缺血性卒中的影像学

近年来，神经影像学技术的发展使人们能更多地获得并理解缺血性卒中的病理学信息，尤其是在卒中早期能准确检出缺血和梗死组织。由于存在缺血半暗带的患者更有可能从治疗中获益，因此识别这些患者至关重要。文章对缺血性卒中的不同神经影像学技术，包括CT、MRI、数字减影血管造影、正电子发射体层摄影、单光子发射体层摄影、超声及图像融合技术的研究进展进行综述，并概述其在临床应用中的不同作用。     

血管内皮生长因子的脑保护作用和对动物模型的治疗进展

随着对缺血性脑血管病防治的深入研究，缺血半暗带血供的恢复越来越引起人们的重视。大约15％的脑血管病患者脑循环储备力下降，这样就增加了脑梗死的可能性。目前，对这种疾病的治疗主要包括抗血小板聚集、抗凝和血管内手术治疗等方法。然而药物治疗存在出血等并发症，血管内治疗复杂和创伤大。因此，临床上需要一种安全、创伤小、更有效地促进脑内毛细血管再生的方法。最近的研究表明，血管内皮生长因子（vascular endothelial growth factor，VEGF）能促进缺血半暗带区血管再生，有助于侧支循环的建立。我们通过列举临床和动物实验VEGF的神经保护作用，介绍VEGF对脑缺血动物模型治疗的最新进展，为缺血性脑血管病的临床防治提供理论依据。     

抗栓治疗在急性脑梗死治疗中的应用和评价

急性缺血性卒中的治疗主要集中在恢复缺血局部的脑血流和保护缺血性神经元上，对于已失去溶栓可能的患者，关键是如何最大限度地挽救缺血半暗带神经元。针对抗栓治疗中抗血小板聚集、降纤和抗凝疗法在治疗急性缺血性卒中中的不同机制，提出了在急性期联合应用3种疗法的可能性。     

远程缺血后处理对急性缺血性脑卒中缺血再灌注损伤的保护

<正>缺血性脑卒中通常是由于血管狭窄或闭塞引起,在有效时间窗内重新恢复或开通病变血管,实现缺血脑组织的再灌注是缺血性脑卒中急性期治疗的重要措施。目前,急性缺血性脑卒中的治疗,无论是公认和首选的静脉溶栓,还是动脉溶栓、桥接、机械取栓、血管成形、支架术等血管内介入治疗,最终目的均为开通血管,实现缺血脑组织再灌注。但在脑缺     

糖尿病足部溃疡的治疗

出于改善治疗结果的期望，现将内外科糖尿病足的治疗方法在此作一综述。 1 评估 1．1病因分析 临床上常将糖尿病足部溃疡分为：神经性；缺血性；神经缺血性。神经性溃疡的主要原因是感觉神经病变而致感觉缺失的足部承受组织破坏性机械负荷所致。单纯缺血性溃疡无神经病变少见，占糖尿病足溃疡的10％～15％，一般发生在严重的周围血管病变并有创伤为诱因的情况下。     

缺血性卒中的影像学

近年来,神经影像学技术的发展使人们能更多地获得并理解缺血性卒中的病理学信息,尤其是在卒中早期能准确检出缺血和梗死组织。由于存在缺血半暗带的患者更有可能从治疗中获益,因此识别这些患者至关重要。文章对缺血性卒中的不同神经影像学技术,包括CT、MRI、数字减影血管造影、正电子发射体层摄影、单光子发射体层摄影、超声及图像融合技术的研究进展进行综述,并概述其在临床应用中的不同作用。     

