周围神经缺血再灌注损伤动物模型的改良

目的研究周围神经缺血再灌注损伤动物模型的改良与建立。方法采用无损伤动脉夹暂时阻断大鼠一侧髂总动脉起始处血流,同时夹闭髂内、髂外动脉,一段时间后打开动脉夹,观察不同缺血再灌注时间下动物肢体功能情况,以及周围神经缺血导致的脊髓电镜下超微结构的改变,明确改良动物模型的实验效果。结果缺血时间的延长动物后肢的瘫痪症状逐渐加重。电镜观察脊髓神经元显示随再灌注时间的延长,神经元损害明显加重。结论用无损伤动脉夹阻断一侧髂总动脉和髂内、髂外动脉的周围神经缺血再灌注损伤的动物模型是对以往模型的改良。该模型制备操作简单,对动物的损伤更小,可得到理想的实验效果。     

兔心肌缺血及缺血再灌注模型的制备

目的　探讨制备兔心肌缺血及缺血再灌注损伤模型的最佳选择血管。方法　 30例兔心脏乳胶灌注后解剖观察左冠状动脉及分支的走行。活体观察左冠状动脉分支的位置和形态 ,制备模型并验证模型效果。结果　典型左室支 2 2例 ,占73 3%。前降支呈现三种类型 :Ⅰ型 17例占 5 7% ,Ⅱ型 10例占 33% ,Ⅲ型 3例占 10 %。结论　在制备兔心肌缺血及缺血再灌注损伤模型时应以左冠状动脉的左旋支发出的左室支为模型制备的首选血管 ,具有操作简便效果可靠的优点     

褪黑激素抗缺血再灌注损伤

缺血再灌注损伤（ischemia-reperfusion injury,IRI）是临床常见的病理过程,其发生发展过程涉及到自由基、钙超载 、白细胞的呼吸爆发等损伤作用。长期以来主要围绕以上几个方面进行对IR损伤的防治。褪黑激素(melatonin,MEL)是由松果体分泌的一种吲哚类激素,能够增强机体多个系统功能,近年来研究发现其通过抗氧化以及在分子水平发挥抗器官IR损伤作用。     

缺血再灌注损伤和细胞因子

缺血再灌注损伤（IRI）是一种重要的病理生理现象。研究发现细胞因子在IRI发病机制中扮演重要角色。从目前的研究看,以细胞因子为治疗靶标防治IRI导致的器官损害是有前景的。     

肢体缺血再灌注损伤的病理形态变化

本文介绍肢体缺血再灌注损伤时的病理形态变化，肌肉组织主要表现为水肿、部分肌纤维坏死及炎细胞浸润；微循环与微血管出现障碍的一系列损伤等。     

AMPK与心脏缺血再灌注损伤

腺苷酸活化蛋白激酶（AMPK）作为一种能量调控器,对心脏尤其是当心脏面临缺血性损伤对能量需求显著增加的时候具有重要作用。活化的AMPK能够增加葡萄糖摄取和糖酵解,加速脂肪酸氧化增加心肌组织的能量供应,并能抑制心肌细胞凋亡来保护心肌组织。     

缺血后处理减轻兔缺血再灌注心肌细胞损伤

目的探讨缺血后处理对在体兔心肌缺血再灌注心肌细胞凋亡和线粒体结构与功能的影响以及可能机制。方法80只兔随机分为假手术组(sham组)、心肌缺血再灌注组(IR组)、缺血预处理组(IP组)、缺血后处理组(PC组)以及缺血后处理加5-羟葵酸(5-HD)干预组(PC+5-HD组)。用TUNEL法检测心肌细胞凋亡,用透射电镜观察心肌细胞的超微结构,用荧光法检测线粒体膜电位,比色法测线粒体Ca2+浓度、丙二醛(MDA)浓度、超氧化物岐化酶(SOD)活性。结果与IR组比较,PC组和IP组兔心肌细胞凋亡减少,心肌及线粒体形态结构改变明显减轻,线粒体跨膜电位、SOD活性明显升高、线粒体Ca2+浓度、MDA浓度均下降(P<0.05),5-HD部分降低上述作用。结论PC可能通过提高线粒体跨膜电位、降低线粒体氧自由基水平、减轻线粒体钙超载而减轻心肌细胞损伤,其机制可能与线粒体功能损伤有关。     

