A new experimental model of ARDS and pulmonary hypertension in the dog

The aim of this study was to establish a stable and reproducible model of pulmonary artery hypertension with concomitant ARDS-like changes of lung function and lung morphology. In eight anesthetized and ventilated dogs, 0.01 ml/kg oleic acid (OA) was given i.v. followed by repetitive injections of 100 microns glass beads (GB) into the right atrium until a mean pulmonary artery pressure of 35-40 mmHg was reached. Mean right ventricular (RVP) and pulmonary artery (PAP) pressures, pulmonary vascular resistance (PVR), lung compliance and resistance, PaO2, intrapulmonary shunt and colloidosmotic pressure (COP) were closely monitored for 150 min. PAP, RVP, and PVR considerably increased subsequent to OA/GB injection, and stabilized at a high level within 70 min, showing only a minimal decrease (PAP, RVP) or no change (PVR) during the following 80 min. A significant decrease of PaO2 and pulmonary compliance as well as an increase of resistance and intrapulmonary shunt were found as early as 30 min after the last embolization and they remained unchanged for 120 min. Reduction of COP suggested transcapillary leakage of macromolecules. Histology revealed an interstitial and intraalveolar edema. We conclude that the combined injection of oleic acid and glass beads provokes microvascular lung injury and results in stable pulmonary artery hypertension with concomitant ARDS-like changes of lung function. Thus, an acute model is provided in the dog allowing for the study of cardiac function in ARDS complicated by pulmonary artery hypertension.     

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)     

Right ventricular diastolic abnormalities in rheumatoid arthritis and its relationship with left ventricular and pulmonary involvement. A tissue Doppler echocardiographic study

Objectives To investigate right ventricular diastolic function in rheumatoid arthritis (RA) and its relationship with left ventricular and pulmonary involvement.Methods Thirty-five RA patients and 30 healthy subjects were submitted to conventional Doppler (CE) and tissue Doppler echocardiography (TDE) to assess left and right systolic and diastolic function and to estimate maximal arterial systolic pulmonary pressure (PAP). To detect pulmonary involvement, pulmonary function tests and high-resolution computed tomography (HRCT) scans were performed in all RA patients.Results An abnormal RV filling, as expressed byan inverted tricuspid (Tr.) E/A ratio, was detected in 12 (34%) of the 35 RA patients and in 2 (7%) of the 30 controls (P<0.004). If compared to CE findings, prevalence of RV diastolic abnormalities were found higher in patients with RA by TDE (RV annulus Em/Am ratio <1 (in 31 (89%) of 35 patients) (P = 0.002). Twenty-two (63%) of 35 patients had abnormal HRCT findings. Pulmonary involvement with pulmonary hypertension (PHT) (36±5 mmHg) was detected in 10 (29%) of 35 RA. In this group, increase of RV annulus and basal Am wave, decrease of Tr. E/A ratio and RV annulus Em/Am ratio were statistically significant compared to RA (12 (34%) of 35) patients with pulmonary involvement who had normal PAP (19±5 mmHg), (P = 0.014, P = 0.006, P = 0.015, P = 0.049, respectively).Conclusions This study points out an impaired RV filling in a significant part of RA patients without overt heart failure. Impairment of RV diastolic function may be a predictor of subclinic myocardial and pulmonary involvement in patients with RA.     

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.     

Inhaled nitric oxide improves hemodynamics in patients with acute pulmonary hypertension after high-risk cardiac surgery

