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1.
目的 评价吸入性一氧化氮 (INO)在心外管道全腔静脉肺动脉连接 (ETCPC)术后早期疗效。方法 ETCPC术后早期吸入NO者为试验组 ,未吸入NO者为对照组 ,各 16例。记录两组吸入及停用INO前后心排出量、肺血管阻力 (PVR)、呼吸指数、肺动脉 -左房压力阶差 (PLG)。记录两组呼吸机辅助时间、ICU滞留时间、胸腔引流管留置时间及住院时间。结果 试验组NO吸入后呼吸指数从 2 . 6 1±0 .32下降至 1. 4 1± 0 .2 1,t=2 . 35 ,P <0 .0 5 ;PLG(mmHg)从 11± 2降至 7± 3,t =2 .76 ,P <0 . 0 1;氧合指数从 16. 3± 18升高至 191± 2 1,t=2 . 74 ,P <0 .0 1;心指数 (CI ,L·min-1·m-2 )从 2 . 84± 0 . 2 3增加至 3 .12±0 . 2 0 ,t=2 . 2 4 ,P <0 .0 5 ;肺血管阻力从 4 . 2 3± 0 .5 3下降至 3 .77± 1 .4 2 ,t =2 . 2 8,P <0 . 0 5 ;中心静脉压(CVP ,mmHg)从 17 .0± 1 9下降至 15 .0± 1. 2 ,下降约 11 .8% ;INO停用前后各项上述指标未见明显差异。与对照组相比较 ,呼吸机辅助时间从 (76± 2 5 )h缩短为 (5. 6± 19)h ,t=2 . 2 8,P <0 . 0 5 ;重症监护时间从 (6± 2 )d缩短至 (4± 2 )d ,t=2 . 33,P <0. 0 5 ;胸腔引流管留置时间及住院时间差异无统计学意义。结论 INO对ETCPC术后远期疗效无明显影响 ,但 相似文献
2.
目的 评价吸入一氧化氮 (NO)对双向腔肺动脉吻合 (BCPS)术后肺血流灌注不足病儿的作用。方法 2 0例病儿吸入NO 2 5~ 15 0百万分之一体积 (ppm) ,定时记录各项血流动力学和呼吸功能指标 ,定期监测二氧化氮 (NO2 )、高铁血红蛋白 (MetHb)含量。结果 吸入NO后 ,中心静脉压从( 2 1 4±4 8)mmHg( 1mmHg =0 133kPa)降至 ( 15 3± 5 9)mmHg,跨肺压从 ( 16 2± 5 3)mmHg降至( 8 8± 4 2 )mmHg ,肺泡 -动脉氧分压差从 ( 391 7± 15 1 9)mmHg降至 ( 2 94 0± 312 5 )mmHg ,呼吸指数从 11 3± 5 3降至 6 8± 3 0 (P <0 0 1) ;动脉血氧饱和度从 0 78± 0 14升至 0 84± 0 9,动脉血氧分压与吸入氧浓度之比从 ( 6 7 0± 30 1)mmHg升至 ( 88 8± 2 6 1)mmHg(P <0 0 1)。吸入NO期间 ,NO2 和MetHb含量分别为 ( 0 1± 0 2 )ppm和 ( 1 2± 0 4) %,均在安全范围内。结论 一氧化氮作为一种选择性肺血管扩张剂 ,用于双向腔肺动脉吻合术后肺血管阻力暂时性增高的病儿 ,可改善其肺血流灌注和氧合功能 ,无明显毒副作用。 相似文献
3.
目的 观察联合使用一氧化氮 (NO)和腺苷 (AD)对肺动脉高压的影响。方法 选用上海种白猪 10头 ,建立急性缺氧性肺动脉高压模型 ,采用分别使用吸入NO 2 0× 10 -6和静脉持续每分钟滴注AD 5 0 μg/kg体重 ,以及联合使用NO和AD的方式 ,在各时段进行各项血流动力学指标测定。结果 联合使用NO和AD ,平均肺动脉压力从 (37± 7)mmHg(1mmHg =0 .133kPa)降至 (2 0± 1)mmHg(P <0 .0 1) ,心排指数从 (2 .30± 0 .5 0 )L·min-1·m-2 升至 (2 .76± 0 .46 )L·min-1·m-2 (P <0 .0 5 )。结论 NO和AD联合治疗幼猪急性缺氧性肺动脉高压 ,在降低肺动脉压力的同时 ,还可增加心输出量。 相似文献
4.