视网膜缺血再灌注损伤机制的研究进展

视网膜缺血再灌注损伤(RIR)是造成视神经损害和致盲的常见眼科临床疾病病理过程。大量学者通过建立不同的实验模型研究视网膜缺血再灌注损伤的机制,研究发现视网膜缺血再灌注损伤的机制与兴奋性氨基酸、氧自由基、一氧化氮、基因调控、钙超载、炎症因子等因素密切相关。对视网膜缺血再灌注损伤机制的深入研究对临床治疗视网膜缺血再灌注损伤造成的眼科疾病具有非常重要的意义。     

缺血—再灌注损伤机制的研究进展

随着临床新技术开展。缺血器官恢复灌流成为现实。然而恢复灌流器官往往不仅功能未恢复,反而使结构损伤和功能障碍更加重了,故称为缺血再灌注损伤(IRI)。IRI的机制至今未能完全阐明,但从近来的大量研究看,IRI与自由基、钙代谢紊乱、血管内皮损伤及白细胞浸润等现象密切相关。 一、自由基的作用机制 自由基的产生:正常情况下,ATP代谢产物次黄嘌呤能迅速被黄嘌呤氧化酶(XOD)转变为黄嘌呤,进而     

肢体缺血后处理对兔急性心肌缺血再灌注损伤的影响

目的:探讨肢体缺血后处理对兔急性心肌缺血再灌注损伤的影响及其可能机制。 方法:健康新西兰大白兔30只，随机分为3组(每组10只)：对照组(Con)、心肌缺血后处理组(MIP)和肢体缺血后处理组(LIP)。缺血前、缺血后及再灌注结束后分别测定血浆磷酸肌酸激酶(CK)活性和丙二醛(MDA)含量；实验结束后，测心肌梗死面积并检测心肌组织髓过氧化物酶(MPO)活性。 结果:MIP和LIP组心肌梗死面积均明显低于Con组(P﹤0.01)；再灌注180 min末血浆CK活性检测证实心肌梗死面积的这种差异；MIP和LIP组再灌注180 min末MDA含量明显低于Con组(P﹤0.01)；MIP和LIP组中性粒细胞在缺血心肌的聚集程度，即组织MPO活性(U/100 g)均明显轻于Con组 (P﹤0.01)。 结论:心肌缺血再灌注前肢体短暂缺血具有显著的心肌保护作用。这种远隔器官缺血后处理心脏保护作用可能与减轻活性氧的损伤及抗氧化作用加强有关。     

Autoregulation by the right coronary artery in dogs with open chests; comparison with the left coronary artery

Experiments were conducted to study autoregulatory responses of the right and left coronary arteries in dogs with open chests. The right and left circumflex coronary artery were cannulated and perfused with blood from the femoral artery via a pressurized reservoir. The perfusion pressure was varied in steps over a wide range and coronary blood flow rates were measured. Both the right and left coronary arteries exhibited autoregulation but the pressure at the lower end of the autoregulatory range was lower in the right (39.8±9.1 mm Hg) than in the left circumflex coronary artery (57.6±14.5 mm Hg). The slope of the pressure-flow relationship in the autoregulatory range was less steep in the right than the left circumflex coronary artery. The closed-loop gain when the perfusion pressure was less than 100 mm Hg was greater in the right than in the left circumflex coronary artery. Increases in the right ventricular afterload produced by pulmonary artery constriction decreased the closed-loop gain, shifted the autoregulatory range upward and to the right, and made the slope steeper. These results indicate that more effective autoregulation is carried out by the right than the left circumflex coronary artery.     

