对心肌预缺血保护作用的实验研究心肌声学造影超声心动图三维重建

目的 探讨心肌声学造影超声心动图三维重建（3D－MCE）对心肌预缺血（IP）的估测。方法 套扎健康犬左前降支或左旋支,建立开胸犬IP模型。IP组犬4只及再灌注（IR）组犬5支分别于基础状态、缺血4h、缺血后再灌注1h,应用经胸三维超声探头,经左房注射自制的声振5％白蛋白对其进行3D－MCE检查,并三维重建。动物处死后将左室短轴分为5－6个断面,用TTC病理染色确定危险心肌与梗死面积。结果 ①3D－MCE显示心肌总质量及造影剂充盈缺损心肌质量与病理实测值高度相关（r分别为0．93,0．92）。②3D－MCE及TTC染色结果均显示IP组心肌受损范围小于IR组。③IP组再灌注1h后灌注缺损心肌质量与再灌注即刻差异无显著性意义,P＞0．05。IR组再灌注1h后灌注缺损心肌质量较再灌注即刻增加,P＜0．05。结论 3D－MCE在定量诊断心肌梗死和心肌缺血范围时,可重复动态观察IP对活体心肌的保护作用。     

经静脉心肌声学造影技术评价ATP敏感钾通道的开放对心肌缺血的保护作用

目的：证实经静脉心肌声学造影（MCE）,能够准确的测量缺血和梗死心肌的范围,并以此技术研究ATP敏感钾通道（KATP通道）开放对缺血心肌的保护作用。方法：21条犬随机分为三组：IR组：冠脉左前降支（LAD）闭塞90min,再灌注120min.NIC组：LAD闭塞前10min,静脉给尼可地尔100μg/kg,随后给予10μg/kg/min持续静滴至再灌注结束。CLIB＋NIC组：在IR组LAD闭塞前20min,静脉给予优降糖0．3mg/kg10min,随后步骤同NIC组。各组均在闭塞前状态、闭塞后1h、再灌注2h测定血流动力学指标;用图像分析仪测量TTC染色和危险心肌范围（AAR）和梗死心肌范围（IA）;经静脉注射全氟显示MCE,在左心室中部水平摄取短轴切面图像,冠脉闭塞1h心肌灌注缺损的范围为AAR,再灌注2h心肌灌注缺损的范围为IA。结果：冠脉闭塞1h,各组心输出量（CO）较基础状态低（P＜0．01）,再灌注2h,NIC组CO与闭塞前相比明显恢复,TTC测定AAR范围：各组之间无显著性差异（P＞0．05）。TTC测量IA范围：NIC组较IR组和GLIB＋NIC组明显缩小（P＜0．01）,MCE结果显示：与TTC染色的AAR有显著的相关性（r=0.975).IR组及GLIB＋NIC组的IA范围与TTC染色的IA范围也有显著的相关性（r=0.949)。结论：KATP通道开放剂尼可地尔能使心梗范围明显减小,经静脉MCE可准确测定缺血和梗死心肌范围。     

心肌声学造影定量评价缺血预适应对犬心肌缺血再灌注损伤的保护作用

目的应用新技术心肌声学造影（MCE）评价缺血预适应（IP）对犬心肌缺血再灌注（IR）损伤的保护作用。 方法将15条杂种犬随机分为两组：IR组，持续缺血3h后再灌注2h；IP＋IR组，在持续缺血前进行4次短暂性缺血5min，中间间隔5min再灌注。采用前降支动脉套扎建立IP开胸犬模型，分别于基础状态、缺血3h和再灌注2h行MCE；测量两组左室射血分数（EF），计算EF恢复值；处死犬后，采用2％红四氮唑将心肌染色，测量坏死区（NA）和危险区（RA）面积，计算NA／RA，与MCE缺损面积比较。 结果两组缺血3h和再灌注2hEF值较基础状态明显下降，再灌注2h后均有改善；再灌注2hIP＋IR组EF恢复程度好于IP组。各组缺血再灌注后心内膜下心肌出现不同程度的坏死区，MCE和TTC染色2种方法测量值高度正相关。MCE和TTC染色显示IP＋IR组NA／RA值较IR组降低。 结论MCE为定量评价IP对IR损伤的保护作用提供了一种有效方法。     

缺血-再灌注不同时间点给予尼可地尔对犬心肌梗死范围的影响

目的　证实尼可地尔是通过激活心肌细胞 KATP通道而起到使梗死心肌范围明显缩小的作用 ;进一步了解在冠状动脉 (冠脉 )闭塞心肌缺血前后和再灌注时给予尼可地尔产生的心肌保护作用是否相同 ,为临床上应用 KATP通道开放剂防治急性心肌缺血性疾病提供依据。方法　 35条犬随机分为 5组 ,每组 7只。缺血再灌注组 (IR组 ) :冠脉左前降支 (L AD)闭塞 90 min,再灌注 12 0 min。缺血前给予尼可地尔组 (PNIC组 ) :L AD闭塞前 10 min经静脉给予尼可地尔 10 0μg/ kg,随后给予 10μg· kg- 1 · min- 1 持续静脉滴注至再灌注结束。缺血后 15 m in给予尼可地尔组 (INIC组 ) :L AD闭塞后 15 m in经静脉给尼可地尔 10 0μg/ kg,随后给予10 μg· kg- 1· min- 1持续至再灌注结束。再灌注开始时给予尼可地尔组 (RNIC组 ) :L AD闭塞 90 min,再灌注开始时立即静脉给尼可地尔 10 0 μg/ kg,随后给予 10 μg· kg- 1· m in- 1持续至再灌注结束。KATP通道阻滞剂组(GL IB+INIC组 ) :在 L AD闭塞前 10 min经静脉给予优降糖 0 .3m g/ kg 10 min,随后步骤同 INIC组。各组均在冠脉闭塞前、冠脉闭塞后 1h、再灌注 2 h测定血流动力学指标 ;再灌注 2 h后用图像分析仪测量氯化三苯四唑 (TTC)染色的梗死心肌范围 (IA)和危险心肌范围 (     

心脏缺血预适应对中性粒细胞功能与活性氧释放的影响

目的:观察缺血预适应中中性粒细胞黏附、浸润及活性氧释放的特点,旨在探讨预适应保护效应与白细胞功能及活性氧的关系。方法:①实验于2000-06/2001-12在解放军广州军区广州总医院医学实验科及南方医科大学南方医院心内科实验室完成。选用杂种犬12条,雄性7条,雌性5条。②麻醉后,开胸游离前降支冠状动脉,稳定30min,造成心肌缺血模型。造模后将犬随机分为2组:缺血再灌注组(n=6),缺血1h后再灌注2h;缺血预适应组(6条),在缺血1h前给予血流阻断5min,灌注5min,反复4次,然后缺血1h,再灌注2h。③分别于基础(缺血和再灌注之前)、缺血1h、再灌注2h各时间点,采用流式细胞术测定中性粒细胞CD11b/CD18表达,按梗死面积%=梗死区面积/危险区面积×100%公式计算心肌梗死范围。按南京聚力生物医学工程提供试剂盒说明测定血清丙二醛水平和超氧化物歧化酶活性。计算髓过氧化物酶活力(kU/g)=ΔA460/(12×组织酶量/3),ΔA460为460nm处吸光度1min增大的值,3为反应的总体积,12为Sigma公司规定的每毫升1mg邻联茴香胺的吸光度;组织酶量指每0.1mL所用酶液中含酶的量。④两组间比较用配对t检验,多组间比较用方差分析,多组间两两比较用SNK方法。结果:犬12条均进入结果分析。①心肌梗死范围:缺血预适应组明显小于缺血再灌注组(P<0.01)。②中性粒细胞膜CD11/CD18表达:缺血再灌注组缺血1h、再灌注2h明显高于基础和缺血预适应组(P<0.05～0.01)。③髓过氧化物酶活性:缺血预适应组缺血和坏死心肌明显低于缺血再灌注组(P<0.05),两组缺血和坏死心肌明显高于正常心肌(P<0.05)。缺血预适应组正常心肌组织低于缺血再灌注组,但差异不明显(P=0.11)。血清丙二醛水平:缺血再灌注组缺血1h和再灌注2h明显高于基础和缺血预适应组(P<0.05)。血清超氧化物岐化酶活性:缺血1h缺血再灌注组明显低于基础和缺血预适应组(P<0.05)。再灌注2h虽然也有此变化,但差异不明显(P>0.05)。结论:缺血预适应能阻抑缺血再灌注所致的中性粒细胞黏附、浸润及活性氧的损害,这可能是发挥缺血预适应保护的重要作用之一。     

兔心脏缺血再灌注损伤后重组水蛭素的保护作用及其机制

背景重组水蛭素能否通过抑制白细胞浸润来拮抗心肌缺血/再灌注(ischemia/reperfusion,IR)损伤,从而起到对心肌的保护作用?目的观察重组水蛭素对缺血心肌内白细胞浸润的影响,进一步探讨重组水蛭素对心肌保护的作用机制.设计随机对照的实验研究.地点、材料和干预本实验在第四军医大学唐都医院心血管病实验室完成.选取24只日本大耳白兔随机分为2组,每组12只.IR组;心脏左冠状动脉前降支IR动物模型,缺血45 min、再灌注120 min,再灌注前后静脉应用生理盐水;重组水蛭素组缺血45 min、再灌注120 min,再灌注前15 min静注重组水蛭素(1 mg/kg),再灌注时继以持续静滴重组水蛭素[1 mg/(kg·h)]120 min.主要观察指标心肌梗死范围及缺血心肌内白细胞浸润的变化.结果重组水蛭素组的心肌梗死范围为(11.7±2.4)%,与缺血再灌注组的(21.2±5.3)%比较,梗死范围明显缩小(t=7.436,P＜0.01).缺血再灌注组的髓过氧化物酶(myeloperoxidase,MPO)活性为(56.01±3.83)nkat/g,重组水蛭素组(35.51±1.67)nkat/g.重组水蛭素组缺血心肌内白细胞聚集较缺血再灌注组显著减少(t=3.935,P＜0.05).结论重组水蛭素能够抑制再灌注期缺血心肌内白细胞浸润,拮抗心肌IR损伤.     

计算机辅助心肌超声造影定量评价心肌灌注的实验研究

目的 探讨计算机辅助心肌超声造影(MCE)定量评价心肌灌注的应用价值.方法 根据阻断和再灌注冠状动脉时间不同,将家兔分为两组:阻断30 min再灌注60 min(I组)和阻断120 min再灌注60 min(Ⅱ组).于冠状动脉阻断时和再灌注后行MCE,造影图像经自制计算机辅助软件处理后,自动得出每个节段的标化造影剂密度(CI),并对心肌灌注进行彩色编码.根据心肌灌注缺损(MPD)和异常的彩色编码区分别计算出危险心肌和梗死心肌面积,并分别与荧光微球染色和氯化三苯基四氮唑染色(TTC)结果对照分析.结果 再灌注后,I组和Ⅱ组的危险节段心肌CI值均较非危险节段减低(P＜0.01),标化后,仅Ⅱ组危险节段的标化C1值比非危险节段明显减低(P＜0.01),而I组危险节段的标化CI值与非危险节段间无明显差异.以标化CI为-70像素为截断值,识别梗死节段的敏感性为95%,特异性为87%.阻断冠状动脉时,MPD和异常彩色编码测量的危险心肌面积与荧光染色呈正相关(r=0.84,P=0.003和r=(0.91,P＜O.001);再灌注时,MPD和异常彩色编码测量的梗死心肌面积与TTC结果呈正相关(r=0.75,P＜0.001和r=0.89,P＜0.001).结论 计算机辅助MCE可以定量评估心肌灌注,识别危险和梗死心肌区域.     

心肌声学造影评价硝酸甘油对犬心肌缺血再灌注损伤的延迟保护作用

目的　探讨心肌声学造影 (myocardial contrastechocardiography,MCE)技术评价硝酸甘油对犬心肌缺血再灌注损伤的延迟保护作用的价值。方法　 12只健康成年杂种犬随机分成缺血再灌注组和硝酸甘油组 ,缺血再灌注组不给予任何药物 ,保持基础状态 ,单纯给与左冠状动脉前降支结扎 180 min,再灌注 12 0 min,在持续缺血和再灌注阶段行心肌声学造影 ,硝酸甘油组 ,用微量静脉泵以 2μg/(kg· min)速度静滴硝酸甘油 1h,2 4 h后结扎左冠状动脉前降支 ,其余步骤同缺血再灌注组。于左室乳头肌水平测定正常灌注区与缺血低灌注区心肌视频密度时间 -强度曲线参数 ,及缺血和再灌注阶段左室壁造影剂显影缺损区 (分别代表心肌危险区面积和坏死区面积 ) ,并与伊文思蓝及红四氮唑 (triphenyl tetrazolium chloride,TTC)心肌组织染色结果对照。结果　心肌造影时间 -强度曲线中 ,两组缺血低灌注区峰值强度 ,时间 -强度曲线下面积 ,比正常灌注区明显减低 ,峰值减半时间比正常灌注区延长 ,差异有显著性 ,缺血再灌注组、缺血低灌注区与正常灌注区心肌视频密度时间 -强度曲线参数比值较硝酸甘油组降低更明显 ,差异有显著性 ,MCE所测定的心肌坏死区面积与危险区面积之比与伊文思蓝及 TTC心肌组织染色结果成正相关。硝酸甘油可使心肌     

心肌声学造影评价缺血后处理对犬心肌缺血再灌注损伤的保护作用及与钾离子通道的关系

目的 采用心肌声学造影(MCE)评价缺血后处理(IPostC)对犬心肌缺血再灌注损伤的作用,及K ATP通道的作用.方法 21只犬左冠状动脉前降支(LAD)阻断180 min,再灌注120 min,分3组:对照组(Con组),无干预;IPostC组,再灌注前给予3次再灌注30 s-缺血30 s过程;格列苯脲组(Gli IPostC组),再灌注前给予K ATP通道阻断剂Gli,其余同IPostC组.MCE评价心肌血流灌注及坏死面积.结果 再灌注后与Con组比较,IPostC组低灌注区MCE峰值强度和曲线下面积增高,峰值减半时间缩短,坏死心肌面积减小.Gli IPostC组各参数介于另2组之间,3组差异显著.结论 IPostC可以减少犬心肌缺血再灌注损伤,其作用机制可能与开放K ATP通道有关.MCE可检测心肌坏死面积,定量心肌血流灌注,评价IPostC的心脏保护作用.     

实时心肌超声造影评价急性心肌缺血的实验研究

目的 评价实时心肌超声造影(MCE)识别大鼠急性心肌梗死心梗范围的准确性,及定量分析缺血心肌血流灌注的特性.方法 雄性Wistar大鼠20只,结扎冠脉左前降支,制备急性心肌梗死(AMI)模型.分别采集基础状态及梗死状态下的RT-MCE 图像.分别在缺血区和灌注正常的心肌取感兴趣区,得出造影成像的强度-时间曲线,读出峰值视频强度PI、A、β、A·β值.结果 MCE显示梗死区灌注充盈缺损,灌注缺损区面积(30.67±6.42)%与病理染色证实的心梗面积相关性好(r=0.87).心梗区PI较正常灌注区低 (5.45±3.07) dB vs (23.03±5.27) dB (P<0.05).灌注缺损区的A、β、A·β值等均与正常心肌MCE灌注参数值间存在显著差异(P<0.05).结论 MCE能无创地准确估测梗死面积.梗死区MCE血流灌注指标显著降低.     

Determination of creatine kinase isoenzyme MB activity in serum using immunological inhibition of creatine kinase M subunit activity. Activity kinetics and diagnostic significance in myocardial infarction.

This is a new method for the determination of creatine kinase isoenzyme MB activity in serum. The method uses direct activity measurement of creatine kinase B subunit activity after blocking of CK-M subunit activity by inhibiting antibodies. The test takes no longer than 15 min. The method yields an intra-serial C.V. of 2.0-12.9%, and a C.V. from day to day of 5.5%. The detection limit is 3.4 U/l creatine kinase MB. In the 95 cases with proven myocardial infarction several types of creatine kinase MB activity kinetics could be determined. The percentage of creatine kinase MB of peak CK-total is 6-25%, with a mean of 11.1%. The amount of creatine kinase MB with respect to total CK activity after reinfarction is higher than the amount after initial infarction.     

Dissociable correlates of two classes of retrieval processing in prefrontal cortex

Although substantial evidence suggests that the prefrontal cortex (PFC) implements processes that are critical for accurate episodic memory judgments, the specific roles of different PFC subregions remain unclear. Here, we used event-related functional magnetic resonance imaging to distinguish between prefrontal activity related to operations that (1) influence processing of retrieval cues based on current task demands, or (2) are involved in monitoring the outputs of retrieval. Fourteen participants studied auditory words spoken by a male or female speaker and completed memory tests in which the stimuli were unstudied foil words and studied words spoken by either the same speaker at study, or the alternate speaker. On "general" test trials, participants were to determine whether each word was studied, regardless of the voice of the speaker, whereas on "specific" test trials, participants were to additionally distinguish between studied words that were spoken in the same voice or a different voice at study. Thus, on specific test trials, participants were explicitly required to attend to voice information in order to evaluate each test item. Anterior (right BA 10), dorsolateral prefrontal (right BA 46), and inferior frontal (bilateral BA 47/12) regions were more active during specific than during general trials. Activation in anterior and dorsolateral PFC was enhanced during specific test trials even in response to unstudied items, suggesting that activation in these regions was related to the differential processing of retrieval cues in the two tasks. In contrast, differences between specific and general test trials in inferior frontal regions (bilateral BA 47/12) were seen only for studied items, suggesting a role for these regions in post-retrieval monitoring processes. Results from this study are consistent with the idea that different PFC subregions implement distinct, but complementary processes that collectively support accurate episodic memory judgments.     

俯卧位通气对高海拔地区肺复张治疗无效急性呼吸窘迫综合征患者氧合的影响

目的 探讨俯卧位通气对高海拔地区肺复张术(RM)治疗无效急性呼吸窘迫综合征(ARDS)患者的治疗作用.方法 从海拔2260m的地区医院筛选RM治疗无效的41例ARDS患者[平均氧合指数( PaO2/FiO2)较RM前升高＜20％视为RM无效],依不同病因分为肺内源性ARDS组(ARDSp组)和肺外源性ARDS组(ARDSexp组),每组再按信封法随机分为俯卧位组和仰卧位组,即ARDSp俯卧位组(11例)、ARDSp仰卧位组(9例)、ARDSexp俯卧位组(10例)、ARDSexp仰卧位组(11例).在通气前及通气1、2、3、4h监测动脉血氧分压( PaO2)、PaO2/FiO2、静态顺应性(Cst)、气道阻力(Raw)的变化.结果 通气lh时,ARDSexp俯卧位组PaO2/FiO2( mm Hg,l mm Hg=0.133 kPa)即较通气前显著升高(157.4±40.6比129.3±48.7,P＜0.05),并随通气时间延长呈持续增高趋势,4h达峰值(219.1 ±41.1);且ARDSexp俯卧位组通气3h内PaO2/FiO2较其他3组显著增高,另3组间则差异无统计学意义.ARDSp俯卧位组、ARDSexp俯卧位组通气4h时PaO2/FiO2均较相应仰卧位组显著增高(208.8±39.7比127.4±47.1,219.1±41.1比124.9±50.8,均P＜0.05).4组通气前后Cst无显著改变,各组间差异也无统计学意义.ARDSp俯卧位组通气4h时Raw(cmH2O·L-1·s-1)较通气前显著降低(6.8±1.7比10.7±1.8,P＜0.05),且明显低于其他3组;其他3组各时间点Raw组内及组间比较差异均无统计学意义.结论 俯卧位通气作为ARDS机械通气重要策略之一,可以改善RM无效高原ARDS患者的氧合,为抢救患者赢得宝贵的时间.     

Digital imaging among medical facilities

The Department of Veterans Affairs (VA) in the USA operates a network of 172 medical centres which all utilize a hospital information system (HIS) which has been developed and is currently maintained by the VA. During the past several years, an image management and communication module has been developed, installed and clinically utilized at the Washington DC and Maryland VA Medical Centres. This image management and communication system, referred to as the decentralized hospital computer program (DHCP) imaging system, is fully integrated with a commercial picture archiving and communication system (PACS). The system is utilized to capture, archive, and display all images generated within the hospital including radiology, nuclear medicine, pathology, endoscopy, bronchoscopy, and dermatology, intraoperative photographs, ECG data, and a limited number of paper documents. The ultimate goal of the project is to have all patient text and image data available at any clinical workstation to any authorized user anywhere within the network of medical centres. Clinical requirements for an imaging workstation include ease of use, rapid and reliable access to the complete set of patient information, and images which are of acceptable quality to meet the requirements of the user and the subspecialty. Patient confidentiality and data security must be safeguarded at all times. Integration of the images with the remainder of the patient's database was found to be critical to the success of the project. The experience at the Washington and Maryland facilities suggests that an imaging system that is successfully integrated with a hospital information system can provide substantial clinical and economic benefits both within and among medical centres. Clinical acceptance and utilization of the system has been excellent, particularly in diagnostic radiology where DHCP Imaging has been interfaced to a commercial PAC system. Based upon this initial experience, the VA has begun to deploy the system throughout its large network of medical centres.     

Myocardial elastography at both high temporal and spatial resolution for the detection of infarcts

Myocardial elastography is a novel method for noninvasively assessing regional myocardial function, with the advantages of high spatial and temporal resolution and high signal-to-noise ratio (SNR). In this paper, in-vivo experiments were performed in anesthetized normal and infarcted mice (one day after left anterior descending coronary artery [LAD] ligation) using a high-resolution (30 MHz) ultrasound system (Vevo 770, VisualSonics Inc., Toronto, ON, Canada). Radiofrequency (RF) signals of the left ventricle (LV) in longitudinal (long-axis) view and the associated electrocardiogram (ECG) were simultaneously acquired. Using a retrospective ECG gating technique, 2-D full field-of-view RF frames were acquired at an extremely high frame rate (8 kHz) that resulted in high-quality incremental displacement and strain estimation of the myocardium. The incremental results were further accumulated to obtain the cumulative displacements and strains. Two-dimensional and M-mode displacement images and strain images (elastograms), as well as displacement and strain profiles as a function of time, were compared between normal and infarcted mice. Incremental results clearly depicted cardiac events including LV contraction, LV relaxation and isovolumetric phases in both normal and infarcted mice, and also evidently indicated reduced motion and deformation in the infarcted myocardium. The elastograms indicated that the infarcted regions underwent thinning during systole rather than thickening, as in the normal case. The cumulative elastograms were found to have higher elastographic SNR (SNR(e)) than the incremental elastograms (e.g., 10.6 vs. 4.7 in a normal myocardium, and 6.0 vs. 2.4 in an infarcted myocardium). Finally, preliminary statistical results from nine normal (m = 9) and seven infarcted (n = 7) mice indicated the capability of the cumulative strain in differentiating infracted from normal myocardia. In conclusion, myocardial elastography could provide regional strain information at simultaneously high temporal (>/=0.125 ms) and spatial ( approximately 55 microm) resolution as well as high precision ( approximately 0.05 microm displacement). This technique was thus capable of accurately characterizing normal myocardial function throughout an entire cardiac cycle, at the same high resolution, and detecting and localizing myocardial infarction in vivo.     

Clinical Pharmacokinetics of Morphine

Morphine, the most widely used mu-opioid analgesic for acute and chronic pain, is the standard against which new analgesics are measured. A thorough understanding of the pharmacokinetics of morphine is required in order to safely and effectively use this analgesic in a wide variety of patients with different levels of organ function. A MEDLINE search was conducted to identify literature published between 1966 and January 2002 relevant to the pharmacokinetics of morphine. These publications were reviewed and the literature summarized regarding unique and clinically important elements of morphine disposition relative to its parenteral administration (including intravenous, intramuscular, subcutaneous, epidural and intrathecal administration), absorption profile (immediate release, controlled release, and sublingual/buccal, and rectal administration), distribution, and its metabolism/ excretion. Special populations, including infants, elderly, and those with renal/liver failure, have a unique morphine pharmacokinetic profile that must be taken into account in order to maximize analgesic efficacy and reduce the risk of adverse events.