taiwan
5. Department of Cell Biology and Anatomy, National Cheng Kung University, Tainan 701, Taiwan
6. Department of Neurology, China Medical University, An-Nan Hospital, Tainan 709, Taiwan
*: Equal contributors
Abstract
Animal and clinical studies have revealed that hyperglycemia during ischemic stroke increases the stroke's severity and the infarct size in clinical and animal studies. However, no conclusive evidence demonstrates that acute hyperglycemia worsens post-stroke outcomes and increases infarct size in lacunar stroke. In this study, we developed a rat model of lacunar stroke that was induced via the injection of artificial embolic particles during full consciousness. We then used this model to compare the acute influence of hyperglycemia in lacunar stroke and diffuse infarction, by evaluating neurologic behavior and the rate, size, and location of the infarction. The time course of the neurologic deficits was clearly recorded from immediately after induction to 24 h post-stroke in both types of stroke. We found that acute hyperglycemia aggravated the neurologic deficit in diffuse infarction at 24 h after stroke, and also aggravated the cerebral infarct. Furthermore, the infarct volumes of the basal ganglion, thalamus, hippocampus, and cerebellum but not the cortex were positively correlated with serum glucose levels. In contrast, acute hyperglycemia reduced the infarct volume and neurologic symptoms in lacunar stroke within 4 min after stroke induction, and this effect persisted for up to 24 h post-stroke. In conclusion, acute hyperglycemia aggravated the neurologic outcomes in diffuse infarction, although it significantly reduced the size of the cerebral infarct and improved the neurologic deficits in lacunar stroke.
Keywords: lacunar stroke, animal model, hyperglycemia, embolization, microsphere
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