目的对肺灌洗(Lavage)诱导的急性肺损伤(ALI)家猪实施以氟碳(PFC)为媒介的部分液体通气(PLV)及吸入20ppm的一氧化氮(NO),比较二者对肺气体交换及血液动力学的影响.方法24头健康家猪,麻醉后经气管导管肺内以生理盐水反复灌洗,直至动脉氧分压(PaO2)<100mmHg达1h,记录气体交换及血液动力学各参数作为急性肺损伤的基础值.随机分为PLV组、NO组及对照组,PLV组肺内灌以相当于肺功能余气量(30ml/kg)的PFC,然后以普通呼吸机行常规气体通气,补充PFC4ml·kg-1·h-1以弥补蒸发损失;NO组吸入20ppmNO,对照组不给予其它治疗,各组每小时记录气体交换及血液动力学各参数的变化.结果PLV组实施PLV1h后,PaO2即从ALI时的(53±11)mmHg升高至(142±133)mmHg,4h后达(318±109)mmHg,与ALI时比较差异有显著性(P<0.01),亦显著高于对照组(P<0.05).实施PLV1h后Qs/Qt从ALI时的(57±9)%降至(42±13)%,4h后降至(26±10)%,较ALI时差异有显著性(P<0.01),并于2h后显著低于对照组(P<0.05).NO组的MPAP在整个实验过程中显著低于对照组(P<0.01).NO组吸入NO1h后,PaO2即呈上升趋势,4h后从ALI时的65±14升至(114±36)mmHg,与对照组比较差异有显著性(P<0.05).同时肺内分流(Qs/Qt)及肺泡-动脉氧压差(AaDO2)降低.MAP及体循环血管阻力(SVR)与对照组比较无显著性改变.结论以氟碳为媒介的部分液体通气及吸入20ppm的NO均能有效的改善ALI动物肺气体交换.吸入NO能显著降低MPAP,而PLV更能显著的升高PaO2. 相似文献
5.
目的 研究全腔静脉肺动脉连接术 (TCPC)术后降钙素基因相关肽 (calcitonin gene relatedpeptide,CGRP)的变化情况及肺循环内无搏动血流对其分泌的长期影响。 方法 实验组为 1 3例心外管道TCPC术后患者 ,对照组为 1 3例房间隔、室间隔缺损心内修复术患者 ,对 2组患者分别于术前、术后第 1天、第 5天、第 4周和术后 6个月测量血CGRP含量。实验组患者术后经右心导管测量心脏指数 (cardiacindex ,CI)及肺血管阻力 (pulmonaryvascularresistance ,PVR)。 结果 术前实验组CGRP含量显著低于对照组 (t=3 1 2 ,P <0 0 1 ) ;术后 2组CGRP均出现一过性升高 ,第 4周对照组恢复正常 ,而实验组仍显著高于对照组 (t=3 1 4 ,P <0 0 1 ) ,且术后 6个月仍保持高水平 (t=2 32 ,P <0 0 5)。CGRP含量与PVR呈显著负相关 (r=- 0 99,t=9 82 ,P <0 0 5) ,与CI呈显著正相关 (r =0 98,t=6 95 ,P <0 0 5)。 结论 TCPC手术完全旷置右心后 ,肺循环无搏动血流会刺激肺组织CGRP分泌增加 ,由此所引起的肺血管阻力降低 ,可能对手术患者的早期恢复有利 相似文献
6.