Reactive hyperaemic flow characteristics of the right coronary artery compared to the left anterior descending coronary artery in the open-chest dog

Reactive hyperaemia, the cardiovascular response to transient occlusion of a vessel, was examined and compared in the right coronary artery (RCA) and the left anterior descending coronary artery (LAD) in the same heart of an open-chest dog. First, to study the relationship between reactive hyperaemia and occlusion time in the RCA and LAD, respective flows were measured and reactive hyperaemia was induced with different occlusion times. Occlusion time required for half the maximum peak percentage reactive hyperaemic flow (%PRH), t _1/2, for the RCA was approximately twice that of the LAD: 11.4±2.3 s versus 5.9±1.4 s. Maximum %PRH of the RCA was significantly greater than that of the LAD while the percentage repayment of the RCA was lower than that of the LAD. Augmentation of right ventricular oxygen consumption shortened t _1/2 and increased percentage repayment significantly. Second, to determine critical pressure, which was defined as the perfusion pressure below which reactive hyperaemia was abolished completely, the RCA and LAD were perfused through a shunt from the carotid artery, perfusion pressure was varied in the range of 100 to 20 mmHg and reactive hyperaemia was induced. Critical pressure in the RCA was significantly lower than in the LAD: 32.2±5.7 mmHg versus 41.5±5.0 mmHg. These results suggest that the RCA has a greater flow reserve than the LAD. These results were consistent with the difference of oxygen metabolism between the right and left ventricles. The difference of oxygen metabolism between the two ventricles would, at least partly, account for these results.     

Aberrant penetrating posterior descending artery from proximal right coronary artery

We report a rare variant of the posterior descending artery (PDA) in a 51-year-old African-American male discovered in coronary CT angiography. Arising from the proximal right coronary artery near its ostium, the anomalous PDA penetrated posteriorly toward the atrioventricular junction septum, exited through the inferior pyramidal space into the posterior interventricular groove and continued in the groove as a short PDA. Along its course it gave rise to small branches to the medial wall of the right atrium, the atrioventricular node region, and the inferoseptal wall of the right ventricle.     

Superdominant right coronary artery with absent left circumflex artery

Noninvasive imaging of coronary artery disease is rapidly replacing angiography as the first line of investigation. Multislice CT is the non-invasive modality of choice for imaging coronary artery disease and provides high speed with good spatial resolution. CT coronary angiography in addition to detecting and characterising atherosclerotic coronary artery disease is also a good imaging tool for evaluating anomalies of coronary arteries. Superdominant right coronary artery with absent left circumflex artery is one such rare coronary artery anomaly which is well evaluated with multislice CT angiography. The authors report one such case of superdominant right coronary artery with absent left circumflex artery imaged with 64-slice MDCT.     

Pulmonary sequestration with right coronary artery supply

Pulmonary sequestration is an unusual malformation consisting of isolated nonfunctioning lung segments lacking communication with functional tracheobronchial trees. Systemic blood supply is commonly from the thoracic aorta, but arteries occasionally arise from other sites. We report a rare form of pulmonary sequestration with arterial supply from the right coronary artery.     

短暂性脑缺血再灌注对大鼠脑PGRN表达的影响

目的检测短暂性脑缺血再灌注早期,大鼠的额颞叶皮质、海马及纹状体中颗粒蛋白前体(progranulin,PGRN)的表达变化,为进一步探讨PGRN对脑缺血的治疗提供实验基础。方法 SPF级成年SD大鼠随机分为2组,假手术组(shamoperation group)和实验组(MCAO group)。用线栓法制作右侧大脑中动脉阻塞(MCAO)1 h,然后再灌注30 min、2 h、12 h、24 h模型,以缺血侧为实验组(ipsilateral group),其对侧为对照组(contralateral group)。假手术组为处理对照。用TTC染色法观察缺血梗死体积。用免疫荧光组织化学法和Western-blot分别检测PGRN的细胞定位及其表达变化。结果 TTC染色表明,脑缺血区域呈现白色,而对照无缺血区为红色。免疫组织化学结果提示,PGRN在神经元中大量表达,在小胶质细胞中有少量表达,而在星形胶质细胞中几乎无表达。Western blot结果提示,与对照组相比,缺血再灌注后2 h大鼠脑额颞叶皮质的缺血侧与非缺血侧PGRN含量均显著上调。在海马区缺血再灌注能瞬间降低PGRN水平,随着时间延长PGRN表达水平在24 h逐步恢复到正常水平。与皮质和海马相比,纹状体在短时间再灌注后PGRN具有较高的表达,特别是在缺血再灌注24 h后。结论短暂性脑缺血再灌注能显著影响PGRN在大鼠脑缺血区及半暗带区的水平,提示PGRN可能参与缺血后脑的调节。     

