Twenty-four-hour real-time continuous monitoring of acute focal cerebral ischemia in rabbits based on magnetic inductive phase shift

基于磁感应相移的兔急性局灶性脑缺血24小时实时连续监测

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作者:Shuang-Lin Zhao, Gui Jin, Ze-Lin Bai, Jing-Bo Chen, Meng-Wei Li, Gen Li, Wei Zhuang, Yue-Ning Liu, Ming-Xin Qin

Background

As a serious clinical disease, ischemic stroke is usually detected through magnetic resonance imaging and computed tomography. In this study, a noninvasive, non-contact, real-time continuous monitoring system was constructed on the basis of magnetic induction phase shift (MIPS) technology. The "thrombin induction method", which conformed to the clinical pathological development process of ischemic stroke, was used to construct an acute focal cerebral ischemia model of rabbits. In the MIPS measurement, a "symmetric cancellation-type" magnetic induction sensor was used to improve the sensitivity and antijamming capability of phase detection.

Conclusions

Our experimental study indicated that the MIPS technology has a potential ability of differentiating the development process of cytotoxic edema from that of vasogenic edema, both of which are caused by cerebral ischemia.

Methods

A 24-h MIPS monitoring experiment was carried out on 15 rabbits (10 in the experimental group and five in the control group). Brain tissues were taken from seven rabbits for the 2% triphenyl tetrazolium chloride staining and verification of the animal model.

Results

The nonparametric independent-sample Wilcoxon rank sum test showed significant differences (p < 0.05) between the experimental group and the control group in MIPS. Results showed that the rabbit MIPS presented a declining trend at first and then an increasing trend in the experimental group, which may reflect the pathological development process of cerebral ischemic stroke. Moreover, TTC staining results showed that the focal cerebral infarction area increased with the development of time CONCLUSIONS: Our experimental study indicated that the MIPS technology has a potential ability of differentiating the development process of cytotoxic edema from that of vasogenic edema, both of which are caused by cerebral ischemia.

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