目的研究吸入不同浓度一氧化氮(NO)对犬感染性急性呼吸窘迫综合征(ARDS)的效应。方法 感染性ARDS建立后,12只纯处毕格犬随机分成两组,单纯机械通气组(对照组,n=6),机械通气+吸入NO组(NO组,n=6)。NO吸人浓度分别为10、20、40、80 ppm,各浓度吸1 h,然后降至10 ppm吸6 h。通过以下指标变化分析判断吸入NO对ARDS的影响:体、肺循环血液动力学参数;氧合指数(PaO2/FiO2)、分流率(Qs/Qt)、肺动态顺应性(cdyn)、死腔量(VD/VT)及气道阻力(Rrs);外周血中性粒细胞计数;血、尿中亚硝酸根/硝酸根浓度(NO2-/NO3-);血正铁血红蛋白含量及动物存活时间。结果 吸人10、20、40、80 ppm.NO,PaO2/FiO2增加超过50%,Qs/Qt下降<25%,VD/VT下降至0.36,PVRI下降近50%,一定程度改善Cdyn,与单纯机械通气组相应时相点比,差异有显著性(P均<0.01),动物存活时间为(10.2±1.7)h显著高于对照组(4.4±1.2)h(P<0.01);NO浓度由80 ppm降至10 ppm时,改善的Qs/Qt,PaO2/FiO2,PVRI,VD/VT及Cdyn等指标又回落,实验最后阶段,随病程发展,肺部情况恶化;吸入NO可减轻外周血白细胞下降程度,与对照组相比差异有显著性(P<0.01)。结论 吸入10~80 ppm NO可明显降低犬感染性ARDS时肺血管阻力,改善通气,血流比例,对ARDS产生一定的治疗作用。 相似文献
7.
目的探讨手助腹腔镜(HALS)能否模拟完成扩大右半结肠切除术中血管骨骼化淋巴结清扫。方法2001年11月至2004年9月由同一组医生对30例右半结肠癌患者分别完成HALS(腹腔镜组)和开腹手术(开腹组),各15例。分析比较两组患者的临床资料。结果腹腔镜组与开腹组的手术时间分别为(214.0±16.5)min和(245.0±24.6)min(t=2.248,P<0.05);术中出血量分别为(78.4±24.3)ml与(203.3±48.5)ml(t=4.927,P<0.05);术后肛门排气时间分别为(53.4±6.7)h与(67.3±9.7)h(t=2.530,P<0.05);术后住院天数分别为(11.5±1.11)d与(17.9±4.0)d(t=3.413,P<0.05);肠旁各站淋巴结数N1分别为(15.3±2.6)枚与(16.2±3.3)枚(t=0.48,P>0.05);N2分别为(5.6±1.6)枚与(5.9±2.2)枚(t=0.213,P>0.05),N3分别为(4.3±2.2)枚与(6.1±1.5)枚(t=1.429,P>0.05),两组患者术后并发症发生率分别为20.0%(3/15)与33.3%(5/15),(χ2=0.0227,P>0.05)。结论HALS可以很好地完成扩大右半结肠切除、术中血管骨骼化淋巴清扫这一高难度手术。 相似文献
8.
目的 探讨心外管道全腔静脉肺动脉连接手术对肺血分布的确切影响。方法 应用99锝 大颗粒聚合蛋白 ( 99mTc MAA)肺灌注显像 ,对 17例心外管道全腔静脉肺动脉连接术病人手术前、后肺血灌注情况进行定量研究。结果 17例病人术后肺放射性核素计数值为 ( 313 7± 40 1)× 10 3,显著高于术前的 ( 2 6 6 8± 33 6 )× 10 3(t=2 2 3,P <0 0 5 )。术后右肺与左肺血流灌注量比值为 1 14± 0 15 ,高于术前的 1 0 2± 0 12。术后肺野上段血流灌注量显著降低 (t=2 93,P <0 0 1) ,下段血流灌注量显著增加 (t=3 14,P <0 0 1)其上 /下段比值为 0 2 3± 0 0 9。显著低于术前为 0 43± 0 0 8(t=3 19,P <0 0 1)。结论 心外管道全腔静脉肺动脉连接手术仍可保持右肺的相对优势灌注血流。术后明显的坠积性肺淤血状态可能与远期肺动静脉瘘并发症发生率增加 ,以及活动耐力受限有关 ,但仍有待于进一步随访证实。 相似文献
9.