不同推拿手法对食蟹猴轻度颈动脉粥样硬化模型的影响

目的　探讨不同颈椎推拿手法对食蟹猴轻度颈动脉粥样硬化（CAS）模型稳定性的影响。 方法　将18只食蟹猴建立轻度CAS模型,并以高脂饲料喂养8周,用彩超证实其造模成功。再将18只食蟹猴随机分为3组（每组6只）,分别是：颈椎旋转组、推桥弓组和模型对照组。分别对颈椎旋转组和推桥弓组的食蟹猴进行相应的手法干预,共干预30 d,模型对照组不做特殊干预。最后将动物麻醉后处死,取颈总动脉分别进行HE染色、拉曼实验和压力实验。 结果　HE染色可见颈总动脉血管内壁损伤严重,有斑块形成。拉曼试验中,3组均有明显的1450 及1660 脂质特征峰,但三组特征峰的相对强度差异无显著性意义（P > 0.05）。压力实验中,三组中食蟹猴颈动脉斑块破裂压力检测结果显示无显著性意义（P > 0.05）。 结论　在食蟹猴轻度CAS病变中,短期内施用颈椎旋转手法和推桥弓手法并不会改变斑块的稳定性。     

Extremely high origin of the right coronary artery from the ascending aorta.

Coronary artery anomalies, especially variations in the level of origin, are frequent. In most cases, the origin lies just a few millimeters superior to the supravalvular ridge; ectopic origins of more than one centimeter above this border are rare. We report a case in which the right coronary artery arises from the ascending aorta 38 mm above the supravalvular ridge.     

高频超声预测急性高同型半胱氨酸血症兔模型冠状动脉内皮损伤的实验研究简

目的探讨高频超声预测急性高同型半胱氨酸血症兔模型冠状动脉内皮功能损伤的价值。方法将实验兔随机分为2组,每组9只。分别灌服3.3 g/kg体质量的L-蛋氨酸（M组）、等量自来水（N组）。然后于0、4、8、12、24h检测其血浆中一氧化氮（NO）、内皮素（ET）含量.同时利用高分辨率超声检测其髂外动脉血管内皮依赖性舒张功能（EDD）、血管内皮非依赖性舒张功能（EID）.并与兔冠状动脉病理结果相对照。结果M组兔血浆中NO在上述各时间点与N组相比均明显降低,ET在上述各时间点与N组相比明显升高;M组兔灌服L-蛋氨酸0、4、8、12、24h后,髂外动脉EDD分别为13.98％±1.96％、3.50％±1.61％、-1.53％±3.01％、-2.49％±1.83％、-5.03％±1.62％,较N组显著降低;而EID无明显改变。病理结果显示,兔冠状动脉内皮细胞大部分脱落,弹力板裸露,内皮细胞线粒体肿胀,内质网扩张,心肌细胞空泡化。结论兔骼外动脉外周血管的内皮功能变化可间接反映冠状动脉内皮损伤.为临床无创、简便预测冠心病提供了新思路。     

不同平面腘动脉损伤血清肌酸激酶动态变化的临床特点

目的　 探讨不同平面腘动脉损伤致患肢创伤严重程度的临床意义,评估腓肠动脉在腘动脉创伤修复中的作用。 方法　收集2010年1月~2019年12月收治的单侧膝关节周围骨折（含脱位）患者103例。其中,合并腘动脉损伤患者68例,根据损伤平面是否高于腓肠动脉分为高位组（16例）和低位组（52例）;其余35例为对照组。对比分析3组患者术前、术后1、3、7、15 d肌酸激酶（creatine kinase,CK）。 结果　高位组CK值显著大于低位组,低位组大于对照组（F=217.709,P<0.001）;同一时间点（术前、术后1、3、7、15 d）3组患者CK值两两比较均有明显差异（P<0.001)。高位组CK各时间点比较均有统计学差异（P<0.05）;低位组术前与术后7 d（P=0.930）、术后1 d与术后3 d（P=0.195）比较无统计学差异。 结论　高位组患肢缺血、损伤程度重于低位组;腓肠动脉是腘动脉不同损伤平面CK差异的主要原因,具有代偿作用。