症状性颈动脉狭窄血管内支架置入术临床应用

目的回顾性分析我院自2005年10月-2012年2月共收治的80例症状性颈动脉狭窄患者，探讨症状性颈动脉狭窄患者血管内治疗方法和疗效。方法对80例症状性颈动脉狭窄患者行血管内支架成形术，通过临床症状、数字减影血管造影（DSA）评价其疗效，并随访3。18月。结果80例患者手术全部成功，术后即刻造影显示狭窄程度明显改善，平均狭窄程度从术前的狭窄率为（78±11）％下降到治疗后的狭窄率为（16±3）％。术后无颅内出血、栓塞等严重并发症发生。术后随访2例有新的短暂性脑缺血发作（TIA）发作，但无新的脑梗死，DSA复查发现3例再狭窄其狭窄率均约32％但无症状。结论血管内支架成形术是治疗症状性颈动脉狭窄的一个相对安全、有效的手段。     

Statins: the new aspirin?

3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, have been described as the principal and the most effective class of drug to reduce serum cholesterol levels. Statin therapies have been shown to reduce cardiovascular events, including myocardial infarction, stroke, and death, significantly, by altering vascular atherosclerosis development in patients with or without coronary artery disease symptoms. Extensive use of statins has led to the increase of some undesirable effects that are heavily counterbalanced by the benefits. Indeed, pleiotropic effects extend far beyond cholesterol reduction and involve non-lipid-related mechanisms that modify endothelial functions, immunoinflammatory responses, smooth muscle cell activation, proliferation and migration, atherosclerotic plaque stability, and thrombus formation. In this review, we describe in detail the targets and mechanisms of action of statins. Received 6 June 2002; received after revision 6 September 2002; accepted 6 September 2002 RID="*" ID="*"Corresponding author.     

35例累及颈动脉间隙病变的影像分析

目的:探讨邻近或转移性病变累及颈动脉间隙的影像特点.方法:搜集35例疾病经临床病理证实患者的影像资料,分析其病变累及颈动脉间隙的影像学表现.结果:转移性淋巴结20例(占57%)均推压、包绕颈动脉间隙内血管.淋巴瘤7例(占20%)均为推移颈动脉间隙内血管.其他病变(8例,占23%)如神经鞘瘤等均以推压为主,使颈动脉间隙内血管移位.10例恶性肿瘤及1例病灶感染(占31%)则表现为病变与血管之间的脂肪层消失.结论:转移性淋巴结多为包绕颈动脉间隙内的血管.淋巴瘤及良性肿块主要是推移颈动脉间隙内的血管.     

Integrins and cardiovascular disease

Cardiovascular diseases involve abnormal cell-cell interactions leading to the development of atherosclerotic plaque, which when ruptured causes massive platelet activation and thrombus formation. Parts of a loose thrombus may detach to form an embolus, blocking circulation at a more distant point. The integrins are a family of adhesive cell receptors interacting with adhesive proteins or with counterreceptors on other cells. There is now solid evidence that the major integrin on platelets, the fibrinogen receptor α _IIb  β ₃ , has an important role in several aspects of cardiovascular diseases and that its regulated inhibition leads to a reduction in incidence and mortality due to these disorders. The development of α _IIb  β ₃ inhibitors is an important strategy of many pharmaceutical companies which foresee a large market for the treatment of acute conditions in surgery, the symptoms of chronic conditions and, it is hoped, maybe even the successful prophylaxis of these conditions. Although all the associated problems have not been solved, the undoubted improvements in patient care resulting from the first of these treatments in the clinic have stimulated further research on the role of integrins on other vascular cells in these processes and in the search for new inhibitors. Both the development of specific inhibitors and of mice with specific integrin subunit genes ablated have contributed to a better understanding of the function of integrins in development of the cardiovascular system.     

Endothelium-derived nitric oxide and vascular physiology and pathology

In 1980, Furchgott and Zawadzki demonstrated that the relaxation of vascular smooth muscle cells in response to acetylcholine is dependent on the anatomical integrity of the endothelium. Endothelium-derived relaxing factor was identified 7 years later as the free radical gas nitric oxide (NO). In endothelium, the amino acid L-arginine is converted to L-citrulline and NO by one of the three NO synthases, the endothelial isoform (eNOS). Shear stress and cell proliferation appear to be, quantitatively, the two major regulatory factors of eNOS gene expression. However, eNOS seems to be mainly regulated by modulation of its activity. Stimulation of specific receptors to various agonists (e.g., bradykinin, serotonin, adenosine, ADP/ATP, histamine, thrombin) increases eNOS enzymatic activity at least in part through an increase in intracellular free Ca²⁺. However, the mechanical stimulus shear stress appears again to be the major stimulus of eNOS activity, although the precise mechanisms activating the enzyme remain to be elucidated. Phosphorylation and subcellular translocation (from plasmalemmal caveolae to the cytoskeleton or cytosol) are probably involved in these regulations. Although eNOS plays a major vasodilatory role in the control of vasomotion, it has not so far been demonstrated that a defect in endothelial NO production could be responsible for high blood pressure in humans. In contrast, a defect in endothelium-dependent vasodilation is known to be promoted by several risk factors (e.g., smoking, diabetes, hypercholesterolemia) and is also the consequence of atheroma (fatty streak infiltration of the neointima). Several mechanisms probably contribute to this decrease in NO bioavailability. Finally, a defect in NO generation contributes to the pathophysiology of pulmonary hypertension. Elucidation of the mechanisms of eNOS enzyme activity and NO bioavailability will contribute to our understanding the physiology of vasomotion and the pathophysiology of endothelial dysfunction, and could provide insights for new therapies, particularly in hypertension and atherosclerosis.     

Velocity and myosin phosphorylation transients in arterial smooth muscle: effects of agonist diffusion

Summary Transients in myoplasmic [Ca²⁺] and in phosphorylation of the 20,000 dalton light chain of myosin have been reported following stimulation of vascular smooth muscle by various agonists. Since these transients are rapid compared with the time required to attain a steady-state stress, agonist diffusion rates may be a significant limitation in activation. The purpose of this study was to estimate the effect of agonist diffusion rates on the time course of activation as assessed by mechanical measurements of stress development and isotonic shortening velocities and by determinations of the time course of myosin phosphorylation. The approach was to measure these parameters in K⁺-stimulated preparations of the swine carotid media of varying thicknesses and to estimate the theoretical contributions imposed by diffusion rates and the presence of a diffusion boundary layer surrounding the tissue. The results show that the time course of parameters which are tissue averages such as stiffness, active stress, and myosin phosphorylation is dominated by agonist diffusion rates. The sequence of events involved in excitation-contraction coupling including agonist actions on the cell membrane, Ca²⁺ release, activation of myosin light chain kinase, and cross-bridge phosphorylation appear to be very rapid events compared with stress development. Estimates of unloaded or lightly loaded shortening velocities which are not simple tissue averages appear to provide an imporoved estimate of activation rates.Supported by a grant from the National Institutes of Health 5-PO1-HL19242. K. E. Kamm was supported by a National Heart, Lung, and Blood Institute Research Service Award HL-05957.     

Liver X receptors in cardiovascular and metabolic disease

Liver X receptors (LXRs) α and β are nuclear oxysterol receptors and metabolic sensors initially found to regulate cholesterol metabolism and lipid biosynthesis. Recent studies have elucidated the importance of LXR in the development of cardiovascular diseases and metabolic disorders. LXR agonists prevent development of atherosclerosis by modulation of metabolic as well as inflammatory gene expression in rodent models. Moreover, LXR activation inhibits hepatic gluconeogenesis and lowers serum glucose levels, indicating possible application of LXR activation in the treatment of diabetes mellitus. However, first-generation LXR agonists elevate hepatic and serum trigylceride levels, making subtype-specific agonists and selective LXR modulators rather than unselective LXR agonists a potential pharmacological strategy. This review summarizes the multiple physiological and pathophysiological implications of LXRs and observations that identify LXRs as potential targets for therapeutic interventions in human cardiovascular and metabolic disease. Received 30 August 2005; received after revision 10 October 2005; accepted 4 November 2005     

生理浓度抗氧化剂对高密度脂蛋白氧化修饰的抑制作用

观察、比较了生理浓度VitC、VitE和白蛋白对体外Cu^2 氧化高密度脂蛋白（HDL）的抑制能力。在体外Cu^2 氧化HDL的反应体系中，同时加入生理浓度的VitC、VitE或白蛋白，通过检测硫代巴比妥酸值（TBARS）和氧化延滞时间的变化，分析3种抗氧化剂对HDL氧化的抑制作用。结果发现，3种抗氧化剂均明显降低HDL的脂质过氧化程度，延长氧化延滞时间，其中以白蛋白作用最为显。结果提示白蛋白是比VitC和VitE更强的HDL抗氧化剂。     

Scavenger receptor family proteins: roles for atherosclerosis, host defence and disorders of the central nervous system

In this review, we summarize the structure and function of the scavenger receptor family of proteins including class A (type I and II macrophage scavenger receptors, MARCO), class B (CD36, scavenger receptor class BI), mucinlike (CD68/macrosialin, dSR-CI) and endothelial (LOX-1) receptors. Two motifs have been identified as ligand-binding domains a charged collagen structure of type I and II receptors, and an immunodominant domain of CD36. These structures can recognize a wide range of negatively charged macromolecules, including oxidized low-density lipoproteins, damaged or apoptotic cells, and pathogenic microorganisms. After binding, these ligands can be either internalized by endocytosis or phagocytosis, or remain at the cell surface and mediate adhesion or lipid transfer through caveolae. Under physiological conditions, scavenger receptors serve to scavenge or clean up cellular debris and other related materials, and they play a role in host defence. In pathological states, they mediate the recruitment, activation and transformation of macrophages and other cells which may be related to the development of atherosclerosis and to disorders caused by the accumulation of denatured materials, such as Alzheimer's disease. Received 17 September 1997; received after revision 16 March 1998; accepted 17 March 1998     

Bis(7)-Tacrine Ameliorates Cognitive Impairment Caused by Cerebral Hypoperfusion in Rats

The effects of bis(7)-tacrine, a novel acetylcholinesterase inhibitor, on cognitive impairment and neuronal degeneration induced by permanent ligation of bilateral common carotid arteries (2VO) were investigated using the Morris water maze in rats. Once daily oral administration of bis(7)-tacrine (0.025, 0.05 and 0.1 mg\5kg-1) was started 14 days after 2VO operation. Over a three-week treatment bis(7)-tacrine effectively reversed 2VO-induced spatial memory deficits in a dose-dependent fashion. Furthermore, histological observation showed bis(7)-tacrine decreased the neuropathological changes in the 2VO rats brain. These results suggest that bis(7)-tacrine has therapeutic potential for the treatment of dementia caused by chronic cerebral hypoperfusion.