吸入伊洛前列素行急性肺血管扩张试验在先天性心脏病合并重度肺动脉高压术前评估中的作用

目的 评价吸入伊洛前列素的急性肺血管扩张试验在先天性心脏病(CHD)肺动脉高压(PH)患者心脏外科手术适应证选择中的作用.方法 对2006年6月至2008年12月46例CHD合并重度PH患者的临床资料进行回顾性分析.其中男性15例,女性31例,平均年龄(12±9)岁.所有患者术前均接受心导管检查和吸入伊洛前列索试验,患者平均肺动脉压(mPAP)(80±13)mm Hg(1 mill Hg=0.133 kPa),平均肺小动脉阻力指数(PVRI)(17±10)wood·m2.将吸入伊洛前列素试验肺血管阳性反应定义为在体循环压力不变或上升的情况下,PVRI下降≥20%,并作为选择手术适应证的重要条件.药物试验阳性患者在心脏外科修补术后均放置肺动脉漂浮导管,监测术后肺动脉压力、阻力以及心功能状况.结果 46例患者中,药物试验阳性29例(63.1%),吸药后PVRI由(15±6)wood·m2降至(9-4-4)wood·m2,肺循环体循环阻力比(Rp/Rs)由0.7±0.2降至0.4±0.2(P值均<0.05).药物试验反应阴性者17例(36.9%),吸药后PVRI由(21±10)wood·m2降至(19±9)wood·m2(P<0.05),Rp/Rs由1.0±0.5降至0.9±0.5(P>0.05).23例患者接受了心脏外科手术治疗,全部存活.其中药物试验阳性组21例,术后mPAP降至(27±10)mm Hg.药物试验阴性组仅2例接受外科修补术,术后mPAP均>45 mm Hg.结论 吸入伊洛前列素试验阳性患者术后肺动脉压力和PVRI明显降低,可作为评价合并PH的CHD手术适应证的一种蕈要手段.     

吸入伊洛前列素对先天性心脏病矫治术患者体外循环后肺动脉高压的影响

目的 评价吸入伊洛前列素对先天性心脏病矫治术患者体外循环后肺动脉高压的影响.方法 选择体外循环下先天性心脏病矫治术患者58例,年龄14～60岁,气管插管后右颈内静脉置漂浮导管监测肺动脉压.体外循环下行先天性心脏病矫治术,体外循环结束后平均肺动脉压仍>25mm Hg,此时通过压缩式雾化器吸入伊洛前列素10μg,于吸药前即刻(T_0)、吸药完毕后即刻,吸药完毕后5、15、30和60min时监测心率、右房压、肺小动脉楔压、平均肺动脉压、平均桡动脉压、肺血管阻力和体循环阻力、心输出量及混合静脉血氧饱和度.结果 先天性心脏病矫治术患者体外循环后存在肺动脉高压患者28例.与吸药前即刻比较,吸药完毕后各时点患者平均肺动脉压和肺血管阻力明显降低,心输出量和吸药完毕后即刻、5 min时混合静脉血氧饱和度明显升高(P<0.05或0.01).结论 体外循环结束后吸入伊洛前列素可有效降低先天性心脏病矫治术患者肺动脉压和肺血管阻力,有助于患者安全、顺利地脱离体外循环.     

通气侧肺吸入伊洛前列素对肺动脉压和缺氧性肺血管收缩的影响

目的 探讨雾化吸入伊洛前列素对大鼠单肺通气(one-lung ventilation,OLV)期间肺动脉压和缺氧性肺血管收缩(hypoxic pulmonary vasoconstriction,HPV)的影响。方法 雄性SD大鼠30只,随机分为A、B、C三组,每组10只。原位离体肺灌注模型建立后,调整气管导管深度致左侧肺OLV,FiO_2为100%,打开连接于呼吸回路的雾化器,A组吸入生理盐水,B组吸入伊洛前列素0.05μg·kg-1·min-1,C组吸入伊洛前列素0.1μg·kg~(-1)·min~(-1),记录灌注10min(T_1)、雾化吸入10min(T_2)和OLV 1h(T_3)的平均肺动脉压(MPAP)及左心房引流液氧分压(PaO_2)。通过测量T_1、T_2和T_3时的左心房引流液PaO_2计算氧合指数(oxygenation index,OI)。实验结束分别取双侧肺组织进行电镜检查。结果 与T_1时比较,T_2、T_3时三组MPAP明显升高(P0.05);T_2、T_3时B、C组MPAP明显低于A组(P0.05),且C组MPAP明显低于B组(P0.05)。与T_1时比较,T_2、T_3时三组OI明显降低(P0.05);T_2、T_3时C组OI明显高于B组(P0.05)。相对于B、C组通气侧,A组通气侧与A、B、C组非通气侧Ⅱ型肺泡上皮细胞核膜外突内陷,部分板层小体排空。结论 在大鼠原位肺灌注模型中,单肺通气期间雾化吸入伊洛前列素能明显降低平均肺动脉压,减少肺内分流并增加氧合。     

