促红细胞生成素对心肺复苏后心肌功能的影响

目的 探讨促红细胞生成素(EPO)对窒息性心搏骤停大鼠心肺复苏(CPR)后心功能不全的心肌保护作用.方法 经夹闭气管8 min建立窒息性心搏骤停-CPR动物模型.按随机数字表法将24只SD大鼠分为3组,每组8只.CPR组窒息致心搏骤停后8 min予胸外按压和机械通气进行复苏;EPO组于自主循环恢复(ROSC)后3 min股静脉注射EPO 5 kU/kg;正常对照组不予任何处理.持续监测左心室收缩压(LVSP)、左心室舒张期末压(LVEDP)、左心室内压上升或下降最大速率(±dp/dt max)等血流动力学指标.于观察终点(ROSC后120 min)处死大鼠,采血测定血清心肌肌钙蛋白Ⅰ(cTnI)含量;光镜和透射电镜下观察心肌组织病理改变;原位末端缺刻标记法(TUNEL)检测心肌细胞凋亡.结果 CPR组和EPO组ROSC后30、60、90、120 min时LVSP、+dp/dt max和- dp/dt max绝对值均较基线水平明显下降.与正常对照组比较,CPR组和EPO组ROSC 30 min时LVSP(mm Hg,1 mm Hg=0.133 kPa)、+dp/dt max(mm Hg/s)、- dp/dt max绝对值(mm Hg/s)即明显下降(LVSP:119.52±12.68、134.32±15.78比165.82土7.05; +dp/dt max:4 457.14±826.22、6 019.85±1 192.19比10 325.93±773.09; - dp/dt max:-3 956.04±952.37、-4 957.22±838.60比-8 421.33±886.65,均P＜0.01),并持续至ROSC 120 min(LVSP:124.62±8.07、145.61±16.70比162.34±7.63; +dp/dt max:4 977.67±350.40、7 471.62±998.32比9 999.39±727.96;- dp/dt max:-4 145.51±729.77、-5 895.64±787.30比-8 089.75±981.52,均P＜0.01);经EPO处理后ROSC各时间点LVSP、+dp/dtmax和- dp/dtmax绝对值均较CPR组显著升高(均P＜0.05).CPR组和EPO组ROSC 120 min LVEDP(mm Hg/s)均较正常对照组明显升高(22.94±3.94、11.18±2.58比2.89±0.70,均P＜0.01),EPO组LVEDP则较CPR组明显下降(P＜0.05).光镜和电镜下观察,CPR组心肌细胞坏死、炎性细胞浸润,心肌细胞胞膜完整性丧失、线粒体肿胀,心肌细胞凋亡增加[凋亡细胞数(个):314.1±30.7比165.2±45.9,P＜0.01];经EPO干预后心肌病理损伤减轻,心肌细胞凋亡较CPR组减少(凋亡细胞数:242.1±20.0比314.1±30.7,P＜0.05).CPR组和EPO组ROSC 120 min血清cTnI (μg/L)均较正常对照组明显升高(20.70土5.96、16.98±3.81比2.60±0.86,均P＜0.01),而CPR组和EPO组比较无差异.结论 EPO可以改善窒息性心搏骤停大鼠CPR后的心功能,减轻心肌损伤,其机制可能与减少线粒体损伤和心肌细胞凋亡有关.     

插入式腹主动脉按压对心搏骤停兔心肺脑复苏的实验研究

目的：探讨插入式腹主动脉按压心肺复苏（IAAC-CPR）对心搏骤停兔心肺脑复苏的效果。方法健康新西兰大白兔10只,雌雄不拘,按随机数字表法分为传统胸外按压心肺复苏（CC-CPR）组和IAAC-CPR组,每组5只。经颈静脉快速推注冰氯化钾并夹闭气管导管制备心搏骤停模型;心搏骤停3 min后开始实施心肺复苏（CPR）,CC-CPR组为呼吸机辅助通气+胸外按压;IAAC-CPR组为呼吸机辅助通气+胸外按压+腹主动脉按压。观察CPR过程中血流动力学和脑皮质血流的变化;记录自主循环恢复（ROSC）时间,观察动物24 h生存情况、24 h神经功能评分及腹部器官情况等。结果 IAAC-CPR组复苏后30、60、90、120 s时脑血流量（CBF,PU值）及平均动脉压（MAP,mmHg,1 mmHg＝0.133 kPa）均明显高于CC-CPR组（CBF 30 s：16.1±6.0比7.8±2.2,60 s：91.6±11.8比57.3±23.2,90 s：259.9±74.9比163.6±50.3,120 s：301.5±60.5比208.4±23.8;MAP 30 s：46.4±9.4比31.4±8.7,60 s：55.8±13.8比34.0±11.5,90 s：61.2±11.5比38.2±10.1,120 s：63.6±11.8比40.2±10.2;均P＜0.05）。与CC-CPR组比较,IAAC-CPR组ROSC所需时间明显缩短（s：182.0±59.0比312.6±86.6,t＝2.787,P＝0.024）,24 h神经功能评分明显下降（分：2.4±1.7比4.6±0.6,t＝2.974,P＝0.023）;而复苏成功率（80.0%比60.0%,χ2＝0.000,P＝1.000）、24 h存活率升高（80.0%比40.0%,χ2＝0.417,P＝0.519）,但差异无统计学意义。ROSC后24 h尸解动物均未发现肝脏损伤。结论在心搏骤停兔复苏早期,IAAC-CPR较CC-CPR取得了更好的脑血流灌注,明显减轻了心搏骤停兔的神经系统功能损伤,且无腹部器官损伤。     

自主循环恢复后轻度低温对心室纤颤兔心功能和心肌结构的影响

目的 观察轻度低温干预对心室纤颤(室颤)兔自主循环恢复(ROSC)后心脏功能、心肌结构和48 h存活率的影响.方法 将新西兰兔按随机数字表法分为4组,采用心外膜电刺激致颤4 min行心肺复苏(CPR)复制动物CPR模型,ROSC后即分别给予常温[(39.0±0.5)℃,n=10]和低温[(33.5±0.5)℃,n=10]处理;同时设常温(n=8)和低温(n=8)对照.各组均监测4h血流动力学指标,观察48 h存活情况;取心肌组织进行病理学观察,检测细胞凋亡[原位末端缺刻标记法(TUNEL)];测定左室心尖组织ATP、ADP、AMP含量[高效液相色谱(HPLC)法],并计算心肌能荷(EC).结果 ①血流动力学:低温对照组和常温对照组比较,心率(HR)、左室压力下降最大速率(-dp/dt max)在基线后各时间段均有下降;左室压力上升最大速率(+dp/dt max)和平均动脉压(MAP)在0.5h有显著差异,而在其他时段均无差异;左室舒张期末压(LVEDP)、左室收缩期末压(LVESP)和股动脉收缩压(SBP)、舒张压(DBP)在各时间段均无显著差异.②复苏后低温组与复苏后常温组比较,HR(次/min)和-dp/dt max(mm Hg/s)在ROSC后0.5、1、2、3、4h均有下降(HR:216.5±33.3比292.9±38.4,218.2±28.0比294.3±37.0,227.5±25.4比291.4±25.3,232.4±27.4比278.1±30.8,230.6±22.0比285.1±38.2;-dp/dt max:1 847.1±241.2比2 383.3±470.9,1 860.7±167.8比2 154.6±319.5,1 822.3±389.7比2 239.7±379.0,1 950.6±412.9比2 229.6±392.4,1 875.7±555.6比2 396.7±420.1,均P＜0.05); LVEDP、+dp/dt max、LVESP、股动脉血压(SBP、DBP、MAP)在ROSC后各时间点均无显著差异.③复苏后低温组48h心肌组织形态损害较复苏后常温组轻.④复苏后低温组心肌细胞凋亡指数(AI)低于复苏后常温组(26.39％比42.02％,P＜0.05).⑤能量检测:复苏后低温组ATP含量(μmol/g)高于复苏后常温组(0.97±0.26比0.65±0.16,P＜0.05).复苏后常温组EC明显低于常温对照组和低温对照组[(0.33±0.13)％比(0.52±0.12)％、(0.55±0.06)％,均P＜0.05],而复苏后低温组EC[(0.41±0.12)％]与两对照组无显著差异.⑥复苏后低温组48 h存活率高于复苏后常温组(100％比60％,P=0.043).结论 室颤兔ROSC后存在心肌结构损害和心功能下降;轻度低温干预可降低48 h死亡率,其保护机制可能与抑制复苏后心肌细胞进一步的损害和凋亡有关;轻度低温对心功能无明显直接抑制,也不引起血流动力学恶化.     

硝酸异山梨酯改善猪心肺复苏后的心功能障碍

目的研究硝酸异山梨酯（isosorbide mononitrate,IM）对室颤型心脏骤停猪自主循环恢复（return of spontaneous circulation,ROSC）后的心功能障碍的影响。方法实验于首都医科大学附属北京朝阳医院实验中心进行。20头五指山小型猪随机（随机数字法）分成 IM组（n ＝10）和对照组（n ＝10）,通过程控刺激方法制作室颤型心脏骤停模型,制模成功后8 min 后行 CPR。IM组在 ROSC 即刻给予 IM [2μg／（kg·min）]6 h;对照组则给予等量生理盐水。比较两组实验动物 ROSC 后24 h 内血流动力学及 ROSC 后72 h 心脏超声和心肌超微结构变化。结果IM组和对照组 ROSC 几率相同;IM组平均动脉压（mmHg,1 mmHg ＝0.133 kPa）在 ROSC 后6 h （88.5±5.6 vs.87.8±6.0,P ＝0.790）与24 h （89.3±3.8 vs.86.9±5.0,P ＝0.245）较对照组差异无统计学意义;IM组心输出量（L／min）在 ROSC 6 h （2.40±0.17 vs.1.60±0.14,P ＜0.01）及24 h （2.49±0.12 vs.2.09±0.16,P ＜0.01）较对照组显著升高;复苏后72 h IM组左心室收缩功能较对照组显著改善,射血分数显著高于对照组（0.67±0.08 vs.0.56±0.09,P ＝0.044）;ROSC 72 h IM组心肌超微结构损伤较对照组减轻。结论硝酸异山梨酯可以改善室颤引起的猪心搏骤停复苏后的心功能障碍。     

胞二磷胆碱提高心肺复苏效果和减轻心肌损伤的作用研究

目的 探讨胞二磷胆碱在心肺复苏(CPR)中对于提高自主循环恢复(ROSC)率和减轻心脏损伤的作用.方法 按随机数字表法将SD大鼠分为对照组(未窒息,5只)、模型组(10只)、肾上腺素组(10只)、胞二磷胆碱组(10只),用窒息法复制心搏骤停(CA)动物模型并进行CPR,各组分别于复苏前5 min和复苏开始时给2次药,对照组和模型组给予等量生理盐水.各组于CPR期间及复苏成功后2h内测定血流动力学指标,然后处死大鼠取心脏组织,检测ATP酶、超氧化物歧化酶(SOD)、丙二醛(MDA)水平,评估大鼠心肌缺血/再灌注损伤情况.结果 胞二磷胆碱组和肾上腺素组ROSC率高于模型组(90％、80％比20％,均P＜0.01),平均复苏时间(s)显著短于模型组(53±10、55±9比95±7,均P＜0.01);复苏后2h末心率(HR,次/min)、平均动脉压(MAP,mm Hg,1 mm Hg=0.133 kPa)均显著高于模型组(HR:222.78±41.55、167.75±11.76比131.50±0.70,MAP:36.53±8.69、39.30±6.45比30.19±5.15,均P＜0.01).胞二磷胆碱组复苏后心功能[左室内压上升/下降最大速率(±dp/dt max)]逐渐平稳并显著高于模型组和肾上腺素组;肾上腺素组虽高于模型组,但下降趋势明显.胞二磷胆碱组Na+-K+-ATP酶(μmol· mg-1· h-1)和SOD活性(U/mg)显著高于模型组和肾上腺素组(Na+-K+-ATP酶:7.35±0.20比5.11 ±0.69、4.70±0.41,SOD活性:320.65±47.25比225.79±24.64、253.67±12.00,均P＜0.01),而MDA含量(mmol/mg)显著低于模型组和肾上腺素组(8.19±1.64比16.59±1.27、14.65±0.93,均P＜0.01),且上述指标与对照组比较无明显差异;模型组和肾上腺素组上述各指标也无明显差异.结论 胞二磷胆碱可提高CPR成功率,并且与肾上腺素相比可减轻心肌缺血/再灌注损伤,改善复苏后心功能.     

呼气末二氧化碳分压在心室纤颤与窒息性心搏骤停心肺复苏中的变化

呼气末二氧化碳分压（PETCO2）已被用来监测胸外按压效果（PC）和作为预测心肺复苏（CPR）预后的一项指标。近期国内研究者进行了一项实验研究,观察心室纤颤（室颤）和窒息性心搏骤停CPR过程中PETCO2的变化。62只雄性SD大鼠随机分为窒息组（n＝32）和室颤组（n＝30）,在CPR进行过程中间隔6 min测量1次PETCO2。结果显示,室颤组胸外按压即刻初始PETCO2水平明显低于窒息组（mmHg：12.8±4.87比49.2±8.13,P＝0.000;1 mmHg＝0.133 kPa）。在室颤组,自主循环恢复的大鼠经过6 min胸外按压时的PETCO2水平明显高于自主循环未恢复的大鼠（mmHg：16.5±3.0比13.2±2.62,P＝0.004）。在窒息组,胸外按压2 min后,自主循环恢复的大鼠PETCO2水平显著高于自主循环未恢复的大鼠（mmHg：20.8±3.24比13.9±1.50 mmHg,P＝0.000）。PETCO2的受试者工作特征曲线（ROC曲线）显示,室颤性心搏骤停和窒息性心搏骤停对自主循环恢复的预测有显著的敏感性和特异性。因此研究人员得出结论：在CPR开始即刻初始的PETCO2水平可能有助于辨别心搏骤停的原因。CPR中PETCO2的变化可预测CPR的结局。     

心肺复苏后早期注射冰盐水的有效性和安全性临床评价

目的：评价心搏骤停患者早期注射冰盐水实现亚低温治疗的可行性、安全性和有效性。方法采用单中心前瞻性随机对照的临床研究方法,以2011年3月到2013年10月北京市大兴区人民医院抢救的心搏骤停进行心肺复苏（CPR）后自主循环恢复（ROSC）的患者为研究对象,按随机数字表法将患者分为两组。ROSC后,冰盐水组患者立即快速静脉注射4℃生理盐水1000 mL来实现亚低温治疗,对照组给予常规头部冰袋降温治疗和腋温监测。所有患者在ROSC即刻和1 h后分别测量直肠温度;记录复苏后6 h胸片出现急性肺水肿、48 h内出现寒战、48 h再次发生心室纤颤（室颤）以及14 d内成功苏醒和死亡的患者例数。结果共有45例患者纳入本研究,其中冰盐水组23例,对照组22例。冰盐水组患者ROSC即刻直肠温度为（36.7±0.9）℃,1 h后降至（34.9±0.7）℃;对照组患者ROSC即刻直肠温度为（36.5±1.0）℃,1 h后升高至（37.9±0.9）℃,两组ROSC后1 h直肠温度比较差异有统计学意义（t＝2.228,P＝0.031）。冰盐水组14 d内成功苏醒患者例数明显多于对照组（13例比7例,χ2＝65.710,P＝0.021）,而出现急性肺水肿（4例比6例）、寒战（2例比0例）、再次发生室颤（4例比5例）和14 d内死亡（11例比12例）的患者例数与对照组比较差异均无统计学意义（均P＞0.05）。结论早期快速静脉注射4℃生理盐水来实现复苏后亚低温治疗脑复苏效果更佳理想,且是可行的、安全的、有效的。     

两种不同复苏方法对院前心搏骤停患者初期复苏效果的随机对照研究

目的：比较主动加压减压心肺复苏(ACD—CPR)和标准心肺复苏(CPR)对于院前发生心搏骤停患者的初期复苏效果，探讨ACD—CPR对院前心搏骤停患者的疗效。方法：将在急诊重症监护室(EICU)发生心搏骤停的92例患者按照区组随机的方法分为ACD—CPR组和标准CPR组，比较两组在复苏开始后1、3、5、10、15和30min时的收缩压(SBP)、自主循环恢复率(ROSC)和入院率。结果：ACD—CPR组3、5、10和l5min时SBP均高于标准CPR组(P均＜0．05)。ACD—CPR组思者的ROSC(52．5％)高于标准CPR组(27．8％)，也具有显著的统计学差异(P＜0．05)。ACD—CPR组的收住院率(21．3％)也高于标准CPR组(15．3％)，但无统计学意义。结论：ACD—CPR在改善院前发生的非创伤性心搏骤停患者初期复苏效果方面，优于标准CPR。     

弥散加权成像观察去甲肾上腺素诱导的高血压灌注对心搏骤停猪脑功能的影响

目的 观察高血压灌注心搏骤停猪自主循环恢复(ROSC)后脑功能的变化.方法 采用电刺激建立猪心室纤颤(室颤)模型,室颤4 min后给予标准心肺复苏(CPR),将ROSC猪按随机数字表法分为两组,每组5只.高血压灌注组立即给予去甲肾上腺素(NE)使平均动脉压(MAP)维持在室颤前血压的130％;正常灌注组给予NE维持MAP为室颤前水平;两组均监测4h观察血流动力学变化;于室颤前及ROSC后1h、3h用弥散加权成像(DWI)技术扫描大脑顶叶皮质,观察脑功能成像的动态变化;于复苏后24 h制备脑组织切片,观察顶叶的病理学变化.结果 与正常灌注组比较,高血压灌注组于ROSC后不同时间点心率(HR,次/min)、MAP(mm Hg,1 mm Hg=0.133 kPa)、心排血量(CO,L/min)、冠状动脉灌注压(CPP,mm Hg)均出现升高趋势(ROSC 30 min HR:167±8比140±15,ROSC 1 h MAP:131 ±9比108±10,ROSC 1 h CO:4.9±0.1比3.4±0.5,ROSC 2 h CPP:118±12比88±1,P＜0.05或P＜0.01).两组复苏前后DWI未见明显异常;复苏后大脑皮质表观弥散系数(ADC)均呈下降趋势,正常灌注组下降趋势较高血压灌注组明显.光镜下观察高血压灌注对脑的保护作用优于正常灌注组.结论 高血压灌注可引起心搏骤停猪复苏后血流动力学的改变,增加脑血流量,对脑具有保护作用,有利于促进神经功能的恢复.     

心脏骤停患者心肺复苏自主循环恢复预后相关因素分析

目的：探究心脏骤停（CA）患者心肺复苏（CPR）自主循环恢复后（ROSC）预后的相关因素,为提高CPR成功率提供临床经验。方法：回顾性分析广东省梅州市人民医院2018年1月到2021年2月525例CPR患者的基线资料、入院信息、CPR信息、治疗情况和结局。结果：以ROSC分组并建立Logistic回归模型,未ROSC组CPR持续时间高于ROSC组（34.39±11.56 min vs 18.59±16.66 min,P<0.001）;CPR所致胸部损伤OR值0.277(95%CI:0.115-0.670)）和CPR持续时间OR值0.006(95%CI:0.002-0.017)可能是ROSC的独立影响因素。以出院状态分组并建立Logistic回归模型,存活出院组CPR持续时间高于非存活出院组（22.08±19.10 min vs 15.86±14.05 min,P=0.041）;以“非存活出院”为参考状态,CPR持续时间、CPR所致胸部损伤和入院时间可能是患者存活出院的影响因素,OR值分别为0.951(95%CI:0.915-0.988),4.457(95%CI:1.297-15....     

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.