Severe pulmonary hypertension and right-sided circulatory failure (RSCF) represent an increasing cause of morbidity and mortality in patients undergoing high-risk cardiac surgery. Increased pulmonary vascular resistance in the setting of cardiopulmonary bypass (CPB) may further lead to decrease blood flow across the pulmonary vascular bed; thereby decreasing left ventricular filling and cardiac output. Current management techniques for RSCF include both nonspecific vasodilator and inotropic agents (often limited by systemic hypotension) and the placement of right ventricular assist devices (associated with increased perioperative morbidity). Inhaled nitric oxide (NOi) represents a novel, specific pulmonary vasodilator that has been proven efficacious in these clinical settings. We evaluated 34 patients in 38 operations who underwent cardiac surgery at Columbia Presbyterian Medical Center, and who received NOi (20 ppm) through a modified ventilatory circuit for hemodynamically significant elevations in pulmonary vascular resistance. Nine patients underwent cardiac transplantation, three patients bilateral lung transplantation, 16 patients left ventricular assist device placement and 10 patients routine cardiac surgery. Patients receiving NOi exhibited substantial reductions in mean pulmonary artery pressure (mPAP) (34.6 +/- 2.0 to 26.0 +/- 1.7 mmHg, p < 0.0001), with improvements in systemic hemodynamics, mean arterial pressure (68 +/- 3.1 to 75.9 +/- 2.0 mmHg, p = 0.006). In five cases, patients could not be weaned from CPB until NOi was administered. Patients were maintained on NOi from 6 to 240 h postoperatively (median duration 36 h). Inhaled NO induces substantial reductions in mPAP and increases in both cardiac index and systemic blood pressure in patients displaying elevated pulmonary hemodynamics after high-risk cardiac surgery. NO is, therefore, a useful adjunct in these patients in whom acute pulmonary hypertension threatens right ventricular function and hemodynamic stability.     

Mental stress increases right heart afterload in severe pulmonary hypertension

Little is known about mental stress effects on the pulmonary circulation in health and disease. The current study was conducted to investigate whether pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) would further increase during standardized mental stress testing in patients with severe pulmonary hypertension. The study was a prospective analysis of seven patients (average age: 40 years, range from 21 to 56 years) with severe pulmonary hypertension (primary: n=4, secondary forms: n=3; resting mean pulmonary artery pressure ranged between 48 and 65 mmHg). Right heart catheterization for the determination of PAP, pulmonary capillary wedge pressure (PCW) and cardiac output (CO) was clinically indicated (diagnostic work‐up, acute drug testing). Patients accomplished a standardized 10 min mental stress test (computer based, adaptive complex reaction‐time task). Pulmonary haemodynamics during stress were compared to resting baseline. During mental stress mean PAP (±SEM) increased by 9·4 ± 2·1 mmHg (P<0·005). Pulmonary vascular resistance increased by 149 ± 25 dyne s cm^–5 (P<0·001). Stroke volume decreased by 6·6 ± 2·2 ml (P<0·03). The data show that moderate mental stress increases right heart afterload in patients with severe pulmonary hypertension owing to elevation of PVR.     

Pulmonary hypertension complicating portal hypertension: portopulmonary hypertension]

Portopulmonary hypertension is a condition with a poor prognosis, which is defined as precapillary pulmonary hypertension complicating portal hypertension mainly due to cirrhosis of various etiologies. A mean pulmonary arterial pressure greater than 25 mmHg at rest with a pulmonary capillary wedge pressure less than 15 mmHg and a pulmonary vascular resistance greater than 120 dynes.sec.cm-5, in the setting of the presence of portosystemic shunting has been proposed as hemodynamic criteria for portopulmonary hypertension. Prevalence of pulmonary hypertension ascertained by right cardiac catheterization was 2% among patients with cirrhosis, and reached to 4% particularly among candidates for liver transplantation. Hyperdynamic systemic circulation seen commonly in patients with cirrhosis appeared to be normalized by complication of pulmonary hypertension with a contraction of circulating plasma volume. Long term treatment by epoprostenol administration or nitric oxide inhalation could induce a gradual decline in pulmonary arterial pressure in patients with poor response to acute vasodilator administration.     

