血必净注射液对内毒素休克狗血流动力学的影响

目的:探讨血必净注射液对内毒素休克时血流动力学的影响及其作用机制。方法:将24只狗随机分为对照组和血必净组,利用大肠杆菌内毒素诱导狗内毒素休克模型。观察血必净注射液对内毒素休克狗血流动力学各指标和血浆乳酸浓度的影响。结果:内毒素注入后两组实验动物的平均动脉压(MAP)均明显下降,平均肺动脉压(MPAP)、心脏指数(CI)均显著升高(P均<0.05)。经血必净注射液进行治疗后,MAP、每搏量(SV)均明显上升,并显著高于对照组(P均<0.05);血必净组的CI无明显变化,但对照组呈进行性下降,并显著低于血必净组(P<0.05)。两组的CVP、MPAP差异无显著性。对照组血浆乳酸浓度明显高于血必净组(P<0.05)。结论:应用大肠杆菌内毒素静脉注射可成功制备狗内毒素休克模型;血必净注射液具有改善内毒素休克状态下血流动力学的作用。     

连续性静-静脉血液滤过对内毒素休克羊血流动力学的影响

目的　探讨连续性静静脉血液滤过( CVVH)对内毒素休克血流动力学的影响及作用机制,并观察其对内毒素休克预后的影响。方法　利用大肠杆菌内毒素( L 2 880 )诱导绵羊内毒素休克模型,随机分为对照组( NHF)和治疗组( HF)两组,观察CVVH(零平衡,40 ml·kg-1·h-1超滤,血流速80 ml/ min)对内毒素休克羊血流动力学的影响。结果　内毒素注入后两组实验动物平均动脉压( MAP)明显下降;平均肺动脉压( MPAP)、心脏指数( CI)显著升高( P<0 .0 1或P<0 .0 5)。实施CVVH后,HF组MAP、每搏量( SV)明显上升,显著高于NHF组( P<0 .0 1或P<0 .0 5) ;HF组CI无明显变化,NHF组进行性下降并显著低于HF组( P<0 .0 5) ;两组MPAP差异无显著性( P>0 .0 5) ;血浆乳酸浓度NHF组明显高于HF组。5h后HF组全部存活,NHF组死亡2只。结论　应用大肠杆菌内毒素静脉注射可成功制备羊内毒素休克模型;CVVH具有改善内毒素休克血流动力学和预后的作用,是治疗内毒素休克的重要手段。     

液体复苏对初进高海拔地区重度失血性休克犬血流动力学的影响

目的 探讨液体复苏对初进高海拔地区重度失血性休克犬血流动力学的影响.方法 13只成年杂种犬由海拔1510 m地区用l d时间运至3780 m的高海拔地区,随机分为三组(n=13).每只犬麻醉后经颈静脉放置漂浮导管,开放股动、静脉通道,经股动脉放血,使MAP维持在(35±5)mmHg,建立重度失血性休克模型.对照组(n=3):休克模型复制后1 h不进行液体复苏;LR组(n=5):休克1 h后输入1.5倍失血量的LR;6%HES组:休克1 h后输入等失血量的6%HES(n=5):三组犬休克模型复制后每小时以5 mL/ks的速度输注LR作为维持量,观察血流动力学变化.结果 对照组犬在休克模型复制后2 h内全部死亡,较休克1h差异具有统计学意义(P<0.05).其他两组液体复苏后2 h时:LR组MAP,CO,PAWP,CVP,LVSWI,RVSWI较休克1 h显著升高(P<0.05),而HR,SVR,PvR较休克l h显著降低(P<0.05);6%HES组CO,PAP,PAWP,CVP.SVR,PVR较休克1 h显著升高(P<0.05),而MAP,HR,CI,LVSWI,RVSWI较休克1 h差异无统计学意义(P>0.05).,结论 初进高海拔地区的重度失血性休克犬,如果不进行有效的液体复苏,死亡均为(3/3);输入1.5倍失血最的TJR是安全有效的;输入等失血量的6%HKS容易导敛心力衰竭.     

多巴胺对内毒素孵育兔肺体动脉血管环张力的影响

目的 比较不同浓度多巴胺对大肠杆菌内毒素脂多糖(LPS)孵育的离体兔肺动脉、体动脉血管张力的影响.方法 选择6只雄性大耳白兔,制备离体肺动脉环和体动脉环各36个.把36个肺动脉环随机分为6组,测试不同浓度多巴胺(4×10-5、8×10-5、16×10-5 μmol/L)对正常肺动脉张力的影响(分别为PN-DOPA4、PN-DOPA8、PN-DOPA16组)及对LPS孵育后肺动脉张力的影响(分别为PL-DOPA4、PL-DOPA8、PL-DOPA16组).体动脉分组与肺动脉分组方法相同,包括正常组(SN-DOPA4、SN-DOPA8、SN-DOPA16)及内毒素组(SL-DOPA4、SL-DOPA8、SL-DOPA16).结果 ①多巴胺对PN-DOPA4及SN-DOPA4组中的血管环均有一定的舒张作用;对PN-DOPA8、PN-DOPA16、SN-DOPA8和SN-DOPA16组的血管环均有收缩作用,随着浓度的加大而升高.②LPS孵育后,多巴胺对PL-DOPA4和SL-DOPA4组血管环舒张作用消失,变为收缩[(22.60±6.68)%比-(2.25±0.58)%,(3.80±0.52)%比-(3.65±0.75)%,P<0.05和P<0.01],对PL-DOPA8组收缩幅度较PN-DOPA8组减少(14.52±0.59)%(P<0.05);对SL-DOPA8组收缩幅度较SN-DOPA8组增高(25.90±1.75)%(P<0.05);对PL-DOPA16组和SL-DOPA16组的张力无显著影响.③LPS孵育后,DOPA4组的肺动脉张力变化(PL/PN)较体动脉张力变化(SL/SN)明显(-10.90±5.06比-1.00±0.24,P<0.05);在DOPA8组SL/SN较明显(1.80±0.35比0.48±0.17,P<0.01).结论 低浓度的多巴胺对正常肺动脉及体动脉血管环有舒张作用;在LPS孵育后,低浓度的多巴胺对肺动脉及体动脉环的作用由舒张变为收缩,且对肺动脉环的张力变化影响最大;不同浓度的多巴胺对LPS孵育后的肺动脉及体动脉血管环均有收缩作用.     

黄芪对感染性休克大鼠保护作用的实验研究

目的:探讨黄芪对感染性休克的作用及其机制.方法:健康成年雄性SD大鼠40只,采用盲肠结扎穿孔术(CLP)制备感染性休克模型.将动物随机均分为假手术组、模型组、黄芪低剂量组和黄芪高剂量组.行CLP前30 min黄芪组经静脉分别注入黄芪注射液10 g/kg和20 g/kg,假手术组和模型组大鼠输注等体积生理盐水(5 ml/kg).CLP后2～20 h每隔2 h经右股动脉测平均动脉压(MAP)和心率(HR);CLP后2、5、9和20 h采血测肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6).结果:模型组动物CLP后MAP进行性下降,HR先快后慢;两个黄芪组均能逆转CLP后MAP下降,HR波动小.模型组TNF-α水平于术后2 h达峰值;IL-6呈先升高后降低的趋势,于9 h达峰值:术后2、5和9 h,假手术组和两个黄芪组的TNF-α浓度均明显低于模型组(P均<0.01);术后5、9和20 h点,假手术组和两个黄芪组IL-6水平均明显低于模型组(P<0.05或P<0.01);黄芪高剂量组TNF-α于术后2 h、IL-6于术后9 h均显著低于黄芪低剂量组(P均<0.05).结论:黄芪通过抑制促炎性细胞因子TNF-α和IL-6的产生,对感染性休克大鼠具有明显的保护作用.     

高渗盐水抢救颅脑损伤所致急性颅内高压的临床研究

目的 探讨高渗盐水(hypertonic saline,HS)在急诊科抢救颅脑损伤所致急性颅内高压患者首次降颅压治疗中的临床疗效.方法 颅脑损伤所致急性颅内高压患者60例,随机分为3%HS组(20例)、10%HS组(20例)和20%甘露醇(mannitol,MT)组(20例).3%HS组静脉给予3%HS 260 mL,10%HS组静脉给予10%HS 80 mL,MT组静脉给予20%MT 250 mL,并于用药前及用药后30、60、90 min和2、3、4、5 h监测颅内压(intracranial pressure,ICP)、平均动脉压(mean artery pressure,MAP),记录尿量,观察生命体征变化,监测血生化指标.结果 ①HS组于用药后30 min ICP达到最大降幅,显著早于MT组(P<0.05),3%HS的降ICP作用可维持至少4 h,优于其余两组(P<0.05).②3%HS和10%HS用药后MAP较用药前显著升高(P<0.05),且3%HS升压作用持续时间较10%HS延长(P<0.05);而20%MT用药后MAP较用药前无显著变化(P>0.05).③静脉快速滴注3%HS、10%HS和20%MT后脑灌注压(CPP)均显著升高(P<0.05); 三组CPP升幅比较差异无统计学意义(P>0.05),但3%HS作用持续时间较10%HS、20%MT显著延长(P<0.05).结论 ①与MT比较,HS抢救颅脑损伤所致急性颅内高压起效更快、更持久,维持ICP更平稳.②两种浓度HS都能显著升高MAP,具有显著扩容作用.③三组均能升高CPP,以3%HS持续时间较长.     

中药注射液血必净对感染性休克犬促凝物质的影响

目的 研究中药注射液血必净对感染性休克犬促凝物质的影响,探讨血必净治疗感染性休克作用机制.方法 在北京朝阳医院基础动物实验窜通过给健康杂种犬静脉内注射内毒素制?感染性休克的动物模型,以收缩压下降大于40 mmHs开始计时,持续稳定60 min,即视为模型成功.按照随机原则将制模的动物分为3组:多巴胺治疗组6只,血必净+多巴胺治疗组(简称血必净组)6只,另设对照组6只.分别按照实验设计的时间点即注射内毒素前(基础),模型成功后用药前,以及用药后3 h检测血管细胞黏附分子(vascular cell adhesion molecule,VCAM)、细胞间黏附分子(inter-cell adhesionmolecule,ICAM)、血管性血友病因子(vonwillibrand factor,VWT)和纤溶酶原激活物抑制物-1(plasminogen activator inhibitor-1,PAI-1)血浆含鼍指标,采用SPSS 13.0统计软件进行统计分析.结果 犬机体促凝功能监测指标VCAM,ICAM,VWT以及PAI-1:血必净组与对照组、多巴胺组相比,在用药后3 h或7 h五项监测指标发生了具有统计学意义的变化(P<0.01或P<0.05),包括降低同观测点的峰值或者延迟峰值的出现;多巴胺组与对照组相比,ICAM,VWT,PAI-1在3 h或7 h也出现具有统计学意义的降低(P<0.01或P<0.05).结论 在应用多巴胺治疗感染性休克犬的基础上加用血必净可以更加有效地降低感染性休克犬体内的促凝物质血浆水平,是中药注射液血必净对感染性休克犬发挥治疗作用的机制之一.     

己酮可可碱对内毒素休克犬的影响

目的 :研究己酮可可碱 (PTX)在内毒素休克时所起的作用。方法 :选用成年杂种犬 12只 ,随机分成 2组 ,第一组 (n =6 )按 2 5 0 μg/kg持续静注内毒素 30min ,第二组 (n =6 )除用同样的方法静注内毒素外 ,在静注内毒素前按 2 0mg/kg静推PTX后按 2 0mg·kg- 1 ·h- 1 持续静注PTX。两组动物从开始到结束持续静注生理盐水维持CVP及PCWP在基础水平。每隔半小时测量一次MAP、MPAP、CVP、PCWP、HR、CO、肠系膜上动脉的血流量。并于 0′、 90′、 180′、 2 40′作动脉血、肺动脉血、肠系膜上静脉血血气分析 ,计算CI,SVI,SVRI,PVRI和DO2 ,VO2 ,O2 ER等。结果 :两组实验动物均产生休克 ,平均动脉压下降 30 %以上。与对照组相比 ,PTX能进一步降低内毒素休克犬的外周血管阻力 ,并使心脏指数及肠系膜上动脉的血流量增加。增加全身及肠系膜上动脉所供胃肠组织的氧输送 (P <0 0 5 )。结论 :己酮可可碱可显著改善内毒素休克犬的血液动力学及缺血脏器的血供、氧供。对感染性休克治疗有益。     

乌司他丁对脓毒症休克犬血流动力学、氧代谢及组织灌注的影响

目的:探讨乌司他丁对脓毒症休克犬血流动力学、氧代谢及组织灌注指标的影响.方法:健康雄性杂种狗14只,内毒素静脉注射复制犬脓毒症休克模型,随机分为对照组(n=7)和治疗组(n=7).对照组只接受林格液复苏.治疗组另外给予首剂乌司他丁1万U/kg,然后持续泵入0.1 7万U/(kg·h).直至12 h后实验结束.脓毒症休克模型稳定后记为0 h,此后每4小时收集血流动力学、氧代谢及组织灌注指标.结果:(1)血流动力学指标:休克后中心静脉压、肺动脉嵌压、右室每搏功指数、肺循环血管阻力指数明显上升(P<0.05),治疗组逐渐回落,8 h后两组比较差异有显著性(P<0.05),治疗组血压在第8小时有明显回升(P<0.05),对照组血压无此趋势,两组比较差异有显著性(P<0.05).复苏后两组的心指数均有上升(P<0.05),治疗组表现尤为明显,但两组差异无显著性(P>0.05).心搏指数、左室每搏功指数休克后明显下降,但两组均迅速回复到基线水平,两组差异无显著性(P>0.05).休克后体循环血管指数明显下降(P<0.05),治疗组逐渐上升,8 h后两组比较差异有显著性(Jp<0.05).(2)氧代谢及组织灌注指标:犬脓毒症休克模型建立后,氧输送、氧消耗、混合静脉血氧饱和度(SVO2)、尿量明显下降(P<0.05),血乳酸、胃黏膜PHi、胃-动脉-PCO2 差上升(P<0.05).治疗组氧输送、SVO2、尿量、胃黏膜PHi逐渐回升,第8小时与对照组比较有明显差异(P<0.05),治疗组氧消耗也有增加趋势,但与对照组比较无明显差异(p>0.05).治疗组血乳酸水平、胃-动脉PCO2差逐渐下降,8 h后与对照组比较差异有显著性(P<0.05).结论:乌司他丁能够明显改善脓毒症休克动物的血流动力学、氧代谢及组织灌注指标.     

丙戊酸对致死性失血性休克犬器官功能和预后的影响

目的 探讨组蛋白去乙酰化酶抑制剂丙戊酸(VPA)对致死性失血性休克犬器官功能和预后的影响.方法 20只成年雄性Beagle犬,采用颈总动脉放血(按全身血容量的42%计算)制备失血性休克模型.将模型犬按随机数字表法分为休克对照组和VPA治疗组,每组10只.VPA治疗组于失血后1.5 h静脉注射(静注)VPA 100 mg/kg(溶于20 ml生理盐水),休克对照组在失血后24 h内静注20 ml生理盐水;失血后24 h起两组犬均实施延迟静脉补液.在非麻醉状态下测定犬失血前(0 h)和失血后不同时间点平均动脉压(MAP)及血浆丙氨酸转氨酶(ALT)、肌酐(Cr)和肌酸激酶同工酶(CK-MB),记录尿量及72 h生存率.结果 两组失血后2 h MAP均显著降低;随后VPA治疗组MAP(mm Hg,1 mm Hg=0.133 kPa)迅速回升,于失血后4、8和24 h显著高于相应休克对照组(58.4±7.6比40.3±5.0,84.4±8.0比56.4±4.4,92.6±10.3比72.6±8.9,P＜0.05或P＜0.01).VPA治疗组0～8、8～24、24～48和48～72 h尿量均显著多于休克对照组,但仍显著少于失血前(0 h).两组失血后血浆ALT、Cr和CK-MB均较0 h显著升高;VPA治疗组失血后4 h起器官功能指标显著低于休克对照组[ALT(U/L):80.1±9.8比112.2±10.1;Cr(μmol/L):74.5±8.3比88.0±7.6;CK-MB(kU/L):10.39±1.10比13.67±1.46,P＜0.05或P＜0.01],但失血后72 h仍显著高于0 h(ALT:79.5±7.1比40.5±4.4;Cr:85.6±7.1比46.6±4.8;CK-MB:7.63±0.86比1.66±0.21,均P＜0.01).VPA治疗组失血后72 h生存率显著高于休克对照组[70%(7/10)比20%(2/10),P＜0.05].结论 犬42%血容量失血后静注VPA能有效提高MAP,增加尿量,减轻器官功能损害,提高72 h早期生存率,有潜力成为战争或突发事故及灾害时低血容量休克现场救治的有效药物.     

局部溶栓加抗凝对急性肺栓塞性肺高压的疗效观察

目的　研究经导管肺动脉局部溶栓加抗凝治疗在急性肺栓塞性肺动脉高压的作用。方法　2 0只小猪自体血栓注入建立急性肺栓塞性肺动脉高压模型。随机分2组,经导管肺动脉局部溶栓加抗凝(A组10只)、局部溶栓不加抗凝(B组10只)。溶栓前、溶栓后2h测肺动脉收缩压(SPAP)、股动脉收缩血压(SABP)、心率(HR)、心输出量(CI)、血气分析(PaO2 、PaCO2 、pH)、纤溶酶 抗纤溶酶复合物(PAP)、DD二聚体(DD)、一氧化氮(NO)。结果　两组SPAP、CI、PaO2 、PaCO2 、PAP、DD、NO均较治疗前有显著变化(P <0 0 5 ) ,A组的SPAP、PAP的变化较B组的变化更显著(P <0 .0 5 )。结论　肺栓塞治疗中,局部溶栓加抗凝的疗效优于单纯局部溶栓。     

静脉注射乌拉地尔对扩张型心肌病心衰患者急性血液动力学效应

目的　探讨乌拉地尔对扩张型心肌病心力衰竭患者急性血液动力学效应。方法　扩张型心肌病心力衰竭患者 15例 ,静脉注射乌拉地尔 2 5mg ,应用Swan Ganz漂浮导管测量用药前、用药 10、3 0、60、90min右心房压 (RAP)、肺动脉压(PAP)及肺毛细血管楔压 (PWP) ,采用热稀释法同步测量心排血量 (CO ) ,无创袖带法同步测量外周动脉收缩压 (SBP)、舒张压 (DBP)、平均压 (MAP) ,心脏监护系统记录心率 (HR) ,计算心脏指数 (CI)、外周血管阻力指数 (SVRI)、肺血管阻力指数 (PVRI)、左心室每搏作功指数 (LVSWI) ,并进行临床观察。结果　与用药前相比 ,用药 10minDBP、MAP、MPAP、PWP、SVRI、PVRI开始降低 (P <0 .0 5 ) ,CO、CI、LVSWI开始增加 (P <0 .0 1) ;用药 3 0minDBP、MAP、MPAP、PWP、SVRI、PVRI降低最明显 (P <0 .0 5 ) ,CO、CI、LVSWI增加最明显 (P <0 .0 1) ;用药 60minDBP、MAP、MPAP、PWP、SVRI、PVRI开始上升 ,CO、CI、LVSWI开始下降 (P <0 .0 5 ) ;用药 90minDBP、MAP上升至用药前水平 (P >0 .0 5 ) ,MPAP、PWP、SVRI仍低于用药前水平 ,CO、CI、LVSWI下降至用药前水平 ;用药后各时刻HR、SBP、RAP无显著变化。所有病人均无不良反应。结论　乌拉地尔可明显改善扩张型心肌病心力衰竭患者急性血液动力学参数     

雾化吸入一氧化氮供体治疗新生猪急性低氧性肺动脉高压

目的探讨雾化吸入一氧化氮供体对新生猪急性低氧性肺动脉高压的作用和安全性。方法持续低氧(FiO2=0.1)1h建立急性低氧性肺动脉高压模型。18头新生猪造模后随机分成3组(每组6只):C组(生理盐水组)、NTG组(硝酸甘油组)和SNP组(硝普钠组),另6头新生猪设为S组(假手术组),作为对照。实验过程中连续监测平均股动脉压(MAP)和平均肺动脉压(MPAP),基础状态、缺氧1h、雾化结束时和雾化后0.5h测定动脉血气分析,雾化结束时测定全血高铁血红蛋白(MetHb)水平和血浆NO代谢产物(NO-2NO-3)的含量。结果缺氧1h后,C组、NTG组和SNP组的MPAP均较S组显著升高(P<0.01);雾化结束时,NTG组和SNP组的MPAP较C组显著下降(P<0.05)。在相同时点,4组新生猪的MAP差异无显著性(P>0.05)。雾化吸入结束时,4组新生猪的全血MetHb和血浆NO浓度差异无显著性(P>0.05)。雾化结束后,未发现有反跳性肺动脉高压。结论雾化吸入NTG或SNP能选择性地降低急性低氧引起的肺动脉高压。     

Pretreatment with pentoxifylline improves the hemodynamic and histologic changes and decreases neutrophil adhesiveness in a pig fecal peritonitis model

We investigated pentoxifylline (PTF) as a pretreatment of septic syndrome in pigs with fecal peritonitis. In the untreated group there was a progressive decrease in mean arterial pressure (MAP), cardiac output, mean pulmonary artery wedge pressure (WP), and a progressive rise in mean pulmonary artery pressure (MPAP), pulmonary vascular resistance (PVR), systemic vascular resistance (SVR), heart rate (HR), and core temperature (T). In those pigs given PTF there was a significantly smaller increase in SVR throughout and in PVR after 270 min. No significant differences were seen in MAP, MPAP, WP, HR, and T. Neutrophil adhesiveness did not change in the untreated group. However, it decreased markedly with PTF, both before and after peritonitis induction. Electron microscopy of the lungs, liver, and spleen in the test group showed severe damage, with endothelial disruption, capillary or sinusoidal occlusion, leukostasis, and neutrophil degranulation. Pretreatment with PTF attenuated these changes.     

Taurolidine attenuates the hemodynamic and respiratory changes associated with endotoxemia

The purpose of this study was to determine if prereatment with taurolidine, a known anti-endotoxin agent, would attenuate the hemodynamic and respiratory responses associated with endotoxin induced lung injury in a large animal model in a randomized controlled study under license from the Department of Health. All animals underwent a general anesthetic. Vascular catheters were placed in the femoral artery and in the femoral vein. A Swan-Ganz Catheter was inserted for measurement of pulmonary artery pressure. Animals were randomized into three groups: Control, with measurements taken at baseline and half hourly up to 90 min; Endotoxin, receiving 5microg/Kg E. coli endotoxin intravenously after baseline measurements; and Endotoxin + Taurolidine, receiving 5g of taurolidine via intraperitoneal infusion 1 h before endotoxin administration. Main outcome measures were mean systemic arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), arterial oxygen tension (pO2), serum endotoxin concentration, and pulmonary myeloperoxidase. Endotoxin induced a significant lung injury characterized by an increase in pulmonary artery pressure, hypoxia, and systemic hypotension. Pretreatment with intraperitoneal taurolidine significantly attenuated these hemodynamic and respiratory changes. Serum endotoxin concentration was also significantly reduced as was lung myeloperoxidase. The data suggest that taurolidine may have a therapeutic role in preventing the lung injury seen in endotoxemia.     

Influence of continuous haemofiltration on haemodynamics and central blood volume in experimental endotoxic shock

In order to asses the influence of continuous haemofiltration (HF) on haemodynamics and central blood volume in endotoxic shock, endotoxinaemia was invoked in 20 swine (28–32 kg). 15 min after doubling the mean pulmonary pressure, the animals were randomly assigned to receive either a zero-balanced veno-venous HF with an ultrafiltration and replacement rate of 600 ml/h (HF group,n=10) or to observe the spontaneous course (E group,n=10) under a constant infusion of endotoxin for 4h. A trend to a higher survival rate in the HF group (6/10 vs. 3/10; group) during the observation period was evident, but not statistically significant. Early initiation of HF during endotoxic shock modifies the haemodynamic response, lowering the pulmonary artery pressure (PAP), PCWP, pulmonary (PVR) and systemic vascular resistance (SVR), compared to the spontaneous course, whereas the decrement of central blood volume was comparable in both groups. These changes cannot be explained by effects of the HF on the volume status, but supports and additional effect by the filtration of small and medium-sized molecules.     

