Animals ; Apoptosis ; Humans ; Ischemia ; pathology ; Neurons ; pathology ; Signal Transduction ; physiology

Angioplasty ; Embolectomy ; Ischemia ; pathology ; surgery ; Mesenteric Artery, Superior ; pathology ; surgery ; Mesenteric Ischemia ; Thrombosis ; pathology ; surgery ; Vascular Diseases ; pathology ; surgery

Humans ; Hypoxia-Ischemia, Brain ; pathology ; Infant, Newborn ; Magnetic Resonance Imaging

Acupuncture Therapy ; Apoptosis ; Brain Ischemia ; pathology ; therapy ; Humans

Obesity is an independent risk factor of cardiovascular diseases. Epidemiological studies have shown that obesity induces the production of inflammatory factors and changes in cardiac hemodynamics, remodeling and function, leading to myocardial damage and heart diseases. The positive effect of exercise on the cardiovascular system has been widely confirmed, while the acute cardiovascular stress caused by exercise cannot be ignored. Compared with the general population, obese people were more prone to arrhythmia and have a higher risk of cardiovascular events during exercise, due to their abnormal cardiac function, myocardial pathological remodeling and low tolerance to corresponding stress. Studies have shown that the intervention of exercise preconditioning (EP) can effectively reduce such risks. EP increases myocardial oxygen consumption through short-term exercise, resulting in relative or absolute myocardial ischemia, inducing the intrinsic myocardial protective effect and reducing the continuous ischemia caused by subsequent long-term exercise. This article reviews the obesity-induced abnormal changes of cardiac function and structure, possible exercise- induced risks of cardiovascular events in obese people and the role of EP in reducing exercise-induced risks of cardiovascular events. We summarize the progress on EP models in obese people, EP prevention against adverse cardiovascular events in obese people, with the aim to provide a theoretical basis for the application of EP in obese people.
Humans ; Exercise ; Obesity ; Myocardium/pathology* ; Myocardial Ischemia ; Cardiovascular Diseases

It is known that ischemic cerebrovascular disease is causing enormous harm to human health on account of the resultant high morbidity and disability rate. In this connexion, the anticipated target is to control the size of focal ischemic cerebral infarction, which is also an important method for judgment of therapeutic efficacy. The key question is to survey the size accurately and objectively; at the same time, the quantitative analysis of focal ischemic cerebral infarction is the pivotal question affecting the experiment conclusion and the reliability level. In this paper are introduced and summarized the methods being recently and commonly used in survey and computation, and the studies made on quantitative analysis of focal ischemic cerebral infarction by 2, 3, 5-triphenyltetrazolium chloride (TTC) staining method. Also are summarized the principles of dyeing in TTC method, the preparatory work, and the commonly used method of surveying and computation. It is the intent of this review to provide relevant data and suggestion for research workers.
Animals ; Brain Ischemia ; pathology ; Cerebral Infarction ; pathology ; Coloring Agents ; Humans ; Reperfusion Injury ; pathology ; Tetrazolium Salts

OBJECTIVETo study the TC index location on a reform LONGA' s animal model of regional experimental cerebral ischemia and reperfusion.

METHODSA total of 300 SD male rats were randomly divided into the pre-test group (n = 30), the original method group (n = 120, Longa' s method) and the reform method group [ n = 150, TC index location is defined by the length of rat incisor teeth root (T point) to the common carotid artery bifurcation (C point) ,the blood flow of a unilateral middle cerebral artery in the rats was reversibly blocked by the TC index location). The morphologic changes and the successful rate of the two methods to establish the rat model were compared.

RESULTSThe successful rate of TC index location modified model method was superior to that of original LONGA' s method,with significant difference in linear correlation analysis.

CONCLUSIONThe reform LONGA' s animal model of regional experimental cerebral ischemia and reperfusion by the TC index location is a good method, and is worth applying in experimental study.

Animals ; Brain Ischemia ; pathology ; Carotid Arteries ; pathology ; Disease Models, Animal ; Incisor ; pathology ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; pathology

Edema ; pathology ; Humans ; Ischemia ; pathology ; Leg ; blood supply ; Ligation ; Male ; Popliteal Vein ; abnormalities ; pathology ; surgery ; Saphenous Vein ; pathology

We have tracked the response of host and transplanted neural progenitors or stem cells to hypoxic-ischemic (HI) brain injury, and explored the therapeutic potential of neural stem cells (NSCs) injected into mice brains subjected to focal HI injury. Such cells may integrace appropriately into the degenerating central nervous system (CNS), and showed robust engraftment and foreign gene expression within the region of HI inury. They appeared to have migrated preferentially to the site of ischemia, experienced limited proliferation, and differentiated into neural cells lost to injury, trying to repopulate the damaged brain area. The transplantation of exogenous NSCs may, in fact, augment a natural self-repair process in which the damaged CNS "attempts" to mobilize its own pool of stem cells. Providing additional NSCs and trophic factors may optimize this response. Therefore, NSCs may provide a novel approach to reconstituting brains damaged by HI brain injury. Preliminary data in animal models of stroke lends support to these hypotheses.
Animal ; Brain/pathology ; Brain Diseases/therapy* ; Brain Diseases/pathology ; Brain Ischemia/therapy* ; Brain Ischemia/pathology ; Gene Therapy* ; Human ; Nerve Tissue/cytology* ; Stem Cells/transplantation* ; Tissue Therapy*

Humans ; Ischemia ; metabolism ; pathology ; therapy ; Ischemic Postconditioning ; methods ; Myocardial Reperfusion Injury ; metabolism ; pathology ; therapy