scholarly journals Automated Ischemic Lesion Segmentation in MRI Mouse Brain Data after Transient Middle Cerebral Artery Occlusion

2017 ◽  
Vol 11 ◽  
Author(s):  
Inge A. Mulder ◽  
Artem Khmelinskii ◽  
Oleh Dzyubachyk ◽  
Sebastiaan de Jong ◽  
Nathalie Rieff ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Mouse Brain ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Lesion Segmentation ◽  
Ischemic Lesion ◽  
Brain Data ◽  
Cerebral Artery Occlusion

scholarly journals MRI Mouse Brain Data of Ischemic Lesion after Transient Middle Cerebral Artery Occlusion

2017 ◽  
Vol 11 ◽  
Author(s):  
Inge A. Mulder ◽  
Artem Khmelinskii ◽  
Oleh Dzyubachyk ◽  
Sebastiaan de Jong ◽  
Marieke J. H. Wermer ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Mouse Brain ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Ischemic Lesion ◽  
Brain Data ◽  
Cerebral Artery Occlusion

Expression of Keap1–Nrf2 system and antioxidative proteins in mouse brain after transient middle cerebral artery occlusion

2011 ◽  
Vol 1370 ◽  
pp. 246-253 ◽  
Author(s):  
Nobuhito Tanaka ◽  
Yoshio Ikeda ◽  
Yasuyuki Ohta ◽  
Kentaro Deguchi ◽  
Fengfeng Tian ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Mouse Brain ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Cerebral Artery Occlusion

scholarly journals Transient Middle Cerebral Artery Occlusion by Intraluminal Suture: I. Three-Dimensional Autoradiographic Image-Analysis of Local Cerebral Glucose Metabolism—Blood Flow Interrelationships during Ischemia and Early Recirculation

1997 ◽  
Vol 17 (12) ◽  
pp. 1266-1280 ◽  
Author(s):  
Ludmila Belayev ◽  
Weizhao Zhao ◽  
Raul Busto ◽  
Myron D. Ginsberg
Keyword(s):  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Glucose Utilization ◽  
Artery Occlusion ◽  
Ischemic Lesion ◽  
Ischemic Core ◽  
Cerebral Artery Occlusion ◽  
Autoradiographic Image

Using autoradiographic image-averaging strategies, we studied the relationship between local glucose utilization (LCMRglc) and blood flow (LCBF) in a highly reproducible model of transient (2-hour) middle cerebral artery occlusion (MCAO) produced in Sprague-Dawley rats by insertion of an intraluminal suture coated with poly-L-lysine. Neurobehavioral examination at 60 minutes after occlusion substantiated a high-grade deficit in all animals. In two subgroups, LCBF was measured with 14C-iodoantipyrine at either 1.5 hours of MCAO, or at 1 hour of recirculation after suture removal. In two other matched subgroups, LCMRglc was measured with 14C-2-deoxyglucose at 1.5 to 2.25 hours of MCAO, and at 0.75 to 1.5 hours of recirculation after 2 hours of MCAO. Average image data sets were generated for LCBF, LCMRglc, and the LCMRglc/LCBF ratio for each study time. Middle cerebral artery occlusion for 2 hours induced graded LCBF decrements affecting ipsilateral cortical and basal ganglionic regions. After 1 hour of recirculation, LCBF in previously ischemic neocortical regions increased by 40% to 200% above ischemic levels, but remained depressed, on average, at about 40% of control. By contrast, frank hyperemia was noted in the previously ischemic caudoputamen. Mean cortical LCBF values during MCAO correlated highly with their respective LCBF values after 1 hour of recirculation (R = 0.93), suggesting that postischemic LCBF recovery is related to the depth of ischemia. Despite focal ischemia, LCMRglc during ~2 hours of MCAO was preserved, on average, at near-normal levels; but following ~1 h of recirculation, LCMRglc became markedly depressed (on average, 55% of control in previously densely ischemic cortical regions). Regression analysis indicated that this depressed glucose utilization was determined largely by the intensity of antecedent ischemia. By pixel analysis, the ischemic core (defined as LCBF 0% to 20% of control) comprised 33% of the ischemic hemisphere, and the penumbra (LCBF 20% to 40%) accounted for 26%. The penumbra was concentrated at the coronal poles of the ischemic lesion and formed a thin shell around the central ischemic core. During 2 hours of MCAO, the LCMRglc/LCBF ratio within the ischemic penumbra was increased four-fold above normal (average, 179 umol/100 mL). In marked contrast, after ~1 h recirculation, this uncoupling had almost completely subsided. The companion study ( Zhao et al., 1997 ) further analyzes these findings in relation to patterns of infarctive histopathology.

