Rapid Noninvasive Continuous Monitoring of Oxygenation in Cerebral Ischemia and Hypoxia

2010 ◽  
Vol 10 (4) ◽  
pp. 213-217 ◽  
Author(s):  
John K-J. Li ◽  
Tijun Wang ◽  
Hongjun Zhang
2008 ◽  
Vol 9 (4) ◽  
pp. e25-e30 ◽  
Author(s):  
Anthony A. Figaji ◽  
Simon I. J. Sandler ◽  
A Graham Fieggen ◽  
Peter D. Le Roux ◽  
Jonathan C. Peter ◽  
...  

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Shuang-Lin Zhao ◽  
Gui Jin ◽  
Ze-Lin Bai ◽  
Jing-Bo Chen ◽  
Meng-Wei Li ◽  
...  

Abstract 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. 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.


1989 ◽  
Vol 9 (4) ◽  
pp. 506-514 ◽  
Author(s):  
J. R. Alger ◽  
A. Brunetti ◽  
G. Nagashima ◽  
K.-A. Hossmann

The sensitivity of cerebral energy metabolism to ischemic and hypoxic stresses following global cerebral ischemia was evaluated in a cat model using 31P nuclear magnetic resonance (NMR) spectroscopic methods. Complete global cerebral ischemia of 5 to 10 min in length was produced at 1 h intervals by reversible arterial occlusion, permitting continuous monitoring of NMR and EEG. Ischemia appeared to produce slightly more severe energy failure in animals that had previously experienced an ischemic injury. Preischemic hypoxia (5% O2 for 5 min) resulted in minor changes in the levels of phosphocreatine and intracellular inorganic phosphate, which were slightly amplified in animals that previously experienced ischemia.


Author(s):  
R.V.W. Dimlich ◽  
M.H. Biros

In severe cerebral ischemia, Purkinje cells of the cerebellum are one of the cell types most vulnerable to anoxic damage. In the partial (forebrain) global ischemic (PGI) model of the rat, Paljärvi noted at the light microscopic level that cerebellar damage is inconsistant and when present, milder than in the telencephalon, diencephalon and rostral brain stem. Cerebellar injury was observed in 3 of 4 PGI rats following 5 minutes of reperfusion but in none of the rats after 90 min of reperfusion. To evaluate a time between these two extremes (5 and 90 min), the present investigation used the PGI model to study the effects of ischemia on the ultrastructure of cerebellar Purkinje cells in rats that were sacrificed after 30 min of reperfusion. This time also was chosen because lactic acid that is thought to contribute to ischemic cell changes in PGI is at a maximum after 30 min of reperfusion.


2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S94-S94
Author(s):  
Kudret Tureyen ◽  
Ramya Sundaresan ◽  
Kellie Bowen ◽  
Raghu Vemuganti

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