Cardiopulmonary effects of the alpha2-adrenoceptor agonists medetomidine and ST-91 in anesthetized sheep

To test the hypothesis that pulmonary alterations are more important than hemodynamic changes in alpha2-agonist-induced hypoxemia in ruminants, the cardiopulmonary effects of incremental doses of (4-[1-(2,3-dimethylphenyl)ethyl]-1H-imadazole) hydrochloride (medetomidine; 0.5, 1.0, 2.0, and 4 micrograms/kg) and 2-(2, 6-diethylphenylamino)-2-imidazol (ST-91; 1.5, 3.0, 6.0, and 12 micrograms/kg) were compared in five halothane-anesthetized, ventilated sheep using a placebo-controlled randomized crossover design. Pulmonary resistance (RL), dynamic compliance, and tidal volume changes in transpulmonary pressure (DeltaPpl) were determined by pneumotachography, whereas cardiac index (CI), mean pulmonary artery pressure (Ppa), and pulmonary artery wedge pressure (Ppaw) were determined using thermodilution and a Swan-Ganz catheter. The most important finding was the fall in partial pressure of oxygen in arterial blood (PaO2) after administration of medetomidine at a dose (0.5 micrograms/kg) 20 times less than the sedative dose. The PaO2 levels decreased to 214 mm Hg as compared with 510 mm Hg in the placebo-treated group. This decrease in PaO2 was associated with a decrease in dynamic compliance and an increase in RL, DeltaPpl, and the intrapulmonary shunt fraction without changes in heart rate, CI, mean arterial pressure, pulmonary vascular resistance, Ppa, or Ppaw. On the other hand, ST-91 only produced significant changes in PaO2 at the highest dose. After this dose of ST-91, the decrease in PaO2 was accompanied by a 50% decrease in CI and an increase in mean arterial pressure, Ppa, Ppaw, and the intrapulmonary shunt fraction without significant alterations of RL and DeltaPpl. The study suggests that the mechanism(s) by which medetomidine and ST-91 produce lower PaO2 are different and that drug-induced alterations in the pulmonary system are mainly responsible for the oxygen-lowering effect of medetomidine.     

Effects of erythrapheresis on pulmonary haemodynamics and oxygen transport in patients with secondary polycythaemia and cor pulmonale

Reducing packed cell volume has been advocated as a therapeutic procedure in patients with polycythaemia secondary to hypoxic cor pulmonale. The aim of this investigation was to evaluate the effects of this manoeuvre on resting pulmonary haemodynamics and tissue oxygenation in 12 such patients. The subjects were studied whilst they were breathing air (n = 12), after breathing 35% oxygen for 30 min (n = 11) and breathing air 30 min after isovolaemic reduction in packed cell volume, from 0.61 +/- 0.02 to 0.50 +/- 0.02 (mean +/- SEM), by erythrapheresis (n = 12). Initial values for the group were: PaO2 6.5 +/- 0.3 kPa; red cell mass 152 +/- 12% predicted; mean pulmonary artery pressure (PAP) 41 +/- 3 mmHg; cardiac index 3.1 +/- 0.31 min-1 m-2. Breathing 35% oxygen reduced PAP by 3.1 +/- 1.0 mmHg (P less than 0.02), cardiac index by 0.28 +/- 0.121 min-1 m-2 (P less than 0.05) and right ventricular stroke work by 0.05 +/- 0.01 J (P less than 0.01). Systemic vascular resistance was unchanged. Systemic oxygen transport increased and peripheral oxygen consumption was unaltered. Erythrapheresis reduced blood viscosity at shear rates 23 S-1 and 230 S-1. PAP fell by 2.4 +/- 1.1 mmHg (P less than 0.05) and cardiac index increased by 0.32 +/- 0.091 min-1 m-2 (P less than 0.01), but right ventricular stroke work was unchanged. Systemic vascular resistance was reduced by 25 +/- 7 kPa S l-1 (P less than 0.01). Systemic oxygen transport decreased but peripheral oxygen consumption was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)     