缺血性卒中的抗血小板治疗进展

随着社会老龄化的加剧 ,缺血性卒中已成为老年期致残、致死的主要原因之一。近年来 ,缺血性卒中的发病还有增加的趋势 ,故该领域的基础研究和防治是当前一项重要的研究课题。自 70年代提出脑卒中的血管缺血学说以来 ,相继发现兴奋性氨基酸神经毒、细胞内钙超载、自由基损伤等在缺血性卒中发生中的作用。局灶缺血再灌注动物模型的建立 ,使缺血中心坏死区和半暗带改变得到了病理学证实。近年提出急性缺血性卒中的治疗在于挽救可逆性缺血组织 ,即保护缺血半暗带 ,防止或缩小缺血引起的脑损害 ,减少梗死灶体积 ,以促进神经功能恢复。在新的动物…     

低能量激光血管内照射血液综合治疗缺血性心脏病

缺血性心脏病是由于心肌缺血、缺氧、代谢障碍及缺血－再灌注、脂质过氧化自由基损伤引起的血液流变学、血液动力学、心肌微循环、心电传导系统及神经内分泌等一系列紊乱。低能量激光血管内照射血液具有抗缺氧、抗脂质过气化、改善血液流变学性质、镇痛及高效抗心律失常等效应，为临床治疗缺血性心脏病提供了一种新的疗法。     

血管内皮细胞生长因子与脑缺血

最近研究发现，脑缺血可诱导血管内皮细胞生长因子（ＶＥＧＦ）及其受体ｍＲＮＡ蛋白的表达，内源性ＶＥＧＦ对缺血脑组织可能具有神经保护作用。缺血脑表面应用外源性ＶＥＧＦ可减小脑梗死体积，减轻缺血性脑水肿，减轻神经元的缺血性损伤。携带ＶＥＧＦ基因的载体有望成为缺血性脑血管病基因治疗的新手段。     

血管内皮细胞生长因子与脑缺血

最近研究发现 ,脑缺血可诱导血管内皮细胞生长因子 (VEGF)及其受体mRNA和蛋白的表达 ,内源性VEGF对缺血脑组织可能具有神经保护作用。缺血脑表面应用外源性VEGF可减小脑梗死体积 ,减轻缺血性脑水肿 ,减轻神经元的缺血性损伤。携带VEGF基因的载体有望成为缺血性脑血管病基因治疗的新手段。     

缺氧对糖尿病血管内皮祖细胞的影响

血管内皮的损害和再生对维持血管的完整性十分重要,血循环中骨髓来源的血管内皮祖细胞有助于血管内皮的修复.局部缺血后,血管内皮祖细胞从骨髓动员到血液中,然后归巢到缺血组织处,在缺血处通过旁分泌生长因子或者渗入血管来促进新生血管形成.糖尿病患者的血管内皮祖细胞在缺氧条件下,功能受到损害,包括动员、附着、迁移、增殖等一系列环节...     

大鼠脑缺血/再灌注损伤后血管内皮细胞生长因子的表达

目的　探讨大鼠局灶性脑缺血 /再灌注后脑组织内血管内皮细胞生长因子 (VEGF)的表达及意义。方法　制备大鼠局灶性脑缺血再灌注模型 ,应用免疫组化 S- P法检测 VEGF蛋白的表达。结果　缺血再灌注损伤后 VEGF表达增加 ,随再灌注时间的延长 ,在缺血灶周边区 ,阳性表达的小血管数量明显增多。结论　脑缺血再灌注损伤可以诱导 VEGF表达增强 ,VEGF可促进毛细血管增生。     

脑缺血白细胞介素-1和抗细胞间黏附分子-1抗体对粒细胞黏附影响的实验研究

目的　探索白细胞介素 1(IL 1)和抗细胞间黏附分子 1(ICAM 1)抗体在脑缺血再灌注损伤时对粒细胞与血管内皮细胞黏附的影响。方法　利用微管吸吮技术 ,研究IL 1和抗ICAM 1抗体对脑缺血后粒细胞与内皮细胞黏附力学特性的影响。结果　粒细胞与内皮细胞黏附力在脑缺血再灌注 4h为 (18.4× 10 ) μdyn ,比正常对照组明显升高 ,加抗ICAM 1抗体后 ,细胞黏附力明显下降。脑缺血再灌注后粒细胞与内皮细胞黏附应力的变化与黏附力的变化基本一致。结论　IL 1可加强粒细胞与内皮细胞的黏附 ,抗ICAM 1抗体对粒细胞与内皮细胞黏附有抑制作用     

Vasculoprotective effect of insulin in the ischemic/reperfused canine heart: role of Akt-stimulated NO production

OBJECTIVES: The objectives of this study were to investigate the vasculoprotective effects of glucose-insulin-potassium (GIK) on ischemia/reperfusion-induced coronary endothelial functional injury and to elucidate the mechanism involved. METHODS: Dogs were subjected to 50 min of coronary occlusion and 4 h of reperfusion. Vehicle, GIK, or GK were intravenously infused 5 min before reperfusion, and the coronary vascular dysfunction and endothelial apoptosis were determined. In a separate study, cultured endothelial cells were subjected to simulated ischemia/reperfusion, and the signaling pathway involved in insulin's anti-apoptotic effect was investigated. RESULTS: In vivo ischemia/reperfusion caused significant coronary vascular endothelial dysfunction as evidenced by reduced endothelium-dependent vasorelaxation, decreased nitric oxide (NO) production, and endothelial cell apoptosis as determined by caspase 3 activation and TUNEL staining. Treatment with GIK, but not GK, markedly improved the endothelium-dependent coronary vasorelaxation (P<0.01 versus vehicle), increased total NO production (P<0.01), and attenuated endothelial apoptosis. In cultured endothelial cells, treatment with insulin also markedly increased NO production and reduced simulated ischemia/reperfusion-induced apoptosis. Moreover, pre-treatment with either Akt inhibitor or NO synthase inhibitor almost abolished the anti-apoptotic effect exerted by insulin but not by SNAP, an NO donor. CONCLUSION: These results demonstrate that in vivo treatment with GIK at reperfusion attenuates ischemia/reperfusion-induced coronary endothelial dysfunction and endothelial apoptosis in an Akt-dependent and NO-mediated fashion. The coronary vasculoprotective effect elicited by insulin may contribute to the previously observed cardiac protective effect of GIK.     

老年大鼠缺血再灌注脑组织血管内皮生长表达及地塞米松对其表达的影响

目的　探讨局灶性脑缺血再灌注后血管内皮生长因子 (VEGF)蛋白表达的意义及地塞米松对其影响。　方法　采用老年雄性大鼠短暂性大脑中动脉闭塞 (MCAO)与再灌注模型 ,应用免疫组织化学方法观察大脑中动脉闭塞 90min再灌注 1～ 7d脑组织VEGF蛋白的表达及腹腔内注射地塞米松 ( 2mg·kg-1 ·d-1 ,持续 7d)对VEGF蛋白表达及脑组织含水量的影响。　结果　实验大鼠再灌注1h ,缺血半暗带神经元及同侧大脑中动脉供血区软脑膜开始表达VEGF ,1d达峰值 (P <0 0 1) ,前者于 1d后快速下降 ,后者维持高水平至 7d。缺血半暗带脑血管内皮细胞在 1～ 7d也有较丰富VEGF表达 (P <0 0 1)。地塞米松处理组缺血区的脑微血管内皮细胞VEGF表达明显减少 (P <0 0 1)。地塞米松在缺血再灌注 1～ 7d明显减少缺血脑组织含水量 (P <0 0 5)。　结论　局灶性脑缺血再灌注可诱导VEGF表达 ,地塞米松可抑制缺血再灌注脑组织血管内皮细胞VEGF表达     

Stem cell niches as clinical targets: the future of anti-ischemic therapy?

This article provides context for the research presented by Napoli et al., reported in this journal. Treatment strategies that target stem cell niches are promising avenues for stimulating inducible angiogenesis in many vascular diseases, such as diabetes mellitus and atherosclerosis. Here we discuss the study carried out by Napoli and colleagues--an analysis of the effects of parathyroid hormone on the vascular stem cell niche in peripheral ischemia. Napoli et al. demonstrate that parathyroid hormone administered in combination with granulocyte colony-stimulating factor induces angiogenesis in a hindlimb ischemia mouse model. This treatment seems to mobilize and localize endothelial cell progenitors specifically to ischemic vascular cell beds. We explore the mechanisms through which the multiple cells within the vascular niche respond to ischemia. The interaction between parathyroid hormone and granulocyte colony-stimulating factor in humans is also discussed. Further assessment is needed to elucidate the factors involved in migration and differentiation of endothelial cell progenitors in ischemia-damaged tissues.     

血管内皮生长因子与心肌缺血

血管内皮生长因子（VEGF）是内皮细胞特异性的促有丝分裂原,属分泌性的糖蛋白。有促进内皮细胞增生,增强血管通透性;加速新血管形成的作用。VEGF通过与其特异性受体结合发挥生物学作用。VEGF在生理和病理状态下新生血管形成中起重要作用。VEGF及其受体在缺血和／或缺 氧的 心肌细胞中表达升高。VEGF蛋白应用于心肌缺血可以通过促进缺血区新生血管形成,提高侧枝血流量而改善心功能。VEGF基因治疗心肌缺血具有广阔应用前景。     

Pathophysiology of preeclampsia: linking placental ischemia/hypoxia with microvascular dysfunction

Studies during the past decade have provided a better understanding of the potential mechanisms responsible for the pathogenesis of preeclampsia. The initiating event in preeclampsia has been postulated to be reduced uteroplacental perfusion as a result of abnormal cytotrophoblast invasion of spiral arterioles. Placental ischemia/hypoxia is thought to lead to widespread activation/dysfunction of the maternal vascular endothelium which results in enhanced formation of endothelin, thromboxane, and superoxide, increased vascular sensitivity to angiotensin II, and decreased formation of vasodilators such as nitric oxide and prostacyclin. These endothelial abnormalities, in turn, cause hypertension by impairing renal function and increasing total peripheral resistance. While recent studies support a role for cytokines and other factors such as lipid peroxides and reactive oxygen intermediates as potential mediators of endothelial dysfunction, finding the link between placental ischemia/hypoxia and maternal endothelial and vascular abnormalities remains an important area of investigation. The quantitative importance of the various endothelial and humoral factors in mediating the vasoconstriction and elevation in arterial pressure during preeclampsia has also not been completely elucidated.     

Therapeutic angiogenesis using vascular endothelial growth factor

Therapeutic angiogenesis using vascular endothelial growth factor can reduce tissue ischemia by simulating the natural process of angiogenesis. Vascular endothelial growth factor not only stimulates endothelial cells to proliferate and migrate, but also mobilizes endothelial progenitor cells and achieves vascular protection. Besides direct administration of angiogenic proteins, plasmids and viral vectors carrying angiogenic genes have been used. Animal experiments have shown promise with evidence of neovascularization and improved perfusion in the target myocardium. Initial phase I and II clinical trials results are encouraging and reflect the potential success of therapeutic angiogenesis as a clinical modality for the treatment of ischemic heart disease. This review discusses the role of vascular endothelial growth factor in therapeutic angiogenesis, along with the problems and considerations of this approach as a treatment strategy.     

血管内皮生长因子在脑缺血中的作用

血管内皮生长因子(vascular endothelial growth factor,VEGF)是一种重要的调节多种内皮功能的血管生长因子.脑缺血后,VEGF不仪能促进血管内皮细胞增殖和迁移,参与血管生成,增加血管通透性,而且在神经保护和神经发生等方面也起着重要作用.文章就VEGF在缺血性脑损伤中的作用进行了综述.