波生坦治疗先天性心脏病术后肺动脉高压的前瞻性随机对照研究

目的 评价应用波生坦治疗婴幼儿先天性心脏病术后肺动脉高压的疗效.方法 30例术前合并肺动脉高压且手术治疗后仍有肺动脉高压的先大性心脏病病儿入选.所有病儿均在低温体外循环辅助下完成心内畸形根治术,术后1周行超声心动图检查,估测肺动脉收缩压＞30mm Hg者随机分配到波生坦治疗组(15例)及对照组(15例)中.研究周期12周,波生坦组:传统治疗+波生坦,波生坦给药方案:10～20 kg病儿,31.25 mg,每日1次(qd)4周,31.25 mg,每日2次(bid)8周;5～10 kg病儿,15.6 mg,qd(4周),15.6 mg,bid(8周);对照组:传统治疗(地高辛、双氢克脲塞).两组病例于术后13周接受门诊随访、调查问卷、超声检查和血液检查.比较两组心功能及临床症状,超声心动图评价血流动力学和肺动脉高压变化,以及血浆内皮素(Endothelin-1,ET-1)变化.结果 两组病例年龄、平均体重、病种分布、基线肺动脉收缩压力、基线血浆ET-1浓度均无统计学差异.心功能改善方而,依据NYHA心功能分级(级数增高定义为心功能恶化,降低则为心功能改善).波生坦治疗组93%的病儿心功能较基线水平改善Ⅰ级,无心功能恶化;对照组只有73%病儿心功能较基线水平改善Ⅰ级,13%病儿心功能较基线水平恶化Ⅰ级.将术后因心肺功能不全再入院及死亡定义为临床恶化,波生坦治疗组无再入院及死亡发生;而对照组13%的病儿发生了临床恶化(1例病儿术后11大死亡,1例病儿术后60天再入院).波生坦治疗组:基线(术后1周)肺动脉收缩压(48.5±9)mm Hg,治疗12周后(29.0±8.0)mm Hg,治疗前后差异有统计学意义(P＜0.01,95%CI:12～27);对照组:基线(术后1周)肺动脉收缩压(45.4±16)mm Hg,12周后(35.1±15.0)mm Hg手术前后差异无统计学意义(P＞0.1).两组之间比较,波生坦治疗组较对照组能更好的降低肺动脉压力(P＜0.05,95%CI:0.1～1 8.3).应用波生坦治疗后血浆ET下降(2.01±0.03)fmol/ml(1 fmol/ml=10-15mol/ml,P=0.03),对照组血浆ET升高(0.15±0.10)fmol/ml(P=0.77).波生坦组有2例肝脏转氨酶升高,停药后自然恢复正常,后未继续服药;无其他明显副作用.结论 波生坦治疗左向右分流的先天性心脏病术后残留肺动脉高压疗效明显,有助于病儿术后心功能及临床症状的恢复.     

先天性心脏病患儿肺动脉,上腔静脉血一氧化氮含量检测及意义

目的:探讨一氧化氮(NO)与先天性心脏病(CHD)引起的肺动脉高压(PH)发病间的关系。方法:应用NO试剂盒检测了CHD患儿肺动脉及上腔静脉血浆中NO含量。结果;(1)伴PH组肺动脉血浆NO含量明显高于不伴肺动脉高压组(37.58±9.99μmol/L:19.03±15.25μmol/L,P<0.01);(2)在PH组中,肺动脉血浆NO含量明显高于上腔静脉血(P<0.01);而不伴PH组,肺动脉和上腔静脉血浆NO含量无显著性差异(P>0.05)。结论:(1)伴PH的先心患儿肺动脉血浆NO含量升高;(2)NO可能介入了CHD引起的PH发病过程。     

体外循环对先天性心脏病合并肺动脉高压患者血浆NO和ADMA浓度的影响

目的 通过观察体外循环(CPB)对先天性心脏病合并肺动脉高压患者血浆一氧化氮(NO)和不对称二甲基精氨酸(ADMA)浓度的影响,分析CPB加重肺动脉高压的原因.方法 拟在CPB下行心内修补术的先天性心脏病患者18例,年龄11～40岁,体重26～59 kg,ASAⅡ或Ⅲ级,心功能Ⅰ～Ⅲ级.根据术前肺动脉收缩压(PASP)分为3组(n=6),Ⅰ组肺动脉压正常(PASP<30 mm Hg);Ⅱ组肺动脉压轻度增高(PASP 30～50 mm Hg);Ⅲ组肺动脉压中重度增高(PASP>50 mm Hg).分别于麻醉诱导前(基础状态)、CPB开始即刻、CPB停机后即刻、3、6和24 h时采集桡动脉血样4 ml,测定血浆NO和ADMA浓度.结果 与基础值相比,Ⅱ组和Ⅲ组CPB停机后即刻、3和6 h时血浆ADMA浓度升高,NO浓度降低(P<0.05),Ⅰ组上述指标差异无统计学意义(P>0.05).与Ⅰ组比较,Ⅱ组和Ⅲ组血浆NO浓度降低,ADMA浓度升高(P<0.05).结论 CPB可引起先天性心脏病合并肺动脉高压患者血浆ADMA浓度升高,NO浓度降低.     

CO2气腹及肠道牵拉引起大鼠应激反应的实验研究

目的研究CO2气腹及肠道牵拉对SD大鼠血浆β-内啡肽(β-endorphin,β-EP)的影响,探讨CO2气腹及肠道牵拉对大鼠围手术期应激反应的影响. 方法选取SPF级雄性SD大鼠120只,随机分为4组,每组30只.A组:CO2气腹组;B组:切口组;C组:切口并肠道牵拉组;D组:对照组.测定A、B和C组大鼠切皮后血浆10 min、20 min和40 min的血浆β-EP浓度,比较CO2气腹及肠道牵拉对应激反应的影响. 结果 CO2气腹组术后10 min、20 min和40 min的血浆β-EP浓度分别为(274.7±66.6)pg/dl、(157.3±63.8)pg/dl和(163.9±74.5)pg/dl,与对照组比较有非常显著升高(P<0.01).切口并肠道牵拉组术后10 min、20 min和40 min的β-EP浓度分别为(376.9±50.8)pg/dl、(298.8±70.0)pg/dl和(266.9±53.7)pg/dl,与气腹组比较两组术后10 min、20 min β-EP有非常显著差异(P<0.01),术后40 min有显著差异(P<0.05).切口并肠道牵拉组与切口组比较两组术后10 min、20 min和40 min β-EP均有非常显著差异(P<0.01). 结论 CO2气腹及肠道牵拉为重要的刺激因素,均可以引起大鼠的应激反应,肠道牵拉可加重应激反应的程度.     

肺血减少型先天性心脏病幼猪远端肺血管病理形态变化的生物学基础

目的采用球囊扩张人工房间隔造口+肺动脉环缩术建立肺血减少型先天性心脏病幼猪动物模型,探讨肺血流减少时未成熟肺血管形态学变化的病理生理机制。方法将出生1~2个月的幼猪20头按随机数字表法分为3组,对照组(C组,n=6):右胸小切口制成一过性肺血减少;轻度至中度肺动脉狭窄组(T1组,n=7),经右心房表面送入球囊扩张器行人工房间隔造口+肺动脉Banding环缩术,术中控制收缩期肺动脉环缩处压差(Trans-PABP)为20~30 mm Hg;重度肺动脉狭窄组(T2组,n=7):术中Trans-PABP≥30~50 mm Hg。3组于术后2个月取右肺中叶外侧段、大小为1.0 cm×0.8 cm×0.8 cm的肺组织,光学显微镜下观察远端肺细小动脉形态学改变,并采用双抗体夹心酶联免疫吸附法(ELISA)检测肺组织中血管内皮细胞生长因子(VEGF)和基质金属蛋白酶2(MMP-2)的含量。结果 T1组、T2组生存动物房间隔造口+肺动脉环缩术均获成功。术后2个月,T1组肺细小动脉内径明显大于C组(82.89±10.72μm vs.74.12±9.28μm;t=-5.892,P0.05),T2组肺细小动脉内径明显大于C组(85.47±5.25μm vs.74.12±9.28μm;t=-6.325,P0.05);T1组单位面积肺细小动脉数量(NAPSC)少于C组(229.70±88.00个/cm2vs.431.50±40.60个/cm2;t=39.526,P0.05),T2组NAPSC少于C组(210.00±40.30个/cm2vs.431.50±40.60个/cm2;t=67.858,P0.05);术后2个月,T1组肺组织MMP-2(58.30±19.60 ng/ml vs.81.20±16.70 ng/ml,t=14.261,P0.05)和VEGF(17.80±3.00 pg/ml vs.21.40±3.80 pg/ml,t=8.482,P0.05)表达较C组明显降低;T2组肺组织MMP-2(42.10±15.20 ng/ml vs.81.20±16.70 ng/ml,t=27.318,P0.05)和VEGF(12.30±3.20 pg/ml vs.21.40±3.80 pg/ml,t=15.139,P0.05)表达较C组明显降低。结论肺血减少型先天性心脏病幼猪肺组织细胞外基质发生构型重建,肺细小血管发育不良或退化。肺血减少时引起细胞外基质中结构性蛋白和细胞因子等成分变化是基质重塑的基础。     

左肺反向循环逆转终末期肺动脉高压

目的 探讨反向肺循环逆转终末期肺动脉高压的机制.方法 选杂种犬30只,随机分成正常对照组(n=10)、肺动脉高压组(n=10)和肺高压反向组(n=10).观察各组的血流动力学参数、动脉血气、外周血一氧化氮(NO)、一氧化氮合酶(eNOS)、内皮素及其肺组织mRNA表达的变化.结果 终末期肺高压模型犬上行左肺反向循环手术后,平均肺动脉压(MPAP)降低[(17.3±3.5)mm Hg,P<0.01],但与正常犬MPAP[(12.6±4.2)mm Hg]相比仍偏高(P<0.05);动脉血氧分压上升到(96.5±6.4)mm Hg(P<0.01),血浆中eNOS升高[(1.53±0.56)μg/ml,P<0.01],NO分泌量增加[(36.25±6.94)μmol/L,P<0.01],ET的含量减少[(21.37±3.82)pg/ml,P<0.01].eNOS-mRNA在术后表达上调,PEET-mRNA在肺高压时表达上调,而在术后表达下调.结论 左肺反向循环具有可行性,可能通过转换血气交换的解剖位置、提高血氧含量、抑制血管收缩因子的产生,增加血管舒张因子的产生降低肺动脉高压.     

前列腺素E1肺动脉途径给药对肺动脉高压患者的降压效果

目的 探讨前列腺素E1肺动脉途径给药对肺动脉高压患者的降压效果.方法 择期行非体外循环冠状动脉搭桥术合并肺动脉高压患者30例,性别不限,年龄65 ～ 82岁,体重60 ～ 88 kg,ASA分级Ⅱ或Ⅲ级,肺动脉收缩压＞40 mm Hg.采用随机数字表法,将其随机分为2组(n=15):中心静脉给药组(C组)和肺动脉给药组(P组).麻醉诱导后行右颈内静脉穿刺置入Swan-Ganz导管用于监测血流动力学指标.切皮后,C组和P组分别通过中心静脉导管和肺动脉导管输注前列腺素E120 ～ 50 ng·kg-1 ·min-1,使肺动脉收缩压降至25～ 30 mm Hg.分别于给药前5 min(To)及给药后5 min(T1)记录心率、平均动脉压、中心静脉压、肺动脉收缩压、肺毛细血管楔压和心脏指数,计算肺血管阻力和周围血管阻力.记录前列腺素E1的用量.结果 与C组相比,P组前列腺素E1用量减少,T1时肺动脉收缩压和肺血管阻力降低,平均动脉压和周围血管阻力升高(P＜0.05).结论 经肺动脉途径给药可提高前列腺素E1降低肺动脉高压的效价,且不影响体循环血流动力学.     

高频部分液体通气对吸入伤犬呼吸循环功能的影响

目的　观察高频部分液体通气 (highfrequencypartialliquidventilation ,HFPLV)对吸入性损伤犬肺力学、氧合和血流动力学参数的影响。　方法　 16条犬经吸入蒸气 ,造成重度吸入性损伤模型 ,并随机分为对照组和治疗组。两组动物致伤后均行高频喷射通气 (highfrequencyjetventila tiot,HFJV) ,治疗组同时经气管导管缓慢注入氟碳液体 (3ml/kg体重 ) ,行HFPLV治疗 ,于通气后3 0、60和 90min时测定两组动物血气、肺顺应性、气道阻力及血流动力学参数。　结果　治疗组PaO2 呈进行性上升 ,在各时相点与致伤后比较差异有显著性意义 (P <0 .0 5 ) ,而对照组各时相点与致伤后比较差异无显著性意义 (P >0 .0 5 ) ;治疗组PaCO2 也逐渐增高 ,于 60、90min显著高于致伤后水平 (P <0 .0 5 )。与对照组比较 ,治疗组各时相点的PaO2 稍有升高 (P >0 .0 5 ) ,PaCO2 于 90min显著增高 (P <0 .0 5 ) ,而两组动 /静态气道阻力、肺顺应性和血流动力学参数比较 ,差异均无显著性意义 (P >0 .0 5 )。　结论　HFPLV与单纯HFJV相比 ,更有利于吸入性损伤的动脉氧合 ,对血流动力学参数无明显不利影响     

吸入一氧化氮对吸入性损伤患者心功能的影响

目的观察吸入一氧化氮(NO)对吸入性损伤患者心功能的疗效,初步探讨其作用机制. 方法选择12例烧伤伴中度以上吸入性损伤的成年患者,随机分为2组.对照组(C组)6例,按常规治疗;治疗组(T组)6例,行常规治疗+吸入体积分数1×10-6 的NO.两组患者均留置各种导管.于治疗前及治疗后6、12、24、48和72 h观察两组患者各项心功能指标和血浆内皮素(ET)及NO含量的变化,对T组患者ET、NO的变化进行相关性分析. 结果 T组心排出量(CO)和心搏出量(SV)在24 h后显著高于治疗前,其变化早于C组 (P﹤0.05～0.01).T组左室每搏功指数(LVSWI)和右室每搏功指数(RVSWI)与C组相比均改善较早,且两组RVSWI比较差异有显著性意义(P<0.05).与C组比较,T组ET水平明显降低(P﹤0.05～0.01),而血浆NO水平明显升高(P<0.01),此两项指标呈负相关(r＝-0.98,P<0.01). 结论吸入体积分数1×10-6的NO可以改善吸入性损伤患者的心功能,其机制可能是NO对肺血管平滑肌张力具有调节作用.     

小儿喉乳头状瘤吸入七氟烷麻醉诱导期间呼吸力学变化

目的 通过热线风速仪观察喉乳头状瘤患儿和普通小儿吸入七氟烷麻醉诱导期呼吸力学的变化,旨在获得预测通气和捕管困难的客观量化指标及对控制通气加深麻醉效果的评估.方法 选择普通患儿(C组)和喉乳头状瘤患儿(L组)各20例,静脉注射氯胺酮1 mg/kg,吸入氧气2 L/min+7%七氟烷实施麻醉诱导.热线风速仪采集四时段呼吸力学数据:静注氯胺酮1 min后(T1),开始吸入7%七氟烷时(T2),吸入7%七氟烷3min后(T3),控制通气2min后(T4).结果 L组T1期呼吸的平均速度[(1.48±0.20)m/s和(1.26±0.18m/s)]、最大速度[(1.72±0.25)m/s和(1.97±0.31)m/s]都高于c组(P<0.05),呼吸频率、吸气时间差异无统计学意义(P>0.05). L组T3、T4期平均吸气速度和最大吸气速度的比值(0.612±0.030和0.613±0.032)小于C组(P<0.05).L组T3期最大吸气速度、呼吸频率下降的幅度[(25±6)%和(19±4)%]少于C组(P<0.05).L组T4期各项指标较T3期无明显变化(P>0.05).结论 喉乳头状瘤患儿吸入七氟烷麻醉诱导期是靠加强呼吸做功来代偿通气不足的,其上气道梗阻情况随麻醉加深更加突出,通过控制通气辅助加深麻醉效果不明显.     

含乌司他丁低温肺保护液在法洛四联症体外循环术中的应用

目的 探讨含乌司他丁(UTI)的低温肺保护液对婴幼儿法洛四联症体外循环肺内炎性反应的保护作用.方法 30例行法洛四联症(TOF)根治术病婴,随机分为肺保护组和对照组,各15例.术前有感染征象(白细胞>12×109/L、体温>38℃,C-反应蛋白>8 mg/L)、有过敏史者除外.肺保护组心脏停跳同时肺动脉灌注低温肺保护液,对照组常规行TOF根治术.围术期监测血浆肿瘤坏死因子(TNF-α)、中性粒细胞CD11b的表达和髓过氧化物酶(MPO),同时监测血气、肺功能及临床指标.结果 血清TNF-α水平肺保护组较对照组低,关胸后0、3 h差异有统计学意义,(11.15±2.47)pg/ml对(14.21±5.55)pg/ml、(12.01±2.69)pg/ml对(15.94±4.86)pg/ml.肺保护组新鲜全血中性粒细胞表面的CD11b平均荧光强度(MFI)水平关胸后3、6 h显著低于对照组,(126.23±36.05)对(156.98±48.34)、(137.27±38.85)对(173.27±67.43).肺保护组MPO水平关胸后3、6、24 h显著低于对照组,(156.52±17.57)U/L对(178.45±35.68)U/L、(178.28±23.63)U/L对(224.66±49.66)U/L、(130.52±57.50)U/L对(96.50±14.49)U/L.肺保护组呼吸机辅助时间明显较对照组短,(17.60±6.39)h对(23.70±8.51)h.肺保护组肺泡-动脉氧阶差(A-aDO2)在关胸后3、6 h显著低于对照组(120.92±33.08)mm Hg(1 mm Hg=0.133 kPa)对(145.52±39.38)mm Hg、(74.76±40.16)mm Hg对(112.50±44.16)mm Hg.肺动态顺应性(Cdyn)在关胸后3、6 h肺保护组显著高于对照组(0.59±0.11)ml·cmH2O-1·kg-1对(0.46±0.17)ml·cmH2O-1·kg-1、(0.67±0.09)ml·cmH2O-1·kg-1对(0.53±0.18)ml·cmH2O-1·kg-1.结论 肺动脉灌注含乌司他丁的低温肺保护液明显减轻体外循环术后肺的炎性反应,具有肺保护作用.     

A comparison of the acute hemodynamic effects of inhaled nitroglycerin and iloprost in patients with pulmonary hypertension undergoing mitral valve surgery.

BACKGROUND: Since the presence of pulmonary hypertension (PHT) affects the prognosis of the patients, it is important to manage and evaluate PHT. The aim of this study was to compare the hemodynamic effects of inhaled nitroglycerin and iloprost during early postoperative period, in patients with PHT undergoing mitral valve replacement surgery. MATERIALS AND METHODS: One hundred patients with PHT (mean pulmonary artery pressure (MPAP) >25 mmHg at rest), were randomized to receive either inhalation of nitroglycerin (group I; n=50) or iloprost (group II; n=50) in the postoperative period. In both groups, baseline hemodynamic parameters were recorded before the treatment (T(0)). Then, patients in group I received 20 microg.kg(-1) nitroglycerin and those in group II received 2.5 microg.kg(-1) iloprost. The same parameters were recorded immediately after the end of the treatment (T(1)). RESULTS: In both study groups MPAP and pulmonary vascular resistance (PVR) were found to be significantly lower at T(1) when compared to that of T(0) period (p<0.05). MPAP and PVR were significantly lower and mean arterial pressure (MAP) was significantly higher in group II when compared to group I at T(1) period (p<0.05). In addition to decreases in PVR and MPAP, iloprost also increased cardiac output (CO)(4.9+/-1.3 vs 5.1+/-0.9, p<0.05) and stroke volume (SV)(48+/-13 vs 56+/-13, p<0.05). CONCLUSION: Inhaled iloprost and nitroglycerin, both effectively reduce MPAP and PVR without affecting MAP, systemic vascular resistance (SVR) and CO. However, iloprost seems to be a more powerful pulmonary vasodilator, therefore we suggest iloprost inhalation in patients with severe PHT.     

Hemodynamic effects of inhaled aerosolized iloprost and inhaled nitric oxide in heart transplant candidates with elevated pulmonary vascular resistance.

OBJECTIVE: An elevated pulmonary vascular resistance (PVR) is described as a predictor of postoperative right heart failure and increased mortality in patients undergoing orthotopic heart transplantation. The use of intravenous vasodilators is limited by their systemic effects. We evaluated the pulmonary and systemic hemodynamic effects of inhaled nitric oxide (NO) and inhaled aerosolized iloprost (IP) in heart transplant candidates with elevated PVR. METHODS: Fourteen male heart transplant candidates due to dilative or ischemic cardiomyopathia with elevated PVR (> or = 180 dyn s cm(-5)) were included in the study. Increasing concentrations of NO (5, 10 and 30 ppm) and 50 microg aerosolized IP were administered by inhalation. Hemodynamic measurements preceded and followed administration of each agent. RESULTS: Inhalation of IP, 10, and 30 ppm NO reduced PVR and mean pulmonary artery pressure (MPAP), but did not affect blood pressure or systemic vascular resistance. Comparing the effectiveness of 10 ppm NO and IP, we found a significant higher reduction of MPAP in patients treated with IP. An increase of cardiac index and stroke index could only be shown with IP-inhalation. CONCLUSIONS: Inhaled iloprost induces pulmonary vasodilation which is significantly greater than the effects of 10 and 30 ppm NO. The results of our study show, that inhaled iloprost induces a reliable hemodynamic response in the evaluation of heart transplant candidates. Further advantages of iloprost inhalation are the lack of adverse reactions and toxic side effects and an easier administration. Due to this facts we recommend iloprost as a routine screening drug for vascular reactivity in HTx-candidates. Based on our results it would be of great interest to investigate the role of iloprost in management of postoperative right heart insufficiency following cardiac transplantation.     

阿魏酸钠对婴幼儿体外循环血管内皮功能的保护作用

目的 观察婴幼儿先天性心脏病心肺转流术(CPB)围手术期一氧化氮(NO)、内皮素(ET-1)和循环内皮细胞(CEC)水平的变化,初步探讨阿魏酸钠对血管内皮功能的保护作用.方法 60例先天性心脏病病儿随机分为阿魏酸钠组(S组)和对照组(C组)各30例.S组于体外循环前静脉滴注阿魏酸钠注射液8 mg/kg,C组予等量平衡盐溶液,检测CPB前(TO)、30 min(T1)、结束时(T2)、手术后2h(T3)、6 h(T4)5个时间点血浆NO和ET浓度,以及T0和T2两个时间点的CEC变化.结果 两组间T0比较差异不明显,12与T0比较CEC浓度均升高明显;T2时与C组比较,S组CEC升高幅度明显被抑制,差异有统计学意义(P<0.05).两组血浆N0浓度T1均降低,差异有统计学意义,组间比较无统计学意义(P>0.05),T2、T3、T4时间点两组NO浓度均有所上升,但均低于T0,差异明显,S组NO降低程度比C组小(P<0.05).两组T1时ET-1稍有降低,随后ET-1升高明显(P<0.01);S组T1、T2、T3、T4时间点均低于C组,差异有统计学意义(P<0.05或P<0.01).结论 体外循环手术可造成NO/ET失平衡状态,CEC数明显增加,证实CPB后存在着血管内皮功能的损伤.阿魏酸钠组术后NO下降幅度,ET、CEC升高的幅度,明显较对照组小,阿魏酸钠可有效拮抗ET的分泌,促进NO的生成,对婴幼儿体外循环手术有较好的血管内皮功能保护作用.

Abstract：

Objective Cardiopulmonary bypass (CPB) and its related ischemia reperfusion injury may cause endothelial cell injury.To study the protective effects of sodium ferulate in vascular endothelial function during CPB by testing the changes of vascular endothelial cell( CEC),nitric oxide( NO) and endothelin-1 ( ET-1 ) in children with congenital heart disease.Methods Sixty patients with congenital heart disease,including 28 males and 32 females were studied.The mean age was (19.7 ±10.4) months and body weight (10.5 ±6.1) kg.There were 37 VSD,8 ASD,7 TOF,5 TAPVC and 3 CAVC,among them 26 patients had pulmonary hypertension.They were randomly divided in to two groups:sodium ferulate group ( group S,n = 30),and control group ( group C,n =30) .Sodium ferulate (8 mg/kg) was given intravenously before CPB.Blood samples were taken from the arterial line at following time points:before CPB (TO),bypass 30 min(Tl ),the termination of CPB (T2 ),2h after operation ( T3 ) and 6h after operation ( T4 ),respectively for determination the concentration of vascular endothelial cell (CEC) in the blood,the concentration of nitric oxide (NO) and endothelin-1 ( ET-1) in the plasma.Results There were no significant difference for the two groups regarding above parameters at TO ( P > 0.05).The level of CEC was significantly elevated after CPB in both groups ( P < 0.05 ) .CEC were lower at T2 in group S than in group C ( P < 0.05 ) .NO was decreased in both groups,but was higher in group S at T2,T3 and T4 ( P < 0.05 ) .The concentration of plasma ET-1 was not significantly different before CPB,but there was a slight decrease at T1,and then it was significantly increased in both groups (P<0.05).But it was lower in group S than in group C at T1,T2,T3 and T4(P<0.05 orP<0.01).Conclusion There was severe endothelial cell damage during CPB.Sodium Ferulate can effectively antagonize the secretion of ET-1 to promote the formation of NO.Therefore,it reduces CPB-induced endothelial cell damage and protects vascular endothelial function during CPB.     

一氧化氮治疗吸入性损伤肺动脉高压量效关系的实验研究

目的探讨吸入不同浓度一氧化氮（ＮＯ）治疗兔烟雾吸入性损伤肺动脉高压的量效关系。方法用右心导管检查术连续测定血流动力学指标,观察吸入体积分数为（１、５、１０、２０、３０、４０、５０、６０）×１０－６的ＮＯ对１５只兔烟雾吸入所致肺动脉高压血流动力学的作用。结果吸入（１、５）×１０－６的ＮＯ对平均肺动脉压（ｍＰＡＰ）、肺毛细血管楔压（ＰＣＷＰ）、肺微血管压（Ｐｍｖ）和肺血管阻力（ＰＶＲ）无明显作用（Ｐ＞００５）;吸入（１０、２０、３０、４０、５０、６０）×１０－６的ＮＯ均有降低ｍＰＡＰ、ＰＣＷＰ、Ｐｍｖ的作用（Ｐ＜００５,Ｐ＜００１）;吸入３０×１０－６的ＮＯ即达到最大扩血管效应（Ｐ＜００５,Ｐ＜００１）,再增加吸入ＮＯ的浓度,ＰＶＲ不再进一步降低（Ｐ＞００５）。结论吸入ＮＯ降低烟雾吸入性损伤早期肺动脉压的体积分数以不超过３０×１０－６为宜。     

人参皂苷单体Re对大鼠心肌细胞缺氧的作用

目的 观察人参皂苷单体Re对大鼠心肌细胞缺氧的保护作用并探讨其机制.方法 SD大鼠乳鼠心肌细胞原代培养,按照随机数字表法分为5组,每组6个样本.正常对照组细胞常规培养;缺氧对照组细胞常规培养48 h再缺氧培养12 h;另外3组细胞先常规培养48 h,分别用20、40、80 g/L人参皂苷单体Re预处理30 min再缺氧12 h,相对应设为单体Re低、中、高浓度组.采用ELISA法检测心肌细胞上清液中乳酸脱氢酶(LDH)活性,荧光漂白恢复(FRAP)实验观察细胞间连接通讯,以FRAP率表示结果.数据处理行组间或配对t检验.结果 (1)与缺氧对照组细胞LDH活性[(403±22)U/L]比较,单体Re低、中、高浓度组均明显降低,分别为(255±16)、(241±13)、(237±24)U/L(t值分别为5.1、5.2、8.3,P值均小于0.05).(2)细胞经激光淬灭后10 min,正常对照组FRAP率为(74.8±3.6)%;缺氧对照组FRAP率为(13.2±5.6)%;单体Re低、中、高浓度组FRAP率分别为(34.3±3.9)%、(36.2±3.1)%、(39.5±2.9)%,与缺氧对照组比较,差异均有统计学意义(t值分别为18.3、-41.9、-6.6,P值均小于0.05).结论 采用人参皂苷单体Re预处理可降低缺氧大鼠心肌细胞LDH的释放,明显改善细胞间连接通讯,对缺氧心肌细胞有明显的保护作用,剂量尤以20 g/L为适宜.

Abstract：

Objective To investigate the protective effect of ginsenoside Re on myocardial cells of neonatal SD rat with hypoxia injury,and to explore its mechanism. Methods The primary passage of myocardial cells collected from neonatal SD rats were divided into A group (with ordinary treatment),B group[exposed to hypoxia (1% O2,5% CO2,94% N2) for 12 hours after being cultured for 48 hours],C group (pretreated with 80 g/L ginsenoside Re for 30 minutes after 48 hours of ordinary culture,then exposed to hypoxia for 12 hours),D group (received the same treatment as used in C group except for using 40 g/L ginsenoside Re),E group (received the same treatment as used in C group except for using 20 g/L ginsenoside Re) according to the random number table,with 6 samples in each group. Myocardial cell supernatants were collected for determination of content of lactate dehydrogenase (LDH) with enzyme linked immunosorbent assay. Fluorescence recovery after photobleaching technique was used to detect gap junction intercellular communication (GJIC).Result was observed by laser scanning confocal microscope. Data were processed with paired t test. Results (1) Compared with that in B group[(403±22)U/L],contents of LDH in E,D,and C groups were obviously decreased[(255±16),(241±13),(237±24)U/L,with t value respectively 5.1,5.2,8.3,P values all below 0.05]. (2) The fluorescence recovery rate in A group was (74.8±3.6)% 10 min after quenching,which was higher than that in B group[(13.2±5.6)%,t=15.2,P<0.01]. The fluorescence recovery rate in C,D,and E groups was respectively (39.5±2.9)%,(36.2±3.1)%,and (34.3±3.9)% 10 min after quenching,all higher than that in B group (with t value respectively -6.6,-41.9,18.3,P values all below 0.05). Conclusions Ginsenoside Re pretreatment,particularly with a dose of 20 g/L,can protect myocardial cells from hypoxia injury,and the effect may be attributable to inhibition of release of LDH and improvement of the GJIC function.