The right ventricle: interaction with the pulmonary circulation

The primary role of the right ventricle (RV) is to deliver all the blood it receives per beat into the pulmonary circulation without causing right atrial pressure to rise. To the extent that it also does not impede left ventricular (LV) filling, cardiac output responsiveness to increased metabolic demand is optimized. Since cardiac output is a function of metabolic demand of the body, during stress and exercise states the flow to the RV can vary widely. Also, instantaneous venous return varies widely for a constant cardiac output as ventilatory efforts alter the dynamic pressure gradient for venous return. Normally, blood flow varies with minimal changes in pulmonary arterial pressure. Similarly, RV filling normally occurs with minimal increases in right atrial pressure. When pulmonary vascular reserve is compromised RV ejection may also be compromised, increasing right atrial pressure and limiting maximal cardiac output. Acute increases in RV outflow resistance, as may occur with acute pulmonary embolism, will cause acute RV dilation and, by ventricular interdependence, markedly decreased LV diastolic compliance, rapidly spiraling to acute cardiogenic shock and death. Treatments include reversing the causes of pulmonary hypertension and sustaining mean arterial pressure higher than pulmonary artery pressure to maximal RV coronary blood flow. Chronic pulmonary hypertension induces progressive RV hypertrophy to match RV contractility to the increased pulmonary arterial elastance. Once fully developed, RV hypertrophy is associated with a sustained increase in right atrial pressure, impaired LV filling, and decreased exercise tolerance. Treatment focuses on pharmacologic therapies to selectively reduce pulmonary vasomotor tone and diuretics to minimize excessive RV dilation. Owning to the irreversible nature of most forms of pulmonary hypertension, when the pulmonary arterial elastance greatly exceeds the adaptive increase in RV systolic elastance, due to RV dilation, progressive pulmonary vascular obliteration, or both, end stage cor pulmonale ensues. If associated with cardiogenic shock, it can effectively be treated only by artificial ventricular support or lung transplantation. Knowing how the RV adapts to these stresses, its sign posts, and treatment options will greatly improve the bedside clinician’s ability to diagnose and treat RV dysfunction.     

Effect of nifedipine on splanchnic and pulmonary vascular capacitance

Summary. This study examines the hypothesis that nifedipine may increase splanchnic vascular capacitance and thus change the distribution of blood between the splanchnic and pulmonary circulation in heart failure patients. Relative regional blood volumes were determined by equilibrium blood pool scintigraphy during a 10 min baseline period and for 30 min after nifedipine 20 mg sublingually, with simultaneous recordings of systemic and pulmonary arterial pressures, hepatic venous wedge pressure, and cardiac output. Eight patients with ischaemic heart failure received nifedipine. Four patients served as controls. Nifedipine reduced mean arterial pressure and systemic vascular resistance in every patient. There were no significant changes in the relative blood volumes of the intestinal, hepatic, or splenic regions or in hepatic venous wedge pressure (reflecting portal venous pressure), suggesting unchanged splanchnic vascular pressure-volume relationship. Nifedipine caused a 6.3±l.0% increase in relative pulmonary blood volume and a slight increase in pulmonary vascular distending pressure from 16.1±2.9 mmHg to 17.5±2.8 mmHg (P < 0.05), suggesting that the increase in pulmonary blood volume was passively mediated. In conclusion, nifedipine did not change splanchnic vascular capacitance, but caused a small increase in pulmonary blood volume, which probably was a passive response to increased distending pressure.     

血清缺氧诱导因子-1α和血管内皮生长因子水平与高原慢性肺心病患者肺动脉压的关系

目的：探讨血清缺氧诱导因子-1α（HIF-1α）和血管内皮生长因子（VEGF）在低氧性肺动脉高压发病中的作用。方法：采用双抗体夹心酶联免疫吸附法（ELSIA）检测高原地区（海拔2 260~3 500m）50例慢性肺心病急性加重期患者（肺心病组）、40例慢性阻塞性肺疾病（COPD）缓解期患者COPD组和40例当地健康体检者（对照组）血清HIF-1α、VEGF含量、动脉血氧分压（PaO2）,并使用彩色多普勒超声心动仪测定肺动脉血流频谱,计算平均肺动脉压（mPAP）。结果：肺心病组血清HIF-1α（325.88±38.02）pg.L-1、VEGF（466.40±52.44）ng.L-1,mPAP（46.22±5.34）mmHg显著高于COPD组[分别为（74.02±8.15）pg.L-1、（98.51±8.22）ng.L-1和（24.77±2.54）mmHg];COPD组显著高于健康对照组[分别为（54.85±7.72）pg.L-1、（74.57±7.58）ng.L-1和（21.47±2.35）mmHg]。肺心病组PaO2（37.21±4.35）mmHg显著低于COPD组（59.21±5.24）mmHg,COPD组显著低于健康对照组（67.35±4.67）mmHg。肺心病组和COPD组血清HIF-1α、VEGF水平与mPAP均呈正相关,与PaO2水平呈负相关。结论：高原慢性肺心病急性加重期患者血清HIF-1α、VEGF水平明显升高,可能与其低氧性肺动脉高压的形成有一定关系。     

