CT Findings of Lung Ischemia Reperfusion Injury in Canine:Correlation with Pathophysiology

目的 评价闭胸式球囊栓塞法制备犬肺缺血再灌注模型的CT表现及其病理生理学基础.材料与方法 选用健康杂种犬11只,球囊栓塞犬左下叶肺动脉2h,然后撤出球囊,建立肺缺血再灌注模型,分别于栓塞前、栓塞2h、再灌注1h、2h、3h、4h分别行CT平扫,同时测量肺动脉主干的压力,抽取静脉血及动脉血做血常规及血气分析,再灌注4h行CT扫描后处死犬得到肺病理标本,进行病理学检查.分析其动态影像学表现、肺动脉压、血气结果及组织病理学表现.结果 10只犬模型制作成功,8只犬数据完整纳入最终分析.栓塞前8只犬双肺未见明显异常.栓塞2h,8只犬均表现为左肺透亮度增加,右肺均出现不同程度的“毛玻璃征”.再灌注过程中,8只犬双肺均出现不同程度“毛玻璃征”,持续4h后仍未恢复正常;非栓塞侧肺组织改变无规律的变化趋势;而栓塞侧肺组织再灌注3～4h时病变程度最重(n＝7).综合评价6个时间点,4只犬左肺病变略重于右肺,4只犬右肺病变略重于左肺.病理学检查见双肺均出现肺毛细血管充血,肺泡间隔增宽,其中4只犬左肺病理改变重于右肺,4只犬左肺病理改变比右肺轻;与上述影像学表现吻合.犬栓塞后至再灌注后4h持续存在低氧血症和酸碱平衡紊乱,但整体上栓塞前后至再灌注后4h肺动脉压、血气分析结果的差异无统计学意义(P＞0.05),综合分析显示再灌注过程中3h时机体病理生理学改变最重.结论 闭胸式球囊栓塞法制备的犬肺缺血再灌注损伤在CT像上主要表现为双肺轻重不一的“毛玻璃”样改变,持续至再灌注4h后仍未恢复正常,可能与肺毛细血管扩张充血、低氧血症和酸碱平衡紊乱等病理生理学改变相吻合.     

犬肺栓塞缺血-再灌注损伤模型的实验研究

目的 建立一种良好的适合进行影像学实验研究的肺栓塞缺血-再灌注损伤动物模型.方法 健康杂种犬20只.采用Seldinger技术穿刺右颈内静脉,置鞘,经鞘置入Swan-Ganz导管,用其球囊栓塞犬的右肺下叶动脉4 h,然后再撤除球囊,使血流再灌注4 h,制成肺栓塞缺血-再灌注损伤模型.在缺血前、缺血4 h和再灌注4 h 3个时间点进行肺部CT扫描.最后处死犬,把双下叶肺组织送检病理和电镜检查.结果 成功制作20只犬的闭胸式活体肺栓塞缺血-再灌注损伤模型,CT、病理和电镜扫描显示均符合肺栓塞缺血-再灌注损伤的变化,即渗透性肺水肿.结论 犬的闭胸式活体肺栓塞缺血-再灌注损伤模型可真实模拟肺栓塞缺血-再灌注损伤的病理生理过程,是一种良好的适合进行影像学实验研究的动物模型.     

犬肺栓塞-再灌注水肿的CT表现及动态观察

目的观察肺栓塞-再灌注水肿的CT表现及特点。材料与方法14只健康杂种犬被麻醉、气管插管。采用Swan-Ganz导管对实验犬进行24h肺栓塞、4h再灌注。栓塞前、栓塞24h、再灌注4h分别测量血气和肺动脉压。栓塞前、栓塞24h、再灌注30min、1、2、3、4h等7个时间点均进行了多排螺旋CT扫描。病理学检查包括透射电镜、光学显微镜和湿/干重比值（W/D）的测定。结果14只犬造模成功,均出现急性、混合性、非心源性的再灌注肺水肿（RPE）。CT表现从磨玻璃影逐渐过渡到结节样实变甚至出现大片实变。病理学主要表现为炎细胞浸润性肺水肿。再灌注4h,肺动脉收缩压（SPAP）平均值〔（25.79±6.25）mmHg〕和PaO2平均值〔（80.74±4.12）mmHg〕与栓塞前正常值〔（22.31±3.77）mmHg和（96.03±6.73）mmHg〕相比差异均具有统计学意义（P均〈0.05）。再灌注侧肺的W/D（6.29±1.23）显著大于对侧肺（4.54±1.19）（P〈0.01）,提示RPE增加了肺组织的含水量。结论低氧血症、肺动脉高压和肺中性粒细胞的激活和扣押是RPE的特点。其CT表现具有多样性。多排螺旋CT扫描能及时有效地反映RPE的动态变化。     

多层螺旋CT灌注成像评价伊达拉奉防治肺栓塞缺血-再灌注损伤疗效的实验研究

目的 探讨多层螺旋CT灌注成像用于评价伊达拉奉防治肺柃塞缺血-再灌注损伤(PTE-IRI)疗效的价值.方法 杂种犬20只,用球囊栓塞犬的右肺下叶动脉4 h,然后再撤除球囊,使血流再灌注4 h,制备PTE-IRI模型.根据实验动物是否用伊达拉奉和应用的时间,用数字表法将实验动物随机分为4组,每组5只,即A组:缺血时和再灌注时均不用伊达拉奉;B组:缺血时用伊达拉奉,再灌注时不用;C组:缺血时和再灌注时均用伊达拉奉;D组:缺血时不用伊达拉奉,再灌注时用.每组又分为缺血前、缺血4 h和冉灌注4 h 3个时间点,分别在这些时间点进行肺部CT平扫及CT灌注扫描.测量右肺下叶局部肺实质的血流量(BF)、血容量(BV)和平均通过时间(MTT),并采用方差分析的方法对其进行比较.结果 实验动物再灌注4 h CT检查主要表现为右肺下叶的肺水肿.(1)右肺CT灌注扫描组间比较:再灌注4 h A、B、C、D组的BF分别是(259.4±15.7)、(293.7±7.9)、(379.4±14.5)、(382.5±16.6)ml·min-1·100 g-1,MTT分别是(3.1±0.2)、(2.6±0.2)、(2.2±0.1)、(1.9±0.2)s;除C组和D组间的BF和MTT差异无统计学意义外(P值均＞0.05),其他各组间BF和MTY差异均有统计学意义(P值均＜0.01);各组间BV差异均无统计学意义(P值均＞0.05).(2)组内比较:A组和B组缺血前和再灌注4 h间的BF[缺血前A组为(397.2±19.2)ml·min-1·100 g-1,B组为(393.2±16.1)ml·min-1·100 g-1]和MTT[缺血前A组为(1.8±0.1)s,B组为(1.8±0.2)s]差异均有统计学意义(P值均＜0.01);缺血前和再灌注4 h A组BV分别为(12.0±0.9)、(12.2±1.0)ml/100 g,B组分别为(11.9±1.5)、(12.2±1.3)ml/100 g,差异均尤统计学意义(P值均＞0.05);C和D组缺血前和再灌注4 h间的BF、MTT、BV差异均无统计学意义(P值均＞0.05).结论 伊达拉奉可减轻肺栓塞缺血.再灌注损伤的程度,多层螺旋CT灌注成像可用于其效果的评价.     

用Swan-Ganz导管建立闭胸式肺栓塞-再灌注损伤犬模型的研究

目的应用Swan-Ganz导管建立一种闭胸式肺栓塞-再灌注动物模型，探讨肺栓塞-再灌注损伤的形成机制。方法选择14只健康杂种犬，体重15～18kg。无菌条件下，从颈外静脉插入1根7FSwan-Ganz导管送至一侧肺的膈叶动脉。通过向球囊充盈或抽出1．2ml稀释对比剂的方式，行肺动脉堵塞和再通。肺栓塞24h后抽空球囊，实现肺的膈叶再灌注4h。实验动物在正常状态下、肺栓塞24h、再灌注4h分别进行血气及肿瘤坏死因子-α（TNF-α）测定。正常状态、肺栓塞24h、再灌注30min及1、2、3、4h分别进行肺部薄层CT扫描。实验末，从双侧肺膈叶取下肺组织标本，分别用于湿／干重比率（W／D）的测量和病理学检查。结果14只犬造模成功，均出现急性混合性再灌注肺水肿。CT主要表现为再通血管远端区域不均匀的磨玻璃样密度增高影。组织病理学检查主要表现为炎细胞浸润性肺水肿。再灌注4h，PaO2为（81±4）mmHg（1mmHg=0．133kPa）、血清肿瘤坏死因子-α（TNF-α）为（16．0±2．5）pg／L，与栓塞前[分别为（96±6）mm Hg和（13．9±2．0）pg／L]差异均有统计学意义（q=-15．29、t=-2．46，P值均〈0．05）。再灌注侧肺的W／D为（6．3±1．2），大于对侧肺的（4．5±1．2）（t=3．83，P〈0．01）。结论Swan-Ganz导管建立的闭胸式肺栓塞．再灌注损伤犬模型，成功地模仿了肺栓塞-再灌注过程。薄层CT扫描能及时反映再灌注肺损伤的动态变化过程。TNF-α在肺栓塞-再灌注损伤的形成中起重要作用。     

兔肺动脉栓塞再灌注肺泡细胞凋亡及调控基因的实验研究

目的 探讨兔肺动脉栓塞／再灌注损伤中的细胞凋亡及其基因调控机制。方法 健康新西兰白兔36只，雌雄不拘，运用5F Berman球囊堵塞左下肺动脉，然后球囊放气，复制肺动脉栓塞缺血再灌注模型，随机分为6组：对照组，假手术组，肺栓塞1h组、肺栓塞2h组，肺栓塞2h再灌注1h组、肺栓塞2h再灌注2h组。实验结束取肺组织，测定肺组织湿干比，采用流式细胞分析法检测肺组织细胞凋亡率和免疫组织化学法检测肺上皮细胞Bax、Bcl-2、Fas／FasL蛋白表达的变化。结果兔肺动脉栓塞时肺组织细胞凋亡明显增加，再灌注后1h、2h凋亡细胞继续增加，并随着再灌注时间延长而增加（P〈0．05），Bax、Fas及FasL蛋白表达在肺动脉栓塞缺血及再灌注后明显增加（P〈O．01）。肺泡上皮细胞凋亡指数与肺组织湿干比、Bax、Fas、FasL蛋白表达之间存在非常显著的正相关关系（r=0．721，0．806，0．820，0．820；P〈0．01），与Bcl-2、Bcl-2／Bax比值呈显著负相关关系（r=-0．602，-0．829；P〈0．01）。结论肺动脉栓塞／再灌注中诱导肺组织细胞凋亡增加，肺组织细胞凋亡和Bax、Bcl-2，Fas、FasL系统活化可能参与了肺栓塞缺血再灌注肺损伤的发生。     

兔急性肺栓塞双源CT双能量肺灌注成像的动态变化及与病理对照

目的：动态观察家兔急性肺栓塞双源CT双能量肺灌注成像表现及其病理学基础,评价双源CT双能量肺灌注成像诊断家兔急性肺栓塞的价值。方法：经股静脉入路注入明胶海绵制作24只家兔急性肺栓塞模型,随机分成4组（即2h组、1天组、3天组和7天组）,每组6只。家兔栓塞前及栓塞后2h、1天、3天和7天行双源CT平扫和双能量扫描。采用双能量软件（LungPBV）进行数据分析处理,分别得到CT解剖图像（CTPA）、双能量肺灌注图像（DEPI）及两者融合图像。以肺叶为单位,分析栓塞前及栓塞后各时间点的肺灌注影像表现,并记录栓塞后肺内灌注异常的肺叶数目;进行家兔肺大体解剖和镜下观察,记录肺栓塞部位及病理表现。以病理为金标准,计算DEPI、CTPA及融合图像诊断肺栓塞的准确性。结果：栓塞前家兔双能量肺灌注图像表现为大致均匀的黄红色伪彩。栓塞后2h组肺灌注图像显示栓塞区呈蓝色;1天组及3天组栓塞区呈蓝黑色;7天组栓塞区呈黑色。DEPI和CTPA诊断肺栓塞的敏感度、特异度、阳性预测值（PPV）和阴性预测值（NPV）分别为100％、95％、95％和100％以及98％、100％、100％和99％;2项指标与病理结果吻合度强（Kappa值-0．933）,融合图像与DEPI一致性好。结论：采用双源CT双能量肺灌注成像技术可观察肺栓塞后肺实质动态灌注变化,并与病理结果有很高的一致性。     

犬急性大块肺动脉栓塞动物模型的建立

目的制作一种适合器械祛栓试验使用的犬急性大块肺栓塞动物模型。方法7只杂种犬,体外制作动物自体血栓,采用经皮股静脉穿刺置入导管,选择性插入一侧肺动脉中央分支动脉后注入制作好的自体血凝块,栓塞一侧肺动脉中央分支动脉,栓塞前后检测血气、肺动脉压及肺动脉造影。实验存活动物于12h后处死,取两侧肺组织进行病理检查。结果1只注射血栓时造成两侧肺栓塞死亡,1只在栓塞12h后肺动脉有部分再通;其余各只均成功栓塞至靶肺动脉的中央分支动脉。结论该方法制作急性大块肺栓塞的动物模型是可行和可重复的,可以为相关试验提供急性大块肺动脉栓塞动物模型。     

宝石能谱CT低剂量对比剂肺动脉成像

目的探讨利用能谱CT低剂量对比剂肺动脉成像诊断肺动脉栓塞及肺梗死的价值。方法对我院2014年1~4月间怀疑肺动脉栓塞的30例患者,行能谱CT低剂量对比剂肺动脉成像,可获得常规CT肺血管造影图像、单能量图像及碘基物质图像,观察肺动脉内有无栓子,记录栓子数、栓子部位以及栓塞程度,分析碘基物质图的影像学表现,记录肺内灌注减低区的位置及数目。结果明确诊断肺动脉栓塞的患者12例,共检出36处肺动脉及其分支栓子,左、右肺动脉主干8处,肺叶动脉16处,肺段动脉12处,共测得肺内灌注减低区16处。结论能谱CT低剂量对比剂肺动脉成像不但能够降低对比剂用量,最大限度减少对比剂的不良反应的发生,而且利用最佳单能量图和碘基物质图及定量测量等工具,能够更准确、安全的诊断肺动脉栓塞及肺梗死。     

双源CT双能量肺灌注成像对肺栓塞的诊断和临床应用价值

目的:探讨双源CT双能量肺灌注成像对肺动脉栓塞的诊断和临床应用价值。方法:对疑诊肺动脉栓塞的78名患者行双源CT肺动脉成像双能量扫描,数据经后处理得到肺动脉血管图像(CTA)和肺灌注图像(PBV)。两位医师对PBV图像进行质量评价和分型,同时观察CTA图像有无栓塞以及栓塞的部位、程度。分析PBV图像的表现与CTA图像、肺部异常改变的关系。用Kappa系数检验两位观察者对PBV图像质量评价和分型的一致性,计算PBV图像诊断肺栓塞的敏感度、特异度、阳性预测值和阴性预测值。结果:两位医师对肺灌注图像质量的分级以及肺灌注图像的分型一致性极强,K值分别为0.87、0.80,P值均<0.01。PBV图像诊断肺栓塞的敏感度为95.30%,特异度为56.40%,阳性预测值为70.70%,阴性预测值为91.20%。对于完全栓塞的患者,其敏感度和特异度均为100%。结论:双源CT双能量肺灌注成像能够显示肺动脉栓塞导致肺血流改变的肺灌注异常。     

Lung ischaemia–reperfusion injury in a canine model: dual-energy CT findings with pathophysiological correlation

Objective:

To evaluate dual-energy CT (DECT) findings of pulmonary ischaemic–reperfusion injury (PIRI) and its pathophysiological correlation in the canine model.

Methods:

A PIRI model was established in 11 canines, utilizing closed pectoral balloon occlusion. Two control canines were also included. For the PIRI model, the left pulmonary artery was occluded with a balloon, which was deflated and removed after 2 h. DECT was performed before, during occlusion and at 2, 3 and 4 h thereafter and was utilized to construct pulmonary perfusion maps. Immediately after the CT scan at the fourth hour post reperfusion, the canines were sacrificed, and lung specimens were harvested for pathological analysis. CT findings, pulmonary artery pressure and blood gas results were then analysed.

Results:

Data at every time point were available for 10 animals (experimental group, n = 8; control group, n = 2). Quantitative measurements from DECT pulmonary perfusion maps found iodine attenuation values of the left lung to be the lowest at 2 h post embolization and the highest at 1 h post reperfusion. In the contralateral lung, perfusion values also peaked at 1 h post reperfusion. Continuous hypoxia and acid–based disorders were observed during PIRI, and comprehensive analysis showed physiological changes to be worst at 3 h post reperfusion.

Conclusion:

DECT pulmonary perfusion mapping demonstrated pulmonary perfusion of the bilateral lungs to be the greatest at 1 h post reperfusion. These CT findings corresponded with pathophysiological changes.

Advances in knowledge:

DECT pulmonary perfusion mapping can be used to evaluate lung ischaemia–reperfusion injury.Ischaemia–reperfusion injury (IRI) occurs under a variety of clinical conditions, including lung and/or cardiac transplantation, cardiopulmonary bypass, pulmonary resection, re-expansion pulmonary oedema, shock, cardiopulmonary resuscitation and pulmonary embolism.^1–3 Pulmonary embolism is a common cause of pulmonary IRI (PIRI), and the incidence of pulmonary embolism is increasing^4,5 with a mortality rate of up to 30%.⁶ With timely identification and treatment of pulmonary embolism, mortality rates can be reduced to <10%.⁷ However, reperfusion after treatment for lung ischaemia can also cause serious complications, such as haemorrhage and pulmonary oedema.⁸ Therefore, it is important to understand both the pathophysiological and imaging appearances of pulmonary IRI. Lung transplantation is also a common cause for PIRI following pulmonary arterial occlusion. Currently, the incidence of PIRI following transplantation is estimated at up to 25%. Post transplantation, PIRI can lead to insufficiency of the primary lung graft, delayed graft function, acute or chronic rejection (e.g. pulmonary oedema and acute respiratory failure), and increased early post-operative mortality and graft failure.^9,10CT is currently the predominant modality for the imaging assessment of thoracic disorders, including PIRI. Dual-energy CT (DECT) allows simultaneous acquisition of dual-energy data sets, allowing for decomposition of the scanned entity based on differences in attenuation between air, soft tissue and iodine.¹¹ One application of this principle in pulmonary imaging is the ability to obtain iodine maps demonstrating the distribution of pulmonary perfusion. The use of CT perfusion mapping has been shown to be relatively sensitive and highly specific for the detection of pulmonary emboli.¹²Recent research into PIRI has focused on the pathological and molecular biological mechanisms.^13–16 To date, there are few reports on imaging and pathophysiological findings in PIRI.^17,18 CT perfusion findings in PIRI have also not yet been described. The aim of this study was to assess PIRI imaging and pathophysiological findings in a canine model.     

肺错构瘤的CT表现及其与其他疾病的鉴别

目的分析肺错构瘤的MSCT表现及其与其他疾病的鉴别。方法对26例行MSCT检查并经手术和病理证实的肺错构瘤进行回顾性分析。结果本组26例均为单发肺错构瘤,其中22例为周围型,位于右肺12例,位于左肺10例;4例为腔内型,其中,1例位于气管中段腔内,1例位于左主支气管内,2例位于左肺下叶支气管内。病灶呈圆形或椭圆形,边缘锐利,9例显示有浅分叶,但均无毛刺。本组22例周围型错构瘤中,3例病灶内含有脂肪密度影;9例病灶内含有钙化影,其中3例为典型的爆米花样钙化;10例病灶呈均匀软组织密度影。4例腔内型错构瘤中,3例病灶内含有脂肪成分,1例含有钙化影。本病主要需于肺炎性假瘤、小叶癌、结核瘤相鉴别。结论肺错构瘤的MSCT表现有一定特征,病灶边缘清楚,内含有脂肪和钙化有助于正确诊断。     

肺隐球菌病的 CT 表现及临床分析

目的：探讨 HIV 阴性患者肺隐球菌病(PC)的 CT 表现。方法回顾性分析26例经病理确诊的 PC 患者的 CT 资料,所有患者均行胸部 CT 平扫,其中8例行增强扫描。结果26例患者中在 CT 上表现为单发病灶11例,多发结节/肿块10例,混合型5例。病灶仅出现在左肺11例,右肺7例,双肺均出现病灶8例。19例可见毛刺,10例见空洞或空泡,8例见晕征。增强扫描1例病灶明显不均匀强化,2例表现为中度不均匀强化,3例轻度强化,2例病灶无强化。结论PC 在 CT 上表现多样,容易误诊为肺癌等其他病变。CT 引导下经皮肺穿刺活检是确诊的有效方法。     

肺真菌病的X线及CT诊断

目的 探讨肺真菌病X线及CT影像表现特征,提高影像诊断水平.方法 回顾分析经病理证实的肺真菌病43例.全部病例均行X线平片及胸部CT检查.结果 左肺14例,右肺21例,双肺多发8例.病灶呈单/多发结节或肿块12例(27.9%);呈单/多发斑片状浸润29例(67.4%);斑片与结节影混合者2例(4.7%).总误诊15例(34.9%),X线平片误诊14例(32.6%),CT误诊5例(11.6%),有4例同时误诊.结论 X线平片及CT对有特征性表现的肺真菌病可做出正确诊断,对于表现不典型者,密切结合临床可提高诊断准确率.     

肺硬化性血管瘤的CT诊断

目的 探讨肺硬化性血管瘤(PSH)的CT表现及诊断价值.方法 回顾性分析经穿刺活检及手术病理证实的肺硬化性血管瘤9例,对其CT表现和病理学特点进行分析.结果 9例中,按部位区分:左肺上叶2例,左肺下叶2例,右肺中叶4例,右肺上叶1例,均为单发病灶;按病灶形态区分:7例为结节状影,境界清晰,1例为长条状,1例为楔形影.CT平扫9例均呈软组织密度,1例边缘可见点状钙化,3例内部可见气体,呈空气新月征,其中3例行增强扫描,均明显强化,其中1例可见血管贴边征.结论 肺硬化性血管瘤在CT平扫中具有良性肿瘤的普遍性特点,空气新月征及增强扫描对肺硬化性血管瘤的诊断有较高价值.     

甲型H1N1流感病毒性肺炎的影像学表现

目的:回顾性讨论12例甲型H1N1流感病毒性肺炎患者的胸部X线和CT表现特征。方法:经临床证实的甲型H1N1流感病毒性肺炎病例12例,男8例,女4例,年龄范围6~51岁,平均年龄21岁。所有患者在发病后1周内均行胸部X线检查及胸部CT扫描。结果:本组病例中,出现临床症状1~4天胸片像表现为阳性者10例,占83%;4~8天胸片像上为阳性者2例,占17%。多数患者的病灶多发。进展期病变发展迅速,常累及多部位及双肺。好转期一般在7~14天。结论:甲型H1N1流感病毒性肺炎主要影像学表现为:①病变位于肺的外周多,多部位受累,双肺各叶均可发生,以双肺下叶为著;②病变多发,大小不等;③早期最常见的影像学表现为斑片状磨玻璃影;④病变变化迅速。     

犬急性骨水泥肺栓塞的实验研究

目的通过股静脉注入骨水泥建立犬急性肺栓塞模型,探讨一定剂量范围内不同量骨水泥肺栓塞引起的生理病理变化间的差异。方法 18只成年家犬随机分成A、B、C 3组,每组6只,麻醉后行胸部CT平扫,穿刺右股静脉、左股动脉并置入血管鞘,经静脉鞘注入聚甲基丙烯酸甲酯(PMMA)A组0.5 ml,B组1 ml,C组2 ml。于注入PMMA前和注入后即刻、30 min及1 h分别检测血气分析、平均肺动脉压;于注入PMMA前、后5 min行肺动脉造影。术后1h行胸部CT平扫+增强。术后2 h将犬处死,开胸解剖观察大体形态后,沿肺动脉分支方向随机取肺组织3块进行病理学检查。结果 18只实验犬经股静脉注入PMMA操作均成功,经CT及病理证实均成功建立急性骨水泥肺栓塞模型。各组实验犬动脉血氧分压、二氧化碳分压在骨水泥注入前后差异均无统计学意义(P>0.05)。仅C组骨水泥注入后即刻平均肺动脉压为(24.12±1.74)mmHg,注入后30 min为(23.84±1.25)mmHg,注入后1 h为(24.17±1.63)mmHg,均较注射前的(16.47±0.55)mmHg差异有统计学意义(P<0.05)。A组、B组平均肺动脉压在骨水泥注入前后差异均无统计学意义(P>0.05)。各组实验犬术后胸部CT平扫均可见两肺高密度影,下肺多见,C组尤为明显。部分实验犬平扫见条索状阴影及肺不张征象。C组部分实验犬胸部增强CT可见肺动脉小分支内部分充盈缺损。肺动脉造影仅C组部分实验犬出现肺内部分细小血管减少,血管纹理稀疏,未见肺动脉主干及分支的充盈缺损。病理学检查均发现肺动脉分支存在骨水泥栓子,未见继发血栓形成。结论≤2 ml的骨水泥致急性肺栓塞的严重程度与注入骨水泥剂量没有相关性。在心肺功能正常情况下,≤2 ml的急性骨水泥肺栓塞不会引起明显的呼吸功能障碍。     

Hydrostatic pulmonary edema: evaluation with thin-section CT in dogs

PURPOSE: To identify the hemodynamic determinants of ground-glass opacification on thin-section computed tomographic (CT) scans of hydrostatic pulmonary edema and to compare attenuation and subjective assessments of ground-glass opacification with extravascular lung water. MATERIALS AND METHODS: Left atrial pressure, pulmonary arterial pressure, effective pulmonary capillary pressure, and extravascular lung water were measured in six dogs before and during progressive increase of effective pulmonary capillary pressure. A thin-section CT scan was obtained at each step. Lung attenuation and subjective assessments of ground-glass opacification were compared with hemodynamic variables and extravascular lung water. RESULTS: Ground-glass opacification was identified when effective pulmonary capillary pressure equaled critical pulmonary capillary pressure. Extravascular lung water increased, and the distribution curve of lung attenuation coefficients shifted to higher attenuation from the second measurement at an effective pulmonary capillary pressure greater than the critical pulmonary capillary pressure. Attenuation was highly correlated (r = 0.98, P < .001) with extravascular lung water; ground-glass opacification was detected before a significant (P = .615, analysis of variance) increase in extravascular lung water. CONCLUSION: Thin-section CT depicts ground-glass opacification when effective pulmonary capillary pressure equals critical pulmonary capillary pressure and before a detectable increase in extravascular lung water. Attenuation reflects extravascular lung water.     

Perfusion characteristics of radiation-injured lung on Gd-DTPA-enhanced dynamic magnetic resonance imaging

RATIONALE AND OBJECTIVES: A contrast-enhanced dynamic magnetic resonance (MR) study was performed experimentally and clinically to describe perfusion characteristics of radiation-injured lung according to pathologic phases. METHODS: The MR study was performed before and at 0.5, 1, 2, 3, 4, and 7 months after 40 Gy-dose irradiation to the right hemithorax in 8 dogs, and clinically in 12 lung lesions of 9 patients with acute or fibrotic radiation pneumonitis. Altered Gd-DTPA kinetics in the affected lungs was assessed by time-signal intensity curves. MR findings were correlated with lung histology and CT images. RESULTS: Within 1 month after irradiation, the irradiated animal lungs showed focal and persistent contrast enhancement relative to nonirradiated lungs. This abnormality was pronounced during the next 2 months. After 4 months, irradiated lungs conversely showed lower enhancement during the Gd-DTPA first-pass but were followed by persistently greater enhancement during Gd-DTPA redistribution phase. Similar differences in enhancement abnormalities between acute and fibrotic radiation pneumonitis were clinically observed. CONCLUSION: These findings indicate that Gd-DTPA kinetics can be altered according to the histopathologic change in early/acute radiation pneumonitis and radiation fibrosis and that the contrast-enhanced perfusion MRI may help differentiate the phases of radiation pneumonitis.     

肺硬化性血管瘤的影像学表现及误诊分析

目的探讨肺硬化性血管瘤的X线、CT表现及误诊原因,提高本病的诊断准确率。方法回顾性分析16例资料完整且经病理证实的肺硬化性血管瘤X线、CT表现。结果左肺8例,右肺8例;均呈圆形或类圆形,边缘光整12例,浅分叶3例,1例边缘不规整;密度均匀12例,CT值约为42HU,点状钙化2例,空气半月征1例,囊变坏死1例,血管贴边征2例;增强10例,明显均匀强化9例,不均匀强化1例。术前误诊8例,误诊为周围型肺癌(n=4),转移瘤(n=2),错构瘤(n=1),曲霉菌球(n=1)。结论 PSH特征性表现为肺内孤立性,圆形或类圆形肿块,边缘光整,明显强化,偶见点状钙化及空气半月征,而对其影像特征及鉴别诊断认识不足是误诊的主要原因。