Immediate hemodynamic effects of high-dose furosemide in normovolemic and hypovolemic dogs

We investigated whether the large dose (7 mg/kg) of iv furosemide often recommended for patients with oliguric acute renal failure impaired hemodynamic function in dogs. Six normovolemic and six hypovolemic animals were anesthetized, intubated, and ventilated. Femoral and pulmonary artery catheters were inserted. After a stable baseline period, the animals received 7 mg/kg of iv furosemide over 30 sec. Mean systemic artery pressure (MAP), mean pulmonary artery pressure (MPAP), CVP, and ECG were continuously monitored. Cardiac output and mean pulmonary arterial occlusion (wedge) pressures (WP) were recorded 2, 6, 12, 18, 24, 30, and 46 min after injection. Neither group demonstrated significant immediate changes in MAP, CVP, MPAP, heart rate (HR), cardiac output, or systemic and pulmonary vascular resistances (SVR and PVR, respectively). Later in the observation period, cardiac output decreased and SVR and PVR increased significantly. The changes were probably associated with decreased plasma volume causing compensatory increases in baroreceptor activity and vascular tone.     

Selective vasodilation by nitric oxide inhalation during sustained pulmonary hypertension following recurrent microembolism in pigs.

PURPOSE: This study establishes a new model of sustained pulmonary hypertension induced by recurrent microembolism in pigs and evaluates the effects of nitric oxide (NO) inhalation in this model. MATERIALS AND METHODS: Fourteen pigs were embolized under general anesthesia with 300-microm microspheres intravenously three times over a period of 7 weeks. Four pigs served as untreated controls. Hemodynamic and gas exchange measurements were performed on days 1 and 7 after the last embolization. RESULTS: Recurrent microembolism caused sustained pulmonary hypertension (mean pulmonary artery pressure [MPAP] 26 +/- 2 and 18 +/- 1 mm Hg on days 1 and 7, respectively) compared with the control group (MPAP 13 +/- 1 mm Hg each for days 1 and 7; P < .05, respectively). Right heart hypertrophy was present at autopsy as indicated by an increase in minimal myocyte diameter. Inhaled NO (5 and 40 parts per million [ppm]) was administered on days 1 and 7. On both days, inhaled NO significantly reduced MPAP and pulmonary vascular resistance without affecting systemic hemodynamics. There were no differences in responses to 5 and 40 ppm inhaled NO. CONCLUSION: We conclude that recurrent microembolization in pigs provides a reliable model of sustained pulmonary hypertension. In this model inhaled NO is a selective pulmonary vasodilator, indicating that active vasoconstriction significantly contributes to sustained pulmonary hypertension after recurrent microembolism.     

Selective vasodilatation by nitric oxide inhalation during sustained pulmonary hypertension following recurrent microembolism in pigs

This study establishes a new model of sustained pulmonary hypertension induced by recurrent microembolism in pigs and evaluates the effects of nitric oxide (NO) inhalation in this model. Fourteen pigs were embolized under general anesthesia with 300-μm microspheres intravenously three times over a period of 7 weeks. Four pigs served as untreated controls. Hemodynamic and gas exchange measurements were performed on days 1 and 7 after the last embolization. Recurrent microembolism caused sustained pulmonary hypertension (mean pulmonary artery pressure [MPAP] 26 ± 2 and 18 ± 1 mm Hg on days 1 and 7, respectively) compared with the control group (MPAP 13 ± 1 mm Hg each for days 1 and 7; P < .05, respectively). Right heart hypertrophy was present at autopsy as indicated by an increase in minimal myocyte diameter. Inhaled NO (5 and 40 parts per million [ppm]) was administered on days 1 and 7. On both days, inhaled NO significantly reduced MPAP and pulmonary vascular resistance without affecting systemic hemodynamics. There were no differences in responses to 5 and 40 ppm inhaled NO. We conclude that recurrent microembolization in pigs provides a reliable model of sustained pulmonary hypertension. In this model inhaled NO is a selective pulmonary vasodilator, indicating that active vasoconstriction significantly contributes to sustained pulmonary hypertension after recurrent microembolism.