Effectiveness of enalapril in chronic cor pulmonale

The aim of our investigation was assessment of enalapril effects in cor pulmonale. 20 patients with chronic obstructive pulmonary diseases complicate with cor pulmonale received combined treatment including enalapril. The course of such treatment led to a significant lowering of systolic and diastolic pressure in the pulmonary artery, systemic arterial pressure, specific peripheral resistance and minute volume in patients with hyperkinetic and mixed types of hemodynamics. Parameters of ECG and exercise tolerance improved. Enalapril is effective in correction of pulmonary and central hemocirculation in chronic cor pulmonale.     

Hemodynamic, renal, and hormonal responses to alpha-human atrial natriuretic peptide in patients with congestive heart failure

Hemodynamic, renal, and hormonal effects of intravenous bolus injection of 50 micrograms synthetic alpha-human atrial natriuretic peptide (alpha-hANP) were studied in eight patients with congestive heart failure. alpha-hANP caused significant reductions in mean blood pressure and systemic vascular resistance. These responses were sustained up to 90 minutes and not accompanied by reflex tachycardia. Cardiac index and stroke volume index increased significantly at 90 minutes and pulmonary capillary wedge pressure, pulmonary arterial pressure, and mean right atrial pressure remained unchanged. Urine volume, urinary sodium excretion, creatinine clearance, and fractional excretion of sodium increased significantly, but fractional excretion of potassium and phosphate did not change. Elevated plasma renin activity, plasma aldosterone, and norepinephrine were suppressed after the injection of alpha-hANP. The bolus injection of this peptide has moderately hypotensive, vasorelaxant, and natriuretic effects in patients with congestive heart failure.     

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.     

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。     

牛心包补片修补心脏缺损并雾化吸入伊洛前列环素降低肺动脉高压

背景：对于先天性心脏病合并肺动脉高压的治疗,传统降低肺动脉高压的药物效果确实,但存在不易监测、停药后反跳等现象;传统的心脏涤纶补片较易引起吻合口变形、血栓、栓塞、溶血和感染等并发症。目的：观察应用戊二醛处理牛心包补片和雾化吸入伊洛前列环素治疗先天性心脏病合并肺动脉高压的效果。方法：选择90例先天性心脏病合并肺动脉高压患者,术中采用戊二醛处理的牛心包补片修补心脏间隔缺损,术后雾化吸入伊洛前列环素30 ng/（min·kg）,日间12 h按1次/4 h给药,夜间12 h按1次/6 h给药,连续给药2 d。记录每次吸入药物前、吸入后即刻、吸入30 min后平均动脉压、平均肺动脉压、体循环阻力指数与肺循环阻力指数,于随访期观察有无心包材料相关并发症和心功能情况。结果与结论：90例患者复查超声心动图见活瓣均已关闭,无分流,心脏间隔缺损无回声中断,心脏收缩功能正常,未发现与牛心包补片相关的不良反应。所有患者不同时间点平均动脉压、体循环阻力指数比较差异无显著性意义。患者吸入药物后即刻平均肺动脉压、肺循环阻力指数明显低于吸入药物前（P 〈0.01）,吸入30 min后平均肺动脉压、肺循环阻力指数亦明显低于吸入药物前（P 〈0.05）。表明应用戊二醛处理的牛心包补片和雾化吸入伊洛前列环素治疗先天性心脏病合并肺动脉高压安全、有效。     