目的探讨脑利钠肽(BNP)在评价功能性单心室患者行全腔静脉-肺动脉连接术(TCPC)后心功能中的价值及其意义。方法选择2004年4~11月间连续在我科随访的TCPC后患者11例(TCPC组),男7例,女4例;年龄8.2±4.1岁;随访时间2.1±1.6年。按照改良R oss标准对临床心功能评分。采集外周静脉血3m l,用酶标免疫法测定血浆BNP浓度。其中6例同期用磁共振成像(M R I)测定心功能,对BNP做相关因素分析。9人健康儿童作为正常对照(对照组)。结果(1)TCPC组血浆BNP水平为400pg/m l(IQR 200-690),较对照组的110 pg/m l(IQR 90-190)增高(P=0.003);(2)M R I测定结果:TCPC组6例患者舒张期末容量指数为65.76±8.65 m l/m2,收缩期末容量指数为31.90±6.36 m l/m2,心搏出量指数为39.09±11.76 m l/m2,射血分数(EF)为0.52±0.06,心脏指数(C I)为2.38±0.58 L/m in.m2,心肌质量指数为103.49±21.57 g/m2,心肌质量/心室舒张期末容量为1.57±0.24;(3)TCPC组BNP水平与手术时年龄呈明显正相关(r=0.632,P=0.041);BNP水平与上述M R I指标、R oss评分、性别、年龄、脉搏血氧饱和度(SpO2)及主心室类型等因素无关。结论TCPC后近2年神经内分泌系统仍处于应激状态,BNP增高可能与TCPC后特有的血流动力学状态有关;血浆BNP水平不能作为正确评估TCPC后心功能状态的指标。 相似文献
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目的 探讨肺动脉高压 (PH)时一氧化氮 (NO)的介导作用及吸入NO对肺、体循环压力和肺血管结构重组逆转的影响。方法 6条PH模型犬 ,采用面罩法间断吸入NO 1周 ,检测肺组织一氧化氮合酶 (NOS)、丙二醛 (MDA)及总钙含量 ;观察吸入NO后血流动力学及动脉血气变化 ;图像分析法测定肺小动脉中膜厚度 (MT) ;监测外周血高铁血红蛋白 (MetHb)含量。结果 PH时 ,肺组织NOS活性为 (0 .5 2± 0 .2 7)nmol·min-1·g-1,较正常明显降低 (P <0 .0 5 ) ,MDA、Ca2 含量明显升高 (P <0 .0 5 )。吸入NO后肺动脉平均压、肺血管阻力明显降低 ,氧分压升高 ,二氧化碳分压降低 ,而体动脉压无变化。吸入NO前后肺小动脉中膜厚度无明显变化 (P >0 .0 5 )。MetHb均低于正常值 15 g/L。结论 NO作用减弱在PH形成中与NOS活性降低密切相关 ,O-2 和Ca2 共同介导 ;吸入NO能选择性降低肺动脉压而不影响体动脉压 ,但对肺血管结构无影响。 相似文献
11.
BACKGROUND: The beneficial effect of inhaled nitric oxide (NO) on pulmonary hypertension is well known. However, the indications for NO inhalation therapy for pulmonary hypertension associated with congenital heart lesions are still unclear. The aim of the current study was to seek a measure that would predict the effectiveness of inhaled NO in infants undergoing cardiac surgery. METHODS: Forty-six infants with pulmonary hypertension were studied. Pulmonary vascular resistance (PVR) measured at the time of cardiac catheterization was used as an indicator and compared with pulmonary arterial pressure/systemic blood pressure ratio (Pp/Ps) at the time of weaning from cardiopulmonary bypass. The effect of 40 ppm of inhaled NO for 15 min was evaluated in patients whose Pp exceeded systemic values. RESULTS: Preoperative PVR correlated positively with Pp/Ps at the time of weaning from cardiopulmonary bypass (r2 = 0.86; P < 0.05; n = 46). A Pp/Ps greater than or equal to 1 was not observed in any cases in which the preoperative PVR values were less than 7 Wood units m2; Pp/Ps ratio greater than or equal to 1 occurred in four patients. Each of these had PVR values greater than 7 Wood units m2. Three of these patients who had PVR values in the 7-12 Wood units m2 range were responsive to inhaled NO. The fourth patient, whose PVR value was greater than 15 Wood units m2, was unresponsive. Lung biopsy specimens were obtained in two patients whose preoperative PVR values were greater than 10 Wood units m2. CONCLUSION: Preoperative PVR correlates reasonably well with postbypass Pp/Ps. 相似文献
12.
PURPOSE: Significant pulmonary hypertension is a predictor of postoperative right heart insufficiency and increased mortality in patients undergoing orthotopic heart transplantation. Since the use of iv vasodilators is limited by their systemic effects, we evaluated the pulmonary and systemic hemodynamic effects of inhaled aerosolized iloprost (IP) in heart transplant candidates with elevated pulmonary vascular resistance (PVR). METHODS: Twenty-nine male heart transplant candidates because of dilated or ischemic cardiomyopathy with elevated PVR were included in the study. After assessing baseline hemodynamics, 50 micro g aerosolized IP were administered by inhalation. RESULTS: Inhalation of iloprost reduced PVR index (PVRI; 416 +/- 180 vs 349 +/- 173 dyn x sec(-1) x m(-2) x cm(-5); P < 0.01) and mean pulmonary artery pressure (MPAP; 28.6 +/- 9 vs 24.2 +/- 9.1 mmHg; P < 0.01), but did not affect blood pressure or systemic vascular resistance. An additional improvement of ventricular performance with an increase of cardiac index (CI; 2.8 +/- 0.7 vs 2.6 +/- 0.7 L x min(-1) x m(-2); P < 0.05) and a decrease of pulmonary capillary wedge pressure (PCWP; 15.6 +/- 6.8 vs 12.8 +/- 7.1 mmHg; P < 0.01) was observed after inhalation of IP. CONCLUSIONS: Inhaled aerosolized iloprost effectively reduces MPAP and is accompanied by an increase in CI and stroke index. Further advantages of iloprost inhalation are the lack of adverse reactions and ease of administration. Iloprost may be a useful drug to screen for vascular reactivity in cardiac transplantation patients. 相似文献
13.
Background: The beneficial effect of inhaled nitric oxide (NO) on pulmonary hypertension is well known. However, the indications for NO inhalation therapy for pulmonary hypertension associated with congenital heart lesions are still unclear. The aim of the current study was to seek a measure that would predict the effectiveness of inhaled NO in infants undergoing cardiac surgery. Methods: Forty-six infants with pulmonary hypertension were studied. Pulmonary vascular resistance (PVR) measured at the time of cardiac catheterization was used as an indicator and compared with pulmonary arterial pressure/systemic blood pressure ratio (Pp/Ps) at the time of weaning from cardiopulmonary bypass. The effect of 40 ppm of inhaled NO for 15 min was evaluated in patients whose Pp exceeded systemic values. Results: Preoperative PVR correlated positively with Pp/Ps at the time of weaning from cardiopulmonary bypass (r2 = 0.86;P < 0.05; n = 46). A Pp/Ps greater than or equal to 1 was not observed in any cases in which the preoperative PVR values were less than 7 Wood units m2; Pp/Ps ratio greater than or equal to 1 occurred in four patients. Each of these had PVR values greater than 7 Wood units m2. Three of these patients who had PVR values in the 7-12 Wood units m2 range were responsive to inhaled NO. The fourth patient, whose PVR value was greater than 15 Wood units m2, was unresponsive. Lung biopsy specimens were obtained in two patients whose preoperative PVR values were greater than 10 Wood units m2. 相似文献
14.
OBJECTIVE: The goal of this study was to evaluate the efficacy of 100% oxygen and inhaled nitric oxide (iNO) in decreasing pulmonary vascular resistance (PVR) and transpulmonary gradient (TPG) in dilated cardiomyopathy patients being evaluated for orthotopic heart transplantation (OHT); who, despite maximal intravenous (IV) dilator therapy, had persistent moderate-to-severe pulmonary hypertension. DESIGN: A prospective nonrandomized clinical study. SETTING: University hospital, major transplant center. PARTICIPANTS: Twenty-one adult patients undergoing OHT evaluation. Interventions: One hundred percent oxygen and iNO at 20 and 40 ppm were sequentially administered to the patients once they were optimized with IV vasodilators and inotropes. MEASUREMENTS AND MAIN RESULTS: Although no significant change was noted with oxygen, iNO 20 ppm reduced the mean pulmonary artery pressure (44.1 +/- 1.7 to 38.6 +/- 1.8 mmHg, p < 0.05), PVR index (823 +/- 47 to 621 +/- 55 dyne/s/m(2)/cm(5), p < 0.05), TPG (22.4 +/- 1.4 to 17.0 +/- 1.5 mmHg, p < 0.05), and right ventricular stroke work index (14.7 +/- 1.2 to 11.1 +/- 1.2 g . m/m(2)/beat, p < 0.05). In 13 of 21 patients, PVR decreased by greater than 25% after iNO therapy. Nine of these patients had PVR and TPG decrease to levels considered acceptable for OHT listing. CONCLUSIONS: iNO can further improve right ventricular hemodynamics even after presumed optimization with IV vasodilators and serves as a test of PVR reversibility during the preoperative assessment of OHT candidates. 相似文献
15.
PURPOSE: Pulmonary hypertension represents a significant predictor of postoperative right heart insufficiency and increased mortality in patients undergoing orthotopic heart transplantation. As the use of intravenous vasodilators is limited by their systemic effects, we evaluated the pulmonary and systemic hemodynamic effects of inhaled aerosolized iloprost in heart transplant candidates with elevated pulmonary vascular resistance. METHODS: Forty-five male heart transplant candidates with dilated or ischemic cardiomyopathy were included in the study. After assessing baseline hemodynamics, 20 microg of aerosolized iloprost was administered by ultrasonic inhalation. All patients were breathing spontaneously. RESULTS: Inhalation of iloprost reduced pulmonary vascular resistance index (395 +/- 205 vs 327 +/- 222 dyne.s.cm(-5).m(-2); P < 0.05) and mean pulmonary arterial pressure (28.7 +/- 10 vs 24.3 +/- 10 mm Hg; P < 0.05). An additional improvement of ventricular performance with an increase of cardiac index (2.7 +/- 0.7 vs 3.0 +/- 0.8 L.min(-1).m(-2); P < 0.05) and a decrease of pulmonary capillary wedge pressure (16.6 +/- 7.7 vs 13.4 +/- 7.3 mm Hg; P < 0.05) was accompanied by a slight decrease of systemic vascular resistance (1280 +/- 396 vs 1172 +/- 380 dyne.s.cm(-5); P < 0.05). However, the mean arterial pressure remained uninfluenced. CONCLUSIONS: Inhaled aerosolized iloprost effectively reduces mean pulmonary arterial pressure and also induces an increase in cardiac index. Further advantages of iloprost inhalation are the lack of adverse reactions and ease of administration. Iloprost represents a useful drug to screen for vascular reactivity in cardiac transplantation patients. 相似文献
16.
BACKGROUND: The inhalation of nitric oxide (NO) in patients with heart failure decreases pulmonary vascular resistance (PVR) and is associated with an increase in pulmonary artery wedge pressure (PAWP). The mechanism for this effect remains unclear. METHODS: In dogs rapid-paced for 8 weeks to induce cardiac dysfunction, we performed left ventricular pressure-volume analysis of unpaced hearts in situ to determine whether during NO inhalation (80 ppm), the mechanism for the rise in PAWP is due to: 1) primary pulmonary vasodilation; 2) a direct negative inotropic effect; or 3) impairment of ventricular relaxation. RESULTS: Inhalation of NO decreased PVR by 51%+/-3.8% (257+/-25 vs 127+/-18 dynes x sec x cm(-5) [NO 80 ppm]; p < 0.001) and increased PAWP (15.4+/-2.4 vs 18.1+/-2.6 mm Hg [NO 80 ppm]; p < 0.001). Calculated systemic vascular resistance remained unchanged. Left ventricular (LV) end-diastolic pressure rose (16.4+/-1.9 vs 19.1+/-1.8 mm Hg [NO 80 ppm]; p < 0.001), as did LV end-diastolic volume (83.5+/-4.0 vs 77.0+/-3.4 mL [NO 80 ppm]; p = 0.006). LV peak +dP/dt was unchanged by NO (1,082+/-105 vs 1,142+/-111 mm Hg/sec [NO 80 ppm]; p = NS). There was a trend toward a stroke volume increase (17.4+/-1.2 vs 18.8+/-1.3 mL; p = NS), but the relaxation time constant and end-diastolic pressure-volume relation were both unchanged. CONCLUSIONS: In this canine model of cardiomyopathy, inhaled NO decreases pulmonary vascular resistance. The associated increase in left ventricular filling pressure appears to be secondary to a primary pulmonary vasodilator effect of NO without primary effects on the contractile or relaxation properties of the left ventricle. 相似文献
17.
目的 观察吸入一氧化氮(nitricoxide,NO)治疗室间隔缺损 (ventricularseptaldefect,VSD)术后肺动脉高压 (pulmonaryhypertension ,PH)的疗效。 方法 2 0例VSD术后PH病人分别吸入 2 0×10 -6 、6× 10 -6 NO ,监测吸入前后的血流动力学、氧合指标。结果 吸入 2 0× 10 -6 NO后明显降低肺动脉压、肺循环阻力、肺内分流率、肺泡动脉血氧分压差 ,提高动脉血氧分压、氧供指数 ;以上指标停吸NO后恢复吸入NO前水平 ;再吸入 6× 10 -6 NO后恢复吸入 2 0× 10 -6 NO后水平 ,并维持至停吸NO后。吸入前后体循环压及阻力无变化。结论 吸入NO是治疗VSD手术后PH的一种有效的方法。 相似文献
18.
PURPOSE: Severe pulmonary hypertension (PH) is a major cause of right ventricular (RV) dysfunction. Various iv vasodilator modalities have been used with limited results because of lack of pulmonary selectivity. The aim of the present controlled study was to evaluate the efficacy of inhaled iloprost, a synthetic prostacyclin analogue, in patients with elevated pulmonary vascular resistance (PVR) immediately after separation from cardiopulmonary bypass (CPB). METHODS: Twelve patients with persistent PH after discontinuation of CPB were included in the study. In all patients standard hemodynamic monitoring was used. Inhaled iloprost was administered via nebulized aerosol at a cumulative dose of 0.2 micro g*kg(-1) for a total duration of 20 min. Complete sets of hemodynamic measurements were performed before inhalation (baseline), during and after cessation of the inhalation period. Echocardiographic monitoring of RV function was also used. RESULTS: Inhaled iloprost induced a reduction in the transpulmonary gradient at the end of the inhalation period in comparison to baseline (9.33 +/- 3.83 mmHg vs 17.09 +/- 6.41 mmHg, P < 0.05). The mean pulmonary artery pressure to systemic artery pressure ratio decreased over this period (0.28 +/- 0.08 vs 0.45 +/- 0.17, P < 0.05). A statistically significant decrease of the PVR to systemic vascular resistance ratio was also observed (0.15 +/- 0.05 vs 0.21 +/- 0.05, P < 0.05). Improved indices of RV function were observed in echocardiographic monitoring. CONCLUSION: Inhaled iloprost appears to be a selective pulmonary vasodilator and may be effective in the initial treatment of PH and the improvement of RV performance in the perioperative setting. 相似文献
19.
烟雾吸入致肺组织细胞损伤后5min,行肺灌洗机械通气4h,观察24。酹明,犬随机分为三组。烟雾吸入后,对照组单纯涓氧;治疗组吸氧加0.0045%NO,连续监测12h血循环动力学化;正常组不致伤。 相似文献
20.
Because nitroprusside NTP infusion used to differentiate between fixed and reversible pulmonary artery hypertension in heart transplant candidates can result in systemic hypotension before reducing pulmonary artery pressures, we observed the effect or inhaled prostacyclin (PGI(2)) on pulmonary artery pressures and transpulmonic gradient (TPG) in patients with NTP-resistant pulmonary artery hypertension. Six patients undergoing evaluation for orthotropic heart transplant (OHTX) with NTP-resistant pulmonary artery hypertension received inhaled PGI(2), with hemodynamic measurements made at baseline, on NTP- and PGI(2) inhaled after returning to baseline. Compared with hemodynamic results with NTP, inhaled PGI(2) caused significant decrease in pulmonary artery systotic pressure, 43.8 +/- 4.8 mm Hg vs 63.2 +/- 2.04 mm Hg (p < 0.001); Mean pulmonary artery pressure, 22.7 +/- 4.18 vs 32.3 +/- 3.39 mm Hg (p < 0.05); and TPG, 11.5 +/- 3.73 vs 17.0 +/- 4.69 mm Hg (p < 0.05), with a 40% decrease in pulmonary vascular resistance/systemic vascular resistance ratio. We conclude that inhaled PGI(2) has benefit in reversing pulmonary artery hypertension resistant to NTP, in patients undergoing OHTX evaluation which is due to its more selective pulmonary vasodilation. 相似文献
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