目的建立紫绀型肺血少动物模型,对肺血减少时未成熟肺小血管进行形态观察和半定量分析,观察肺血减少时未成熟肺小血管的发育特点。方法取紫绀型肺血少动物肺组织,进行固定、制片及染色。光镜和透射电镜观察,形态半定量测量分析肺小动脉中膜厚度(media thickness,MT)及中膜厚度百分比(percentage of media thickness,MT%)、中膜面积(media section area,MS)及中膜面积百分比(percentage of media section area,MS%);计数单位面积肺小动脉数目(arterial numbers of per square centimeter,APSC)和单位面积肺泡数量(mean alveolar nunber,MAN);计算同一张切片所有泡内肺动脉(intraacinar pulmonary arteries,IAPA)中肌型动脉(circular muscular artery,CMA)、部分肌型动脉(partially muscular artery,PMA)和无肌型动脉(non-muscular artery,NMA)的比例。结果同对照组(C组)相比,光镜观察肺血减少组(D组)肺小动脉中层退化和发育不良,管腔扩大,形态不规则,管壁厚薄不均,部分弹力纤维层中断、缺失。PMA和NMA比例较C组高,而CMA比例相对较低(P<0.001)。D组肺小动脉MT、MT%及MS、MS%均显著小于C组(P均<0.001)。D组APSC较C组减少(P<0.01),而MAN与C组差异无显著性(P>0.05)。电镜下显示D组肺小血管内皮细胞胞质肿胀,基膜变薄;弹力纤维排列不整齐,有的区域萎缩变薄或中断;血管中层平滑肌轻度萎缩;细胞器减少,线粒体空泡化;部分肺泡Ⅱ型上皮细胞增生明显,板层体丰富。结论肺血流减少时肺小血管发育不良或退化,形态结构异常影响器官的正常功能,尽早改善肺血少状态是促进肺血管发育和改善全身状况的关键。
目的探讨心率变异性与脓毒血症病情危重程度的关系。方法 68例脓毒血症患者为脓毒血症组,根据患者急性生理与慢性健康评分-Ⅱ(Acute Physiology and Chronic Health EvaluationⅡ,APACHE-Ⅱ)评分分为危重组32例和非危重组36例,68例体检健康者为对照组。入选者均行24h动态心电图和血生化检查等,观察并比较各组全部相邻NN间期差值的均方根值(RMSSD)、每5min NN间期的标准差均值(SDANN)、全部NN标准差(SDNN)、相邻NN间期差值>50ms的个数占总NN间期数的比例(PNN50),以及血乳酸、皮质醇、空腹血糖和血小板计数等指标,分析心率变异性与脓毒血症病情危重程度的关系。结果脓毒血症组RMSSD[(20.19±6.03)ms]、SDANN[(76.78±18.90)ms]、SDNN[(92.32±16.45)ms]、PNN50[(9.15±2.79)%]均低于对照组[(36.87±11.43)ms、(98.57±19.43)ms、(122.56±19.36)ms、(15.46±4.64)%](P<0.05),乳酸[(2.42±1.01)mmol/L]、皮质醇[(334.3±80.5)μg/L]、空腹血糖[(7.03±2.15)mmol/L]高于对照组[(1.03±0.62)mmol/L、(165.9±53.7)μg/L、(4.54±1.28)mmol/L](P<0.05);脓毒血症危重组SDANN[(59.45±9.03)ms]、SDNN[(72.36±13.57)ms]、PNN50[(7.81±2.98)%]均低于非危重组[(88.24±15.36)ms、(107.46±16.49)ms、(9.92±3.04)%](P<0.05),RMSSD[(19.79±6.21)ms]与非危重组[(22.01±5.64)ms]比较差异无统计学意义(P>0.05);脓毒血症危重组乳酸[(3.67±1.34)mmol/L]、皮质醇[(387.8±61.3)μg/L]、空腹血糖[(10.42±2.42)mmol/L]均高于非危重组[(1.78±1.21)mmol/L、(283.7±52.5)μg/L、(6.35±1.05)mmol/L](P<0.05);脓毒血症患者APACHE-Ⅱ评分与SDANN、SDNN呈负相关(r=-0.476,P=0.008;r=-0.451,P=0.006),与乳酸、皮质醇和空腹血糖水平呈正相关(r=0.573,P=0.000;r=0.674,P=0.000;r=0.696,P=0.000);SDANN诊断脓毒血症预后的AUC、灵敏度、特异度和约登指数分别为0.920、82.6%、99.8%和82.4,SDNN诊断脓毒血症预后的AUC、灵敏度、特异度和约登指数分别为0.952、96.9%、89.2%和86.1。结论脓毒血症患者心率变�
Background Large animal cardiopulmonary bypass （CPB） models are expensive,and prevent assessment of neurocognitive function,and difficulties with long-term recovery.The purpose of this study was to establish a novel rat model of cardiopulmonary bypass for deep hypothermic circulatory arrest without blood priming.Methods Twenty adult male Sprague-Dawley rats weighing 450-560 g were randomized to CPB with deep hypothermic circulatory arrest （DHCA） and control groups,with 10 rats each.The experimental protocols,including blood and crystalloid fluid administration,anesthesia,orotracheal intubation,ventilation,cannulation,and heparinization were identical in both groups.After inducing cardiac arrest,the circuit was turned off and rats were left in a DHCA state for 15 minutes.Rats were rewarmed to 34℃ to 35℃ over a period of 36 to 42 minutes using CPB-assisted rewarming,a heating blanket,and a heating lamp along with administration of 0.1 mEq of sodium bicarbonate and 0.14 mEq of calcium chloride.The remaining priming volume was reinfused and animals were weaned from CPB.Results All CPB with DHCA processes were successfully achieved.Blood gas analysis and hemodynamic parameters were in the normal range.The vital signs of all rats were stable.Conclusions Our CPB circuit has several novel features,including a small priming volume,active cooling/rewarming processes,vacuum-assisted venous drainage,peripheral cannulation without thoracotomy or stemotomy,and an accurate means of monitoring peripheral tissue oxygenation.