Hemodynamics of Idiopathic Paroxysmal Atrial Fibrillation

The hemodynamics of induced atrial fibrillation (AF) was investigated in 15 patients (ages 58 ± 11 years) with paroxysmal AF presenting without organic heart disease or hypertension. A hemodynamic study was performed both during sinus rhythm and after the induction of AF. The mean heart rate increased from 73 ± 11 to 128 ± 18 beats/min (P < 0.001) after AF. Systolic and mean aortic pressures did not significantly change, and diastolic aortic pressure increased (78 ± 11 vs 89 ± 12 mmHg, P < 0.01). Left ventricular enddiastolic pressure decreased during AF (9 ± 3 vs 6 ± 2.6 mmHg, P < 0.005), whereas mean pulmonary wedge pressure increased (8 ± 2 vs 12 ± 4 mmHg, P < 0.001). Systolic pulmonary arterial pressure did not show significant variations, and there was a slight but statistically significant increase in the diastolic and mean pulmonary arterial pressures (P < 0.01). The right ventricular end-diastolic pressure decreased during AF (5.6 ± 2 vs 3.8 ± 2 mmHg, P < 0.01 j, whereas mean right atrial pressure showed a trend toward an increase. Stroke volume markedly decreased (P < 0.001) while the cardiac index did not significantly change. Systemic vascular resistance, pulmonary arteriolar resistance, and the arteriovenous O₂ difference showed no significant variations after the induction of AF. These results suggest that in subjects without organic heart disease, paroxysmal AF is well tolerated hemodynamicaily, and the rise in the atrial pressures during AF is not related to an increase in the ventricular end-diastolic pressure.     

Optional active compliance chamber performance in a pulmonary artery-pulmonary artery configured paracorporeal artificial lung

INTRODUCTION: Our group has developed a paracorporeal artificial lung (PAL) attached in a pulmonary artery (PA) to PA in series configuration to address profound respiratory failure and serve as a bridge to transplant and/or recovery. We recently designed, developed and converted our passive pre-PAL compliance chamber to an active, synchronized, counterpulsating assist device to relieve right heart strain and offset increased work placed on the right ventricle when the PAL is attached. In this study, we evaluated the safety and performance of both a valved and non-valved optional active compliance chamber (OACC) in a PA-PA PAL for right heart assistance in normal adult sheep. METHODS: Eleven sheep (30-50 kg) were divided into non-valved OACC (n = 6) and valved (n = 5) OACC groups. To mimic pulmonary hypertension, a C-clamp was placed distal to the OACC-PAL and occluded until a 20% decrease in cardiac output (CO) was achieved. The OACC was activated, and right ventricular pressure (RVP), pulmonary artery pressure (PAP), mean arterial pressure (MAP) and CO were recorded. RESULTS: All eleven animals tolerated the implantation of the OACC PAL. Activation of the OACC resulted in a significant increase in CO. Systolic and diastolic right ventricular pressure decreased in both groups. Lastly, counterpulsation increased the mean PAP in all animals and peak PAP reached 89 mmHg. Despite providing right heart assistance, synchronizing the counterpulsation was technically difficult, and the high peak PA pressures resulted in anastomotic bleeding in all animals and anastomotic breakdown in 4/11 animals. CONCLUSIONS: An OACC PAL perfused by the right ventricle applied in series with the pulmonary circulation reduces ventricular load and improves cardiac efficiency. These preliminary data suggest the potential of an artificial lung in unloading the strained right ventricle and acting as a bridge to transplantation. The augmented peak PA pressures, resulting in bleeding and anastomotic breakdown, and complexity in synchronizing the cardiac cycle with the pulsations of the augmented OACC, compromise this configuration.     

