吸入性伊洛前列素对先心病体外循环后肺动脉高压的影响

【目的】初步评估吸入性伊洛前列素对先心病伴发肺动脉高压患儿停止体外循环(CPB)后降低肺动脉高压的疗效。【方法】选择16例先心病合并肺高压的患儿,在停CPB后超声雾化吸入伊洛前列素30 ng/(kg.min),给药时间约20 min。通过持续脉冲心排量(PiCCO)导管及心内测压管测定用药前后血流动力学指标,比较吸入前、吸入结束后、吸入结束后20 min各项血流动力学参数。【结果】与吸入前比较,吸入伊洛前列素后及停药后20 min肺动脉压/体动脉压,肺循环阻力指数/体循环阻力指数,跨肺压均显著下降(P<0.01,P<0.05),心脏指数用药前后的变化无统计学差异。【结论】停CPB后吸入伊洛前列素,可选择性舒张肺血管,改善肺部血流动力学,改善右心功能。     

雾化吸入伊洛前列环素治疗肺动脉高压的疗效观察与护理

目的:观察雾化吸入伊洛前列环素在治疗肺动脉高压患者中的作用,并实施相应的护理措施。方法:对20例肺动脉高压患者分别给予20μg的伊洛前列环素实施雾化吸入,吸入15min后,通过右心导管接压力连接管测量各部位压力,观察患者肺动脉收缩压、肺动脉平均压、肺动脉舒张压、肺小动脉嵌顿压、心率的变化。结果:经吸入伊洛前列环素雾化治疗后,20例患者肺动脉压力均有下降。患者、血压、心率无明显变化。结论:雾化吸入伊洛前列环素,配合精心的护理,能有效、安全的降低肺动脉压力,达到理想的治疗效果。     

彩色多普勒超声在扩展先天性室间隔缺损合并重度肺动脉高压患者手术适应证中的研究

目的 彩色多普勒超声在扩展先天性室间隔缺损(VSD)合并重度肺动脉高压(PH)患者手术适应证中的应用价值.方法 选取先天性VSD并重度PH患者30例,肘静脉注射腺苷75 μg·kg-1·min-1,应用彩色多普勒超声心动图检测主动脉平均压、肺动脉平均压、肺动脉收缩压、肺动脉舒张压、肺循环阻力、体循环阻力、肺循环阻力/体循环阻力比值、肺动脉/主动脉收缩压比值、肺循环/体循环血流量比值,注射5分钟后肺血管阻力下降>30%和肺动脉平均压下降>10%为急性血管扩张试验阳性.结果 17例急性血管扩张试验阳性者,通过临床药物降压治疗有效后成功手术;13例药物试验阴性者继续降压治疗无效.结论 通过腺苷急性血管扩张试验,可以判断肺动脉高压的可逆性,彩色多普勒超声心动图在扩展先天性室间隔缺损合并重度肺动脉高压患者手术适应征中起到初步筛选的作用.     

先天性心脏病并肺动脉高压患儿术后雾化吸入前列腺素E1对肺循环的影响

目的探讨先天性心脏病并肺动脉高压术后患儿雾化吸入前列腺素E1对肺循环的影响。方法选择先天性心脏病合并肺动脉高压、在全麻低温体外循环下行心内直视手术的患儿60例,按入科顺序随机分为3组各20例。3组患儿在术后常规脱离呼吸机后分别予雾化吸入生理盐水、硝普钠、前列腺素E1。观察比较3组雾化吸入前、吸入10、20、30 min,及停吸后10、30 min时的肺循环指标。结果3组雾化吸入前平均肺动脉压（MPAP）、肺阻力指数（PVRI）、动脉血氧分压（PaO2）及二氧化碳分压（PaCO2）比较,差异均无统计学意义（P〉0.05）。雾化吸入10 min后前列腺素E1组和硝普钠组MPAP、PVRI均显著低于生理盐水组（P〈0.05）。硝普钠组在吸入后30 min已显著降低的MPAP、PVRI在停吸后10 min内相应回升并反跳,且显著高于生理盐水组及前列腺素E1组（P〈0.05）,而雾化吸入前列腺素E1组在结束雾化30 min后未见反跳,且仍显著低于生理盐水组（P〈0.05）。雾化吸入前列腺素E1后动脉血氧分压较吸入硝普钠和生理盐水升高（P〈0.05）,而二氧化碳分压下降（P〈0.05）,且停止雾化吸入后仍有持续作用（P〈0.05）;吸入硝普钠后动脉血氧分压、二氧化碳分压无变化,差异均无统计学意义（P〉0.05）。结论先天性心脏病合并肺动脉高压术后患儿雾化吸入前列腺素E1更有利于降低肺动脉压,明显改善动脉血氧分压,预防肺动脉高压危象的发生。     