scholarly journals Metabolomic Analysis of Mouse Brain after a Transient Middle Cerebral Artery Occlusion by Mass Spectrometry Imaging

2018 ◽  
Vol 58 (9) ◽  
pp. 384-392 ◽  
Author(s):  
Takatsugu ABE ◽  
Kuniyasu NIIZUMA ◽  
Atsushi KANOKE ◽  
Daisuke SAIGUSA ◽  
Ritsumi SAITO ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Mouse Brain ◽  
Cerebral Artery ◽  
Mass Spectrometry Imaging ◽  
Artery Occlusion ◽  
Metabolomic Analysis ◽  
Cerebral Artery Occlusion

Pathophysiology and treatment of focal cerebral ischemia

1992 ◽  
Vol 77 (3) ◽  
pp. 337-354 ◽  
Author(s):  
Bo K. Siesjö
Keyword(s):  
Free Radicals ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Ischemic Lesion ◽  
Glutamate Antagonists ◽  
Content Type ◽  
Cerebral Artery Occlusion ◽  
Fine Print

✓ The mechanisms that give rise to ischemic brain damage have not been definitively determined, but considerable evidence exists that three major factors are involved: increases in the intercellular cytosolic calcium concentration (Ca++i), acidosis, and production of free radicals. A nonphysiological rise in Ca++i due to a disturbed pump/leak relationship for calcium is believed to cause cell damage by overactivation of lipases and proteases and possibly also of endonucleases, and by alterations of protein phosphorylation, which secondarily affects protein synthesis and genome expression. The severity of this disturbance depends on the density of ischemia. In complete or near-complete ischemia of the cardiac arrest type, pump activity has ceased and the calcium leak is enhanced by the massive release of excitatory amino acids. As a result, multiple calcium channels are opened. This is probably the scenario in the focus of an ischemic lesion due to middle cerebral artery occlusion. Such ischemic tissues can be salvaged only by recirculation, and any brain damage incurred is delayed, suggesting that the calcium transient gives rise to sustained changes in membrane function and metabolism. If the ischemia is less dense, as in the penumbral zone of a focal ischemic lesion, pump failure may be moderate and the leak may be only slightly or intermittently enhanced. These differences in the pump/leak relationship for calcium explain why calcium and glutamate antagonists may lack effect on the cardiac arrest type of ischemia, while decreasing infarct size in focal ischemia. The adverse effects of acidosis may be exerted by several mechanisms. When the ischemia is sustained, acidosis may promote edema formation by inducing Na+ and Cl− accumulation via coupled Na+/H+ and Cl−/HCO3− exchange; however, it may also prevent recovery of mitochondrial metabolism and resumption of H+ extrusion. If the ischemia is transient, pronounced intraischemic acidosis triggers delayed damage characterized by gross edema and seizures. Possibly, this is a result of free-radical formation. If the ischemia is moderate, as in the penumbral zone of a focal ischemic lesion, the effect of acidosis is controversial. In fact, enhanced glucolysis may then be beneficial. Although free radicals have long been assumed to be mediators of ischemic cell death, it is only recently that more substantial evidence of their participation has been produced. It now seems likely that one major target of free radicals is the microvasculature, and that free radicals and other mediators of inflammatory reactions (such as platelet-activating factor) aggravate the ischemic lesion by causing microvascular dysfunction and blood-brain barrier disruption. Solid experimental evidence exists that the infarct resulting from middle cerebral artery occlusion can be reduced by glutamate antagonists, by several calcium antagonists, and by some drugs acting on Ca++ and Na+ influx. In addition, published reports hint that qualitatively similar results are obtained with drugs whose sole or main effect is to scavenge free radicals. Thus, there is substantial experimental evidence that the ischemic lesions due to middle cerebral artery occlusion can be ameliorated by drugs, sometimes dramatically; however, the therapeutic window seems small, maximally 3 to 6 hours. This suggests that if these therapeutic principles are to be successfully applied to the clinical situation, patient management must change.

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