Pulmonary and systemic haemodynamic disorders in the adult respiratory distress syndrome

We repeatedly assessed pulmonary and systemic haemodynamics in 40 adult patients undergoing therapy for severe acute respiratory failure of diverse causes (ARDS). Initial measurements were performed just before admission to our Intensive Care Unit (first haemodynamic evaluation) and were repeated during the course of illness, after correcting hypoxemia, hypercapnia and acidosis by mechanical ventilation with high FiO₂ and positive end expiratory pressure, or by extracorporeal membrane oxygenation. In some patients pulmonary blood flow (PBF) was increased by dopamine infusion or reduced by partial veno arterial bypass.First haemodynamic evaluation permitted us to individualize four systemic haemodynamic patterns in the early stage of ARDS; hyperkinetic state (17 cases), hypovolemia (12 cases), myocardial failure (4 cases) or over-perfusion (6 cases).Our measurements pointed out that pulmonary hypertension is a usual finding in ARDS (mean pulmonary artery pressure: 26±7 mmHg for PBF=1–2 1/min/sq.meter); 25±6 mmHg for PBF=2–3 1/min/sq.meter; 26±7 mmHg for PBF=3–4 1/min/sq.meter) with a high pulmonary vascular resistance (PVR=14±3 mmHg/1 for PBF=1–2 1/min/sq.meter; 8±3 mmHg/1 for pBF=2–3 1/min/sq.meter; 5±2 mmHg/1 for PBF=3–4 1/min/sq.meter); we found also that pulmonary hypertension and pulmonary vascular resistance increased progressivly in patients who died.Pulmonary hypertension in ARDS has two haemodynamic consequences:1° It causes an elevated afterload for the right ventricle with an excessive right ventricular stroke-work index wich can produce right heart failure.2° It is probably in part responsible for an abnormally low systemic arterial pressure (47±16 mmHg for PBF=1–2 1/min/sq.meter; 54±11 mmHg for PBF=2–3 1/min./sq.meter; 64±17 mmHg for PBF=3–4 1/min/sq.meter) and a low systemic arterial resistance (24±9 mmHg/1 for PBF=1–2 1/min.sq.meter; 19±5 mmHg/1 for PBF=2–3 1/min/sq.meter; 17±5 mmHg/1 for PBF=3–4 1/min/sq.meter) observed in our patients with ARDS.The major therapeutic goal of respiratory intensive therapy in severe acute respiratory failure (ARF) caused by altered permeability oedema (APE) is to control the arterial hypoxemia that results from a high intrapulmonary shunt. In addition to respiratory therapy, careful attention must be given to the recognition and management of systemic haemodynamic disturbances complicating the early state of A.P.E.: such disorders as a hyperkinetic state, myocardial failure, hypovolaemia or overperfusion can enhance hypoxemia and myocardial failure or hypovolaemia may be worsened by the use of mechanical ventilation with positive end-expiratory pressure (PEEP). Moreover during the course of ARF with the development of progressive pulmonary fibrosis the alteration in the pulmonary arterial tree produces a high right ventricular after-load with the risk of acute Cor pulmonale.This study was undertaken to describe the early haemodynamic disorders coexisting with APE and to assess pulmonary and systemic haemodynamics during the course of ARF [managed with mechanical ventilation and PEEP, and in some cases with extracorporeal membrane oxygenation (ECMO)].     

Efficiency of prostacyclin in the treatment of protamine-mediated right ventricular failure and acute pulmonary hypertension

Protamine is used after cardiopulmonary bypass was stopped in order to reverse the anticoagulant effects of heparin administered during open-heart operations. Adverse hemodynamic responses to protamine are common, ranging from minor perturbations to cardiovascular collapse. The aim of the present study was to investigate whether a prostacyclin is effective in the treatment of protamine-mediated acute pulmonary hypertension and right ventricular failure in the perioperative period of isolated coronary artery bypass grafting (CABG) operations. In sixty-eight (1.78%) of 3800 patients who underwent isolated CABG, acute pulmonary hypertension and right ventricular failure developed during or following the protamine infusion. These 68 patients were included in the study and were randomized into two groups. Thirty-eight of the patients received prostaglandin I(2) (PGI(2)), norepinephrine and dopamine (PGI(2) group), whereas 30 patients received nitroglycerin, norepinephrine and dopamine (control group). Hemodynamic data were recorded before and after the above drug combinