短暂性脑缺血发作与脑缺血耐受研究进展

脑缺血耐受是近年来的研究热点。短暂性脑缺血发作虽然使缺血性卒中危险增加,但同时可诱导神经细胞对再次缺血产生耐受。耐受的机制涉及血管因素、腺苷、兴奋性氨基酸、热休克蛋白、低氧诱导因子-1、促红细胞生成素、KATP通道等。临床观察显示,TIA的持续时间、发作频度、脑梗死间隔时间以及脑梗死体积等均与耐受的发生有关。     

Neuronal plasticity after ischemic preconditioning and TIA-like preconditioning ischemic periods

Transient ischemic attacks (TIAs) have recently become the center of attention since they are thought to share some characteristics with experimental ischemic preconditioning (IPC). This phenomenon describes the situation that a brief, per se harmless, cerebral ischemic period renders the brain resistant to a subsequent severe and normally damaging ischemia. Preconditioning (PC) is not restricted to the brain but also occurs in other organs. Furthermore, apart from a short ischemia, the PC event may comprise nearly any noxious stimulus which, however, must not exceed the threshold to tissue damage. In the last two decades, our knowledge concerning the underlying molecular basis of PC has substantially grown and there is hope to potentially imitate the induction of an endogenous neuroprotective state in patients with a high risk of cerebral ischemia. While, at present, there is virtually no neuropathological data on changes after TIAs or TIA-like PC ischemic periods in human brains, the following review will briefly summarize the current knowledge of plastic neuronal changes after PC in animal models, still awaiting their detection in the human brain.     

炎症与缺血性脑卒中

缺血性脑卒中(IS)是复杂多因素疾病,除传统的高血压、高脂血症、糖尿病和吸烟之外,炎症亦是重要的相关因素.临床上常见IS急性期患者在无明确感染条件下有短时发热或血白细胞升高,提示伴随了炎症过程.     

P-选择素与缺血性脑卒中

血小板活化在缺血性脑卒中的发生、发展过程中起着重要作用,P-选择素（CD62p）的表达是血小板活化的标志。抗CD62p治疗可以减轻缺血性脑损伤症状。因此,研究CD62p在缺血性脑卒中的发生和卒中后再损伤过程中的作用,对缺血性脑卒中的防治具有重要意义。     

Hypertriglyceridemia and ischemic stroke

There are no conclusive data regarding the association between dyslipidemia and the risk of ischemic stroke (IS). Clinical investigations have primarily focused on the association between elevated levels of low-density lipoprotein cholesterol and low levels of high-density lipoprotein cholesterol as stroke risk factors. Much less scientific attention has been aimed at elevated levels of triglycerides. Consequently the potential role of hypertriglyceridemia as an independent risk factor for IS remains controversial. However, accumulating evidence has shown that hypertriglyceridemia is associated with pathophysiological processes such as endothelial dysfunction, atherosclerosis and the production of a prothrombotic state, which could contribute to IS risk. The aim of this review is to critically analyze the contribution of hypertriglyceridemia to the occurrence of IS.     

同型半胱氨酸与缺血性卒中

同型半胱氨酸(Hcy)即2-氨酸-4-巯基丁酸,又名高半胱氨酸,是蛋氨酸(Met)代谢的重要中间产物。1964年,Gibson等率先报告高同型半胱氨酸血症与血管性疾病和血栓形成有关。自1969年McCully提出高同型半胱氨酸血症是导致动脉粥样硬化的主要因素以来,已有大量研究证实高同型半胱氨酸血症是缺血性卒中的独立危险因子,但近年又有临床试验得出不同结论。笔者拟就同型半胱氨酸与缺血性卒中之间的关系作如下综述。一、同型半胱氨酸代谢特点     

Neuroprotection targeting ischemic penumbra and beyond for the treatment of ischemic stroke

Neuroprotection to attenuate or block the ischemic cascade and salvage neuronal damage has been extensively explored for the treatment of ischemic stroke. In the last two decades, neuroprotective strategy has been evolving from targeting a signal pathway in neurons to protecting all neurovascular components and improving cell-cell and cell-extracellular matrix interaction that ultimately benefits the brain recovery after ischemic stroke. The progression from potentially reversible to irreversible injury in the ischemic penumbra has provided the opportunity to develop therapies to attenuate the ischemic stroke damage. Thus, the ischemic penumbra has been the main target for the current neuroprotective intervention. However, despite our increasing knowledge of the physiologic, mechanistic, and imaging characterizations of the ischemic penumbra, no effective neuroprotective therapy has been found so far for the treatment of ischemic stroke. The current acute neuroprotective approach focusing on the damaging mechanisms at the ischemic penumbra is greatly limited by the rapid evolution of the deleterious cascades in the ischemic penumbra. Neuroprotective intervention attempts to promote endogenous repairing in the transition zone of the penumbra for the therapeutic purposes may overcome the unrealistic therapeutic windows under the current neuroprotective strategy. In addition, increasing evidence has indicated ischemic stroke could induce long-lasing cellular and hemodynamic changes beyond the ischemic territory. It is unclear whether and how the global responses induced by the ischemic cascade contribute to the progression of cognitive impairment after ischemic stroke. The prolonged pathophysiological cascades induced by ischemic stroke beyond the ischemic penumbra might provide novel therapeutic opportunities for the neuroprotective intervention, which could prevent or slow down the progression of vascular dementia after ischemic stroke.     

Arterial spin label imaging of acute ischemic stroke and transient ischemic attack

Since acute stroke and transient ischemic attack (TIA) are disruptions of brain hemodynamics, perfusion neuroimaging might be of clinical utility. Recently, arterial spin labeling (ASL), a noncontrast perfusion method, has become clinically feasible. It has advantages compared to contrast bolus perfusion-weighted imaging (PWI) including lack of exposure to gadolinium, improved quantitation, and decreased sensitivity to susceptibility and motion. Drawbacks include reduced signal-to-noise and high sensitivity to arterial transit delays. However, this sensitivity can enable visualization of collateral flow. This article discusses ASL findings in patients with acute stroke and TIA, focusing on typical appearances, common artifacts, and comparisons with PWI.     

血管生成素与缺血性脑血管病

血管生成素（ANG）具有促血管生成作用,本文着重阐述ANG的生理作用及其促血管生成的机制,重点介绍缺血性脑血管病（ICVD）时ANG的表达及其对ICVD的保护及治疗作用。     

Chagas' disease and ischemic stroke

American trypanosomiasis, known as Chagas' disease (CD) is a major Public Health problem in South America. Chronic cardiomyopathy is the most common clinical form of CD. Chagasic cardiomyopathy affects about 30 % of CD patients, and its manifestations begin on average 10-40 years after the initial infection. Chagas' cardiomyopathy is characterized by congestive heart failure, sudden cardiac death, intraventricular conduction defects, arrhythmias and thromboembolism. The relationship between Chagas' cardiomyopathy and ischemic stroke was reviewed. Significant variables that predict ischemic stroke in chagasic patients have been identified: apical aneurysm, cardiac insufficiency and cardiac arrhythmia. Prevalence of apical aneurysm in CD stroke patients has been estimated in 37%. The diagnosis of CD may be established after stroke presentation in at least 40% of patients. Chagasic cardiomyopathy should be included in the differential diagnosis of the etiology of stroke, being a potential source of cardioembolic stroke.     

Relapsing ischemic encephaloenteropathy and cryoglobulinemia

Cryoglobulinemia is a rare cause of encephalopathy. The authors report three patients with strikingly similar clinical features of recurrent encephalopathy accompanied by symptoms of gastrointestinal ischemia. In only one patient was cryoglobulinemia ascertained in life during the final illness. The autopsy examinations all showed diffuse cerebral, enteral, and systemic small vessel lesions immunoreactive for immunoglobulins and typical of mixed essential cryoglobulinemia. This unusual relapsing clinical syndrome is readily misinterpreted as of nonorganic origin despite its potentially fatal prognosis.     

脑血管反应性与缺血性卒中

目的观察缺血性卒中患者脑血管反应性（CVR）变化,确定两者之间的相关性。方法采用经颅多普勒超声（TCD）结合屏气试验检测76例缺血性卒中患者及62例对照病例的屏气指数（BHI）。结果缺血性卒中患者组的BHI明显低于对照组（P〈0.001）,Logistic 回归显示,由BHI所表示的CVR是缺血性卒中的独立影响因素（P=0.000）。结论降低的CVR是缺血性脑卒中的独立危险因素,应该重视CVR在脑缺血发生、发展过程中的独立影响作用。     

对氧磷酯酶与缺血性血管疾病

血清对氧磷酯酶(paraoxonase，PON)是一类与高密度脂蛋白(HDL)密切相关的酶。自20世纪90年代初发现对氧磷酯酶1的活性与动脉粥样硬化的发生密切相关后，对对氧磷酯酶的研究日趋深入。现已证实对氧磷酯酶基因家族及其酶活性参与脂质过氧化物的降解、高密度脂蛋白的抗氧化作用和免疫炎症反应。故探讨对氧磷酯酶与动脉粥样硬化性疾病发生和发展的分子机制，将为缺血性血管疾病的防治提供一条有意义的途径。     

Acidosis and ischemic brain damage

It is now widely accepted that acidosis is an important component of the pathogenetic events that lead to ischemic brain damage. The objective with this article is to recall the evolution of the concept, to describe the conditions under which tissue acidosis arises and causes enhanced brain damage, and to probe into the cellular and molecular mechanisms involved.     

Valvular strands and ischemic stroke

We report the case of a previously healthy 47-year-old woman suffering an acute embolic stroke in the left middle cerebral artery distribution. A filiform structure along the line of the aortic valve was first identified by transesophageal echocardiography, leading to the diagnosis of a valvular strand. These masses are thought to represent giant Lambl's excrescences, although differential diagnoses include several benign cardiac tumors, e.g. papillary fibroelastoma. Valvular strands have previously been associated with embolic events including stroke, although exact pathogenetic mechanisms and further patient management have not yet been fully established. This case report additionally provides a short overview of the currently existing literature. As a conclusion, standard recommendations for patient management and treatment cannot be derived from currently available evidence.