先天性心脏病合并肺高压患儿术后吸入伊洛前列素治疗的护理

目的 探讨先天性心脏病合并肺高压患儿术后吸入伊洛前列素治疗在监护室的护理,以达到有双的治疗.方法 采用回顾分析法,对10例先天性心脏病患儿术后肺高压吸入伊洛前列素治疗过程中的护理进行总结分析.结果 通过规范化的护理,10例患儿肺动脉压力下降,无并发症发生,病情平稳后转回病房.结论 在吸入伊洛前列素治疗的过程中对患儿进行有效雾化吸入的护理,严密观察药物疗效和不良反应,保证了伊洛前列素的治疗效果.     

米力农对先天性心脏病合并肺动脉高压患者肺氧合功能及肺循环动力学的影响

目的:观察肺动脉内注射米力农对先天性心脏病合并肺动脉高压患者的肺氧合功能及肺循环动力学的影响。方法:对先天性心脏病合并肺动脉高压患者18例行右心导管术时,比较单纯高浓度吸氧患者8例与吸氧联合肺动脉内注射米力农患者10例肺动脉平均压与全肺阻力下降及动脉血氧饱和度改善情况的差异。结果:先天性心脏病合并肺动脉高压患者,吸氧联合肺动脉内注射米力农后肺动脉平均压下降[(10.22±4.78vs6.00±3.14)mmHg]与全肺阻力的降低[(3.25±1.13vs1.63±1.98)mmHg],动脉血氧饱和度的提高[(6.93±1.98)%vs(5.01±2.61)%],均优于单纯高浓度吸氧者,差异有统计学意义。结论:米力农能有效降低肺动脉平均压,改善肺氧合功能,是先天性心脏病合并肺动脉高压患者可选择的一种安全、有效的降肺动脉压药物。     

雾化吸入硝酸甘油治疗先天性心脏病合并肺动脉高压的护理观察

目的:探讨雾化吸入硝酸甘油治疗先天性心脏病合并继发性肺动脉高压的护理观察。方法:将我科2006年6月～2011年6月收治的465例先天性心脏病合并不同程度肺动脉高压的患者随机分为两组,治疗组采用硝酸甘油雾化吸入,对照组采用常规治疗。两组治疗1周后,比较两组患者肺动脉平均压、体外循环后呼吸机辅助时间、术后氧分压(PO2)情况。结果:治疗组肺动脉压控制情况较对照组明显有效,两组比较有统计学差异(P<0.05)。结论:硝酸甘油雾化吸入用于先天性心脏病合并肺动脉高压的干预治疗,能取得较好的治疗效果及预期指标。     

雾化吸入伊洛前列素对肺动脉高压患者血液动力学的影响

目的探讨雾化吸入进口伊洛前列素对肺动脉高压患者血液动力学的影响。方法选择各类型肺动脉高压患者共17例,应用Swan-Ganz漂浮导管和有创动脉监测进行血液动力学监测,对比吸入伊洛前列素前后的体、肺循环血液动力学参数和氧合指数,并观察不良反应。结果吸入伊洛前列素后各项血液动力学和氧合参数对比:心率[(87±12)次/分VS(85±14)次/分,P=0.13];平均右房压[(10±5)mmHg VS(9±5)mmHg,P=0.23];平均肺动脉压力[(78±23)mmHg VS(67±19)mmHg,P=0.03];肺循环阻力[(15.8±5.3)woods VS(11.6±4.7)woods,P=0.02];心排量[(4.3±1.1)L/minVS(4.9±1.4)L/min,P=0.04];平均肺血管楔压[(10±4)mmHg VS(10±3)mmHg,P=0.35];混合静脉血氧饱和度[(65±3)%VS(67±3)%,P=0.14];平均体动脉压[(84±12)mmHg VS(83±11)mmHg,P=0.08];体循环阻力[(17.2±5.1)woods VS(15.1±4.0)woods,P=0.08];动脉血氧饱和度[(92±4)%VS(93±3)%,P=0.44];不良反应轻微,呛咳、颜面潮红各2例,头痛1例。结论雾化吸入伊洛前列素可以显著改善肺动脉高压患者肺循环参数,不良反应轻微。     

伊洛前列素雾化吸入给药对先天性心脏病患儿继发肺动脉高压血流动力学的影响

目的:探讨伊洛前列素雾化吸入给药对先天性心脏病患儿继发肺动脉高压的治疗作用。方法:选择一组先天性心脏病患儿用口含器或面罩吸入法吸入伊洛前列素,剂量为25～30 ng/(kg.min),以2 mL生理盐水稀释后,通过PARI Junior BOY N压机压缩雾化吸入,每4 h给药1次,吸入60、120 min后采用连续多普勒超声波技术,测量左右心每搏心排量等血流动力学参数变化。结果:在用药前和用药后60、120 min,血流动力学参数有明显变化,患儿用药后左、右心排血量增加,外周末梢血氧饱和度明显升高,用药1 h显效,于用药2 h达峰值。结论:伊洛前列素雾化吸入可以增加心输出量,改善心功能,提示应用该方法治疗先天性心脏病患儿继发肺动脉高压是有效可行的。     

伊洛前列素雾化吸入给药对先天性心脏病患儿继发肺动脉高压血流动力学的影响

目的：探讨伊洛前列素雾化吸入给药对先天性心脏病患儿继发肺动脉高压的治疗作用。方法：选择一组先天性心脏病患儿用口含器或面罩吸入法吸入伊洛前列素，剂量为25—30ng／（kg·min），以2mL生理盐水稀释后，通过PARI Junior BOYN压机压缩雾化吸入．每4h给药1次，吸入60、120min后采用连续多普勒超声波技术，测量左右心每搏心排量等血流动力学参数变化。结果：在用药前和用药后60、120min，血流动力学参数有明显变化，患儿用药后左、右心排血量增加，外周末梢血氧饱和度明显升高，用药1h显效。于用药2h达峰值。结论：伊洛前列素雾化吸入可以增加心输出量．改善心功能，提示应用该方法治疗先天性心脏病患儿继发肺动脉高压是有效可行的     

Recovery from circulatory shock in severe primary pulmonary hypertension (PPH) with aerosolization of iloprost

Objective: The treatment of decompensated right ventricular failure with vasodilators is difficult due to reduced systemic pressure and/or ventilation/perfusion (V/Q) mismatch with hypoxemia. In a recent study we demonstrated that inhaled vasodilatory prostanoids may offer a new strategy to achieve pulmonary selective vasodilatation and improvement of right ventricular function. We applied this new approach to a patient with circulatory shock due to primary pulmonary hypertension (PPH), complicated by a pulmonary infiltrate, who did not tolerate intravenous prostacyclin. Design: Case report. Setting: Intensive Care Unit (ICU), Medizinische Klinik Gießen, Germany. Patient: A 45-year-old woman with PPH presenting with decompensated right heart failure (ascites, pleural effusion), circulatory shock and commencing renal and hepatic failure, despite maximum therapy including the use of catecholamines. Intervention: Intermittent inhalation of aerosolized iloprost, the stable analogue of prostacyclin, and comparison to inhaled nitric oxide (NO). Subsequent long-term therapy with aerosolized iloprost, 150 fig/day. Measurements and results: In response to inhaled iloprost, pulmonary arterial pressure (PAP) decreased from 65 to 61 mmHg, cardiac index (CI) increased from 1.25 to 1.85 1/min per m², and pulmonary vascular resistance (PVR) decreased from 2416 to 1549 dyn/s per cm⁵ while inhaled NO decreased the PVR from 2280 to 1920 dyn/s per cm⁵ without a decrease in PAP. Both of these interventions increased the arterial pO₂ but did not change the systemic arterial pressure. In contrast, intravenous prostacyclin was not tolerated, due to systemic side effects. During repeated inhalations with iloprost, the baseline hemodynamics and gas exchange improved dramatically and renal and liver functions normalized. During 1 year of continued therapy, the clinical status improved very much, concomitant with improved hemodynamics, and the patient has been taken off the transplantation list. Conclusions: Inhalation of aerosolized iloprost may offer a new life-saving strategy in near desperate cases of pulmonary hypertension in which intravenous prostacyclin cannot be applied due to severe side effects.     

牛心包补片修复心脏间隔缺损的应用

背景：心脏涤纶补片因其质地薄、质量轻、生物相容性好等优点常规用于心脏手术,但最近几年发现,用心脏涤纶补片对心室间隔缺损修补后,一旦发生术后残余漏,较易引起溶血、细菌或真菌感染。目的：探讨应用牛心包补片修复心脏间隔缺损的疗效。方法：采用戊二醛固定的牛心包补片修补152例心脏间隔缺损患者,其中房间隔缺损56例,室间隔缺损78例,部分房室间隔缺损18例。术后复查心电图、胸片、心脏超声,观察其术后早期病情、血流动力学和心脏功能。结果与结论：152例患者均完成修补手术,术后无早期死亡,患者随访2—6个月,牛心包补片在使用过程中及术后早期均未发现漏血、溶血、血栓、感染、排斥反应等并发症。1例患者因合并肺动脉高压,术后第1天出现高血压危象,经过抢救后好转。复查心电图、胸片、心脏超声可见心脏间隔缺损修补完全,无残余分流;肺动脉压力明显下降;活瓣已关闭无分流;心脏功能正常。证实牛心包补片可以有效修复心脏间隔缺损,改善患者的血流动力学和心功能,近期效果满意,是一种良好的心脏间隔缺损修补材料。     

Amplification of the pulmonary vasodilatory response to inhaled iloprost by subthreshold phosphodiesterase types 3 and 4 inhibition in severe pulmonary hypertension

OBJECTIVE: Aerosolized iloprost causes specific pulmonary vasodilation for about 60 mins in patients with severe primary and secondary pulmonary hypertension. Repeated daily inhalations are currently in use for chronic treatment. The aim of the current study was to evaluate if phosphodiesterase type 3 and 4 inhibition might amplify the prostanoid effect on pulmonary vasodilatation by stabilization of intracellular second messenger cyclic adenosine monophosphate. DESIGN: Uncontrolled clinical trial. SETTING: Medical intensive care unit, Department of Internal Medicine, University Hospital, Giessen, Germany. PATIENTS: A total of 11 patients with precapillary pulmonary hypertension (eight with primary pulmonary hypertension; one with pulmonary hypertension associated with calcinosis, Raynaud phenomenon, esophageal dysfunction, sclerodactyly, and telangiectasia [CREST syndrome]; one with pulmonary hypertension associated with systemic lupus erythematodes, and one with chronic pulmonary embolism) were included. All were classified as New York Heart Association class III or class IV. INTERVENTIONS: During right heart catheterization, a single inhalation with iloprost (1.4 microg per inhalation) was performed, and hemodynamics and gas exchange variables were recorded for the next 2.5 hrs. After the iloprost effects had completely leveled off, the dual-selective phosphodiesterase types 3 and 4 inhibitor tolafentrine was infused in seven patients and aerosolized in five patients at doses that were per se ineffective (80 mg per 2.5 hrs intravenously; approximately 0.8 mg deposited by aerosol), followed by a second iloprost inhalation procedure. MEASUREMENTS: Decrease in pulmonary vascular resistance, duration of drug effect, safety, and tolerability of combined pharmacologic intervention. RESULTS: The decrease in pulmonary vascular resistance to sole iloprost nebulization lasted for approximately 60 mins. This response was enhanced and prolonged to approximately 120 mins in the presence of both infused and aerosolized tolafentrine, without loss of pulmonary selectivity. No adverse events were observed. CONCLUSIONS: These data support the principle that subthreshold selective phosphodiesterase types 3 and 4 inhibition amplifies the lung vasodilatory response to inhaled iloprost, with minute doses being sufficient via the inhalative route.     

Nifedipine in chronic cor pulmonale: acute and relatively long-term effects

After 20 mg sublingual nifedipine in 12 men with clinical stable chronic cor pulmonale the mean arterial pressure and systemic vascular resistance fell, cardiac index rose, and mean pulmonary arterial (Ppa) and wedge (Ppaw) pressures, right atrial pressure, and PaO2 remained unchanged. After 20 mg orally every 6 hours for 24 hours in 11 patients, the mean arterial pressure fell further, systemic vascular resistance remained low, and the cardiac index returned to baseline, whereas the Ppa and Ppaw decreased, but the pulmonary vascular driving pressure (Ppa-Ppaw), right atrial pressure, PaO2, and spirometry and ejection fractions remained unchanged. Of eight patients receiving maintenance therapy four developed untoward side effects in 1 to 3 weeks and one was noncompliant. The remaining three patients evaluated at 6 weeks failed to improve and had unchanged resting hemodynamics. Thus in the absence of a potentially reversible hypoxic pulmonary hypertension, nifedipine may not improve pulmonary arterial pressure and cardiac function in clinically stable patients with cor pulmonale.     

Effects of inhaled aerosolized iloprost and inhaled NO on pulmonary circulation and edema formation in ovine lung injury

Although inhaled NO (iNO) has been shown to lower pulmonary pressures and edema accumulation in experimental acute lung injury, its clinical use has been questioned because of a lack of improvement in outcome, rebound phenomena, and potential toxicity. We investigated the effects of aerosolized iloprost, a stable prostacyclin analogue, compared with iNO on pulmonary pressures and lung edema in 20 female sheep with oleic acid lung injury. The most effective dose of iloprost was determined in healthy animals before the experiment. Anesthetized and ventilated sheep received a central venous oleic acid infusion and were continuously infused with Ringer lactate to achieve a positive fluid balance (5 mL.kg(-1).h(-1)). In the iNO group (n = 6), iNO (20 ppm) was administered continuously for 8 h. Animals in the iloprost group (n = 6) received aerosolized iloprost (40 microg 2 h(-1)). Animals in the control group (n = 6) had no further intervention. Oleic acid infusion was associated with impaired oxygenation, pulmonary hypertension, and lung edema in all groups. Although iNO significantly decreased pulmonary vascular resistance index, effective pulmonary capillary pressure, and extravascular lung water index, these parameters were unaffected by iloprost. Oxygenation index (Pao2/Fio2) increased significantly both during NO and iloprost inhalation but also tended to improve in the control group over time. In contrast to iNO, the investigated dose of iloprost was ineffective to attenuate acute lung injury-induced changes in pulmonary hemodynamics and lung edema in this experimental model.     

The effect of food on pharmacokinetics and pharmacodynamics of fenoldopam in class III heart failure.

Eighteen patients with New York Heart Association class III congestive heart failure were given single 100 mg oral doses of fenoldopam with food or fasting in a random-order single-blind crossover trial. Before and after each fenoldopam dose, thermodilution cardiac output, right atrial pressure, pulmonary artery pressure, and pulmonary capillary wedge pressure (PCWP) were measured with a balloon-tipped pulmonary artery catheter, and heart rates and blood pressures were recorded with an automated sphygmomanometer. Compared with fasting, bioavailability of fenoldopam was decreased significantly when administered with food: mean peak plasma fenoldopam level decreased from 26.5 (+/- 4.1 SEM) ng/ml to 10.9 (+/- 1.7 SEM) ng/ml (p = 0.0004) and mean area under the concentration-time curve was decreased from 44.7 (+/- 5.8 SEM) ng.hr/ml to 26.8 (+/- 4.1 SEM) ng.hr/ml (p = 0.0001). Fenoldopam administration to fasting patients resulted in decreases in mean arterial pressure, systemic vascular resistance, and PCWP and significant increases in cardiac index without change in heart rate. The maximum changes in mean cardiac index, systemic vascular resistance, and PCWP were greatest 1 hour after oral administration and did not persist beyond 3 hours after administration. In fasting patients, changes in cardiac index were correlated with plasma fenoldopam levels, whereas changes in PCWP and mean arterial pressure did not correlate significantly with the observed fenoldopam level.     

心脏外科肺动脉高压患者围手术期一氧化氮的吸入治疗

目的 探讨一氧化氮(NO)吸入治疗对合并肺动脉高压心脏外科围手术期患者的有效性与安全性.方法 应用Servo 300A呼吸机或Aeronox NO释放与监测仪,对合并肺动脉高压且临床常规治疗效果不理想的27例成人和1例房间隔缺损修补术患儿进行围手术期NO吸入治疗,NO开始剂量(5～10)×10-6,然后根据病情可缓慢升高至20×10-6.于治疗前后监测患者的肺动脉压(PAP)、动脉压(AP)、肺血管阻力(PVR)和氧合指数(PaO2/FiO2).NO吸入治疗的有效标准为治疗开始后1 h内AP/PAP改善20%以上,或PaO2/FiO2改善20%以上.NO吸入治疗1.5 h后无效者终止该方法.结果 成人患者NO吸入治疗有效率为77.8%(21/27例),治疗持续时间为12～96 h,平均(32.6±10.3)h.1例房间隔缺损合并中度肺动脉高压患儿在房间隔缺损修补术后,肺动脉高压加重,合并严重的低氧血症[PaO2/FiO2为40 mm Hg(1 mm Hg=0.133 kPa),吸入氧浓度(FiO2)为1.00],经NO吸入等综合治疗后效果明显,4 d后撤离呼吸机.治疗中与治疗后,在患者与工作人员中未发现不良事件.结论 NO吸入治疗对心脏外科合并肺动脉高压围手术期病情加重者治疗有效,值得进一步临床探索.     

Effect of molsidomine on hemodynamics in patients with dilated cardiomyopathy

The effect of 4 mg Molsidomine iv. followed by a continuous infusion of 3 mg per hour for 3 hours on arterial blood pressure, pulmonary artery pressure, cardiac index, peripheral and pulmonary vascular resistance and heart rate was evaluated in eleven patients suffering from chronic heart failure caused by non-ischaemic dilatative cardiomyopathy (NYHA II-III). A significant decrease in systemic blood pressure, systolic and mean pulmonary artery pressure and pulmonary wedge pressure was observed and also a marked decrease in total peripheral and pulmonary vascular resistance. There was a slight, but not significant increase in cardiac index. The heart rate did not change significantly. Treatment had to be stopped in one patient because of side effects (hypotension, nausea).     

伊洛前列素对先天性心脏病并肺动脉高压患儿术后cAMP，cGMP及p-Akt，p-P13K表达的影响

【目的】观察吸入伊洛前列素对先天性心脏病（CHD）继发肺动脉高压（PAH）患儿术后血浆环磷酸腺苷（cAMP）,环磷酸鸟苷（cGMP）和磷酸化磷脂酰肌醇3-激酶（P-PI3K）和磷酸化蛋白激酶B（p-AKt）蛋白表达的影响。【方法】对30例经彩超确诊的各类CHD伴PAH择期行矫治手术的患儿（≤12岁）,根据术后有无吸入伊洛前列素随机选择分为两组,每组15例。吸入组术后吸入伊洛前列素25ng／（kg·min）,每4h吸入1次。使用ElISA法检测两组血浆cAMP,cGMP含量,p-PI3K和p-AKt蛋白的表达。【结果】与对照组相比,吸入组吸入伊洛前列素后24h,患儿cAMP增高。PI3K及AKt蛋白表达量也增高。【结论】CHD伴PAH患儿心脏手术后吸入伊洛前列素时,可能通过cAMP介导的激活PI3K通路改善其血液流变学。     

犬肺动脉高压模型连续热稀释法的应用

背景：以往小动物肺动脉高压模型有创测压方法一般根据生物信号采集系统的压力波形图引导,采用右心导管法进行压力测定;由于设备技术和动物体积的限制无法应用肺动脉导管测定心输出量及肺血管阻力。目的：在脱氢野百合碱诱导建立犬肺动脉高压模型中利用Swan-Ganz七腔漂浮导管和Vigilance系统根据连续热稀释法测定心输出量、肺血管阻力,肺动脉压力,探讨连续心排量法在肺动脉高压动物模型中的应用价值。方法：10只比格犬随机分成2组：实验组用脱氢野百合碱右心房注射的方法建立肺动脉高压的动物模型,对照组右心房注射二甲基酰胺做对照;在用药前,用药后8周使用漂浮导管和Vigilance系统分别测定两组犬右心房收缩压、右心室收缩压、肺动脉收缩压、平均肺动脉压力、肺毛细血管楔压及心输出量。结果与结论：实验组用药后肺血管阻力显著上升（P=0．00）,实验组用药后心输出量显著减少（P〈0．05）。使用连续热稀释法测定肺血管阻力和心输出量较传统的间断热稀释法更准确稳定。利用漂浮导管和Vigilance系统根据连续热稀释法原理在脱氢野百合碱诱导的犬肺动脉高压模型中进行肺血管阻力和心输出量测定,该方法具有准确稳定、可重复操作和对实验模型创伤小的优点。