三七总皂甙注射液治疗肺源性心脏病急性发作期心力衰竭疗效观察

目的：观察三七总皂甙注射液联用西药治疗肺源性心脏病（肺心病）急性发作期心力衰竭（心衰）的疗效。方法：６０ 例患者随机分为２ 组,每组３０ 例。对照组给予吸氧、抗生素、氨茶碱、利尿剂和地塞米松等治疗;治疗组除以上治疗外加用三七总皂甙注射液６００ ｍ ｇ 加入５％ 葡萄糖或生理盐水中静滴,每日１ 次,２ 组均连续用药１５ 日后评定疗效、心功能和血气分析。结果：治疗组显效率（５６７％ ）、总有效率（９３３％ ）显著高于对照组（分别为３６７％ 和７６７％ , Ｐ＜ ００１ 和 Ｐ＜ ００５）。治疗组治疗后肺动脉平均压（ Ｐ Ａ Ｍ Ｐ）、肺血管阻力（ Ｐ Ｖ Ｒ）、总外周血管阻力（ Ｔ Ｐ Ｒ）、 Ｐａ Ｏ２ 和动脉血氧饱和度（ Ｓａ Ｏ２）的改善明显优于对照组（ Ｐ＜ ００５ 或 Ｐ＜ ００１）。结论：三七总皂甙注射液与西药合用治疗肺心病急性发作期心衰比单用西药治疗更加有效和安全。     

Long-term Oxygen Therapy in Cor Pulmonale

Fourteen out of a group of 21 patients with cor pulmonale associatedwith obstructive airways disease received controlled oxygentherapy for 24 hours per day during acute exacerbations in hospital,but for only 12 hours per day at home in convalescence. Threepatients derived benefit judged by a reduction in the expectednumber of acute exacerbations of cor pulmonale, but most patientscontinued to deteriorate. It was felt that 12 hours per daywas an insufficient period for oxygen therapy and longer periodswere necessary. Despite this poor response pulmonary arterypressure measured in convalescence was normal or only slightlyelevated in many patients. The aetiology of cor pulmonale andin particular the importance of increased pulmonary vascularresistance in obstructive airways disease is discussed. Thefindings do not support the hypothesis that cor pulmonale isinvariably due to pressure overload of the right ventricle.     

Hemodynamic effects of continuous norepinephrine infusion in dogs with and without hyperkinetic endotoxic shock

We compared, at constant preload maintained by polygeline (gelatin) infusion, the hemodynamic effects of continuous infusion of norepinephrine (0.5, 1, and 1.5 micrograms/kg X min) in anesthetized dogs with and without hyperdynamic endotoxic shock. In both groups, norepinephrine infusion increased systolic, diastolic and mean aortic BP, cardiac index, stroke index, index of myocardial contractility, and mean pulmonary artery pressure. No significant change in right atrial pressure, left ventricular end-diastolic pressure, heart rate, systemic vascular resistance, or pulmonary vascular resistance was observed. Oxygen consumption index and oxygen extraction ratio remained unchanged. Increases in systolic aortic BP were dose-related, whereas maximal effects on other variables were obtained at 0.5 to 1 microgram/kg X min. The rise in aortic pressure resulted from an increased cardiac index but not from an increased systemic vascular resistance. Stroke index increased as contractility improved. The slight alpha-adrenergic effect of continuous, low-dose norepinephrine infusion did not impede the beneficial effects of the marked beta-adrenergic stimulation on cardiac function. The combination of these two effects improved hemodynamic disturbances of hyperdynamic endotoxic canine shock.     

Continuous positive airway pressure is beneficial in treatment of smoke inhalation

This study demonstrates that continuous positive airway pressure (CPAP) improves pulmonary function after smoke inhalation by dogs. Sixteen dogs were anesthetized with iv sodium pentobarbital. Arterial and mixed venous blood gas tensions; carboxyhemoglobin concentration (COHgb); mean systemic arterial (MAP), mean pulmonary arterial (MPAP), and pulmonary arterial wedge (WP) pressures; heart (HR) and respiratory (f) rates; cardiac output (CO); and airway pressure (Paw) were measured. Intrapulmonary physiologic shunt (Qsp/Qt) and pulmonary (PVR) and systemic (SVR) vascular resistances were calculated. The animals then breathed an aerosol of smoke and were divided randomly into 2 groups. The treatment group breathed spontaneously on 8-torr CPAP whereas the control group continued to breathe spontaneously at ambient pressure. After inhalation of smoke, Qsp/Qt, MPAP, PVR, COHgb, HR, and f rose, whereas PaO2 and MAP fell in untreated animals. When CPAP was applied, PaO2 and Qsp/Qt returned nearly to baseline values. Mean f also was significantly lower in the treated animals. We found that the early institution of CPAP improves oxygen exchange in the lungs after the inhalation of smoke.     

还原型谷胱甘肽对慢性肺源性心脏病急性加重期患者血中脂质过氧化物及抗氧化物酶活性的影响

目的:探讨还原型谷胱甘肽对慢性肺源性心脏病急性加重期患者血中脂质过氧化物及抗氧化物酶活性的影响。方法:检测27例健康成年人静脉血全血超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)的活性及血浆脂质过氧化物(LPO)和丙二醛(MDA)的浓度,与慢性肺心病急性加重期组治疗前的此5项指标进行对应比较;选择68例慢性肺源性心脏病急性加重期患者,随机分成两组,试验前均监测静脉血全血SOD、GSH-Px和CAT的活性及血浆LPO和MDA的浓度以及右室压(RVP)、平均肺动脉压(mPAP)等血流动力学指标并评价心功能。试验组在给予常规治疗的同时合并给予还原型谷胱甘肽1.2 g/d,稀释后静脉滴注,疗程2周;对照组只给予常规治疗。2周后,复测上述指标,比较各组治疗前后的变化。结果:(1)肺心病急性加重期组的全血SOD、GSH-Px和CAT的活性比对照组低,而血浆LPO及MDA的浓度比对照组高(均P<0.05)。(2)还原型谷胱甘肽组试验前后比较,全血SOD、GSH-Px和CAT活性明显增高,且血浆LPO和MDA浓度明显降低(均P<0.05);而对照组则无显著变化(P>0.05)。(3)还原型谷胱甘肽组试验前后比较,PVP、mPAP均明显下降(P<0.05);而对照组无显著变化(P>0.05)。(4)还原型谷胱甘肽组心力衰竭纠正的有效率显著高于对照组(P<0.05)。结论:慢性肺源性心脏病急性加重期患者机体的抗氧化能力降低,还原型谷胱甘肽可通过提高机体的抗氧化能力,消除氧自由基和脂质过氧化物起到降低肺动脉和右心室压力、纠正心力衰竭的作用。     

Hemodynamic and respiratory effects of enoximone in acute respiratory insufficiency of chronic obstructive bronchopneumopathy

Hemodynamic effects and gas exchange were studied in twenty COPD patients undergoing mechanical ventilation before and 30 and 60 minutes after an intravenous administration of 1 mg/kg enoximone. Enoximone decreased significantly pulmonary arterial pressure and pulmonary vascular resistances without significantly decrease of systemic vascular resistances 60 minutes after a slight dose of 1 mg/kg. Right ventricular ejection fraction increased; O2 arterial pressure, CO2 arterial pressure, intrapulmonary shunt remained unchanged. We concluded that enoximone induced pulmonary vasodilation in patients with decompensated COPD and increased right ventricular function without deleterious effects in gas exchange.     

血液滤过对严重创伤后并发急性呼吸窘迫综合征患者氧合功能和血流动力学的影响

目的 研究血液滤过对严重创伤后并发ARDS患者氧合功能和血流动力学的影响。方法 选择严重创伤后ARDS患者12例，在呼吸机辅助或控制呼吸下行血液滤过治疗，于血液滤过后1－5d内用Swan-Ganz漂浮导管监测血流动力学和肺氧功能的变化。结果 与血液滤过前比较，滤过后第1天CVP、MPAP、SVRI、PVRI显著降低，整个血液滤过时间PaO2／FiO2升高非常显著，MAP、PCWP、HR、CI、DO2、VO2、ExtrO2、Qs/Qt无显著变化。结论 血液滤过对严重创伤后ARDS患者的血流动力学和氧合功能无明显影响，但可使氧合指数升高。     

夜间无创正压通气对高原地区肺心病缓解期慢性呼吸衰竭患者的康复效应

背景药物治疗慢性呼吸衰竭的效果有限;采用无创通气对慢性肺心病慢性呼吸衰竭患者进行干预,可能不失为一种改善其症状和体征的有效措施.目的观察夜间无创正压通气对高原地区慢性肺心病缓解期慢性呼吸衰竭患者的呼吸肌功能、肺功能的作用.设计完全随机分组设计,对比观察.单位解放军第四医院兰州军区呼吸内科中心.对象选择2002-10/2004-11在解放军第四医院兰州军区呼吸内科中心住院的慢性肺心病缓解期慢性呼吸衰竭患者60例,男38例,女22例.患者均知情同意参加.随机分为2组,治疗组和对照组各30例.方法[1]治疗组采用呼吸机治疗,时间为每晚2200～次日晨700,通气模式为压力支持通气和呼气末正压.在治疗前和治疗5周后测定肺功能、动脉血气、呼吸肌功能和6 min步行距离.对照组病情缓解1周后在出院前测定上述指标,出院后未经任何治疗,5周后复诊测定上述指标.[2]6 min步行距离试验让患者尽最大努力在20 m走廊内行走,完成6 min或以呼吸困难不能坚持为止,用计量表测算步行距离.用电脑膈肌功能测定仪测定口腔最大吸气压、最大呼气压后,用气道阻断法测定最大跨膈压.采用血气分析仪测定动脉血氧分压和二氧化碳分压.用电脑肺功能仪测定第1秒用力呼气量占预计值百分比、第1秒用力呼气量占用力肺活量百分比.[3]组间比较采用t检验,组内比较采用配对t检验.主要观察指标两组干预前后呼吸肌功能、肺功能、动脉血气和6 min步行距离比较.结果纳入慢性肺心病缓解期慢性呼吸衰竭患者60例均进入结果分析.两组患者干预前动脉血气和肺功能各项指标相近(P＞0.05).干预5周后,动脉血氧分压、第1秒用力呼气量占预计值百分比、第1秒用力呼气量占用力肺活量百分比、最大吸气压、最大呼气压、最大跨膈压和6 min步行距离治疗组治疗后明显高于治疗前和对照组治疗后(P＜0.05～0.01),动脉血二氧化碳分压治疗组治疗后明显低于治疗前和对照组治疗后(P＜0.01).结论夜间无创正压通气治疗能显著改善高原地区肺心病缓解期慢性呼吸衰竭患者的动脉血气和肺功能,增强呼吸肌力量.     

The haemodynamic effects of intermittent haemofiltration in critically ill patients

The haemodynamic effects of intermittent high volume venovenous haemofiltration were studied in 13 critically ill patients. The mean negative fluid balance during filtration was 1.2l and the mean duration of treatment 3 h 40 min. The cardiac index fell initially (4.5±0.2 to 3.8±0.2l/min/m²;p<0.05) but then remained stable throughout treatment before returning to baseline at the end of haemofiltration. The mean arterial pressure was unchanged with an increase in the systemic vascular resistance (651±33 to 765±65 dyne·s/cm⁵;p<0.05) suggesting that vascular responsiveness is maintained during haemofiltration.     

Pulmonary vascular effects of dobutamine in experimental pulmonary hypertension

OBJECTIVE: To characterize the dose-related effects of dobutamine on pulmonary vascular tone and associated changes in right ventricular afterload in canine microembolic lung injury .DESIGN: Prospective, interventional study. SETTING: University laboratory. SUBJECTS: Ten anesthetized and ventilated dogs. INTERVENTIONS: Right heart catheterization for the measurement of pulmonary vascular resistance by multipoint mean pulmonary artery pressure (Ppa)/cardiac output (Q) plots, partitioning of pulmonary vascular resistance by the occlusion method, and determination of pulmonary arterial input impedance from spectral analysis of Ppa and Q waves, in ten anesthetized and ventilated dogs, before and after induction of acute microembolic lung injury, and without or with 5, 10, 15, and 20 microg.kg(-1).min(-1) dobutamine. MEASUREMENTS AND MAIN RESULTS: Microembolic pulmonary hypertension was associated with a shift of Ppa/Q plots to higher pressures, a slight decrease in the arterial component of pulmonary vascular resistance, a decrease in characteristic impedance, and an increase in the pulsatile component of right ventricular hydraulic load. At baseline, dobutamine had no effect on Ppa/Q plots at 5 and 10 microg.kg(-1).min(-1) but increased Ppa at 15 and 20 microg.kg(-1).min(-1). In microembolic pulmonary hypertension, the only effect of dobutamine on Ppa/Q plots was a decrease in Ppa at 20 microg.kg(-1).min(-1). Dobutamine had no effect on the partitioning of pulmonary vascular resistance or on pulmonary arterial input impedance spectrum. CONCLUSIONS: Dobutamine at doses up to 10 microg.kg(-1).min(-1) has no flow-independent effect on the normal or the acutely hypertensive pulmonary circulation. Higher doses may be constricting or dilating depending on preexisting tone.