Autophagy is a highly evolutionarily conserved physiological mechanism of organism, including several stages such as autophagosomes formation, the fusion of lysosomes and autophagosomes, and autophagosomes degradation. In physiological conditions, autophagy is responsible for clearing the spoiled organelles and long-lived proteins to maintain the homeostasis of cells and organism. Meanwhile, autophagy is also involved in the formation and development of diseases, but the mechanism has not been confirmed yet. The relationship between autophagy and hypoxic ischemic brain injuries represented by stroke is a research hotpot in recent years, but there is no clear conclusion about autophagy's role and mechanism in hypoxic ischemic brain injuries. We reviewed the activation, function and mechanism of autophagy in hypoxic ischemic brain injuries, in order to provide some perspectives on these researches.
Animals ; Autophagy ; Homeostasis ; Humans ; Hypoxia-Ischemia, Brain ; physiopathology ; Lysosomes

Ischemic tolerance exists in many organs, among which the cerebral ischemic tolerance and its potential clinical applications are most notable. The discovery of new triggers of cerebral ischemic tolerance has brought more interesting insights into the molecular mechanisms. The remote ischemic preconditioning and pharmacological induction of cerebral ischemic tolerance have shown promising clinical safety and feasibility, and therefore may be important breakthroughs in the clinical application of cerebral ischemic tolerance.
Brain Ischemia ; physiopathology ; Erythropoietin ; therapeutic use ; Humans ; Ischemic Preconditioning ; methods

Due to its great clinical significance, brain injury following cardiac arrest (CA) has attracted more attention now. Meanwhile, there are currently no approved real time objective methods used to monitor brain injury following CA. In this study, we adopt the method of nonextensive Kullback-Leibler Entropy in investigating the HRV signals from brain injury and compare the result with that of corresponding EEG analysis. The comparative analysis shows that Kullback-Leibler Entropy can reveal the injury level of brain following CA. And we propose a novel quantitative approach for monitoring brain injury.
Algorithms ; Brain ; pathology ; physiopathology ; Brain Ischemia ; physiopathology ; Electroencephalography ; Heart Arrest ; complications ; Heart Rate ; physiology ; Humans

To study the dynamic changes of CT perfusion parameters during the first 12 h in the embolic cerebral ischemia models. Local cerebral ischemia model were established in 7 New Zealand white rabbits. All CT scans were performed with a GE Lightspeed 16 multislice CT. Following the baseline scan, further CT perfusion scans were performed at the same locations 20 min, 1-6 h and 8, 10 and 12 h after the embolus delivery. Maps of all parameters were obtained by CT perfusion software at each time point. The brains, taken 12 h after the scan, were sliced corresponding to the positions of the CT slices and stained by 2,3,5-triphenyltetrazolium chloride (TTC). On the basis of the TTC results, the ischemic sides were divided into 3 regions: core, penumbra and the relatively normal region. The changes of all parameters were then divided into 3 stages. In the first two hours (the first stage), the CBV dropped more remarkably in the core than in the penumbra but rose slightly in the relatively normal region while the CBF decreased and MTT, TTP extended in all regions to varying degrees. In the 2nd-5th h (the second stage), all the parameters fluctuated slightly around a certain level. In the 5th-12th h (the third stage), the CBV and CBF dropped, and MTT and TTP were prolonged or shortened slightly in the core and penumbra though much notably in the former while the CBV, CBF rose and MTT, TTP were shortened remarkably in the relatively normal region. We experimentally demonstrated that the location and extent of cerebral ischemia could be accurately assessed by CT perfusion imaging. The pathophysiology of the ischemia could be reflected by the CT perfusion to varying degrees.
Blood Flow Velocity ; Brain Ischemia/physiopathology ; Brain Ischemia/*radiography ; Cerebrovascular Circulation ; Stroke/physiopathology ; Tomography, X-Ray Computed

Animals ; Brain Chemistry ; Brain Ischemia ; metabolism ; physiopathology ; Cerebral Cortex ; metabolism ; Dementia ; metabolism ; physiopathology ; Humans ; Microdialysis ; Reperfusion Injury ; metabolism ; physiopathology

Animals ; Aquaporin 4 ; metabolism ; Blood-Brain Barrier ; physiopathology ; Brain Edema ; physiopathology ; Brain Ischemia ; metabolism ; physiopathology ; Capillary Permeability ; physiology ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; physiopathology

PURPOSE: Although early neurological deterioration (END) during the acute stroke period is known to be associated with poor functional outcomes, there is little data regarding the impact of END on long-term outcomes according to the characteristics of END. The aim of this study was to investigate whether there are differences in long-term mortality according to the characteristics of END among acute ischemic stroke or transient ischemic attack patients. MATERIALS AND METHODS: END was defined as any increase (> or =1) in National Institute of Health Stroke Scale score within 7 days after admission. We assessed the characteristics of END, such as the etiology and severity of END, as well as recovery after END. The relationship between 30-day or long-term mortality and each characteristic of END was investigated using multiple logistic analysis or Cox regression model. RESULTS: Among 2820 patients, END was observed in 344 patients (12.2%). After adjustment for age, sex, underlying cardiovascular diseases, stroke severity, and stroke subtypes, END was associated with long-term mortality, whether it was mild or severe and whether or not it was followed by recovery. However, 30-day mortality was strongly related to the severity of END or the absence of recovery after END. Among the causes of END, recurrent stroke and medical illness were related to 30-day mortality, as well as long-term mortality, while brain herniation and intracranial hemorrhagic complications were only associated with 30-day mortality. CONCLUSION: The results of the present study demonstrated that END is associated with higher mortality and the effects of END on short-term and long-term mortality depend on END characteristics.
Aged ; Brain Ischemia/mortality/*physiopathology ; Female ; Humans ; Male ; Middle Aged ; Prospective Studies ; Stroke/mortality/*physiopathology

Stroke has become the second leading cause of death in the world, and the most common type is the ischemic stroke. Due to its rapid onset and complex conditions, ischemic stroke is a major neurological disorder that causes disability. Ischemic stroke mainly results from atherosclerosis, and the pathogenesis of ischemic stroke mainly includes energy metabolism disorders in the brain, the toxicity of excitatory amino acids, oxidative/nitrification stress, inflammatory response, apoptosis, and autophagy. With the characteristics of multi-component and multi-target, traditional Chinese medicine could be used to treat ischemic stroke at different stages. This article summarized the latest research progress on the pathogenesis of ischemic stroke and commonly used traditional Chinese medicine for treatment of ischemic stroke in order to provide references for the further research and clinical treatment of ischemic stroke.
Brain Ischemia ; physiopathology ; therapy ; Humans ; Medicine, Chinese Traditional ; Research ; Stroke ; physiopathology ; therapy

The in vivo measurements of rabbit brain tissue impedance were taken under both normal and ischemic conditions by using two-electrode measurement method in the frequency range from 0.1 Hz to 1 MHz. The dynamic images about the resistivity of cerebral ischemia were reconstructed based on a 16-electrode system. The results of in vivo measurement showed that the ratio of impedance increased can be as high as 75% at frequencies lower than 10 Hz. In the range from 1 KHz to 1 MHz, the ratio showed a constant value of 15%. The electrical impedance tomography (EIT) images obtained suggested that the regions of impedance changes highly correspond to the position of ischemia. It is confirmed that the brain function changes caused by local deficiency of blood can be detected and imaged by EIT method.
Animals ; Brain ; physiology ; Brain Ischemia ; physiopathology ; Electric Impedance ; Female ; Male ; Rabbits ; Tomography ; methods

AIMTo explore the role of femoral nerves section (FNS) on the protection of limb ischemic preconditioning (LIP) against cerebral ischemia/reperfusion injuries.

METHODSModel of brain ischemia induced by Four-vessel occlusion was used. LIP was performed by clamping the bilateral femoral arteries for 10 min 3 times in a interval of 10 min. Rats with vertebral arteries permanently occluded were divided into sham group, cerebral ischemic group, FNS + cerebral ischemic group, LIP + cerebral ischemic group, FNS + LIP + cerebral ischemic group. The changes of neural density (ND) in the CA1 hippocampus were observed 7d after the sham operation or brain ischemia under thionin staining. The expression of c-Fos in the CA1 hippocampus was measured 6 h after the sham operation or brain ischemia under immunohistochemistry method.

RESULTSThionin staining revealed that serious neuronal damage was visualized in the CA1 hippocampus in both cerebral ischemic group and FNS + cerebral ischemic group as compared with sham group. LIP attenuated the neuronal damage of the CA1 subfield induced normally by cerebral ischemia/reperfusion, and ND in LIP + cerebral ischemic group was significantly higher than that in cerebral ischemic group (P < 0.01). But obvious neuronal damage of the CA1 subfield was found in FNS+ LIP + cerebral ischemic group, and ND was significantly decreased as compared with LIP + cerebral ischemic group (P < 0.01). These results suggested that the protection of LIP against cerebral ischemia/reperfusion injuries might be cancelled by preceding section of femoral nerve. It was found that there was almost no c-Fos expression in the CA1 hippocampus in sham group. Changes of c-Fos expression in the CA1 subfield in cerebral ischemic group were similar to that in sham group. But in LIP + cerebral ischemic group, c-Fos expression in the CA1 subfield was markedly increased and the number of positive cells and optical density of c-Fos expression were significantly higher than those in sham and cerebral ischemic group. c-Fos expression in the CA1 subfield was again decreased in FNS + LIP + cerebral ischemic group, and the number of positive cells and optical density of c-Fos expression were significantly lower than those in LIP + cerebral ischemic group.

CONCLUSIONNeural pathway participated in the protective effect of LIP on brain, and increased c-Fos expression in the CA1 hippocampus by LIP after cerebral ischemia/reperfusion, might be a part of neural pathway by which LIP induced brain ischemic tolerance.

Animals ; Brain Ischemia ; physiopathology ; Extremities ; blood supply ; Ischemic Preconditioning ; methods ; Male ; Neural Pathways ; physiopathology ; Rats ; Rats, Wistar ; Reperfusion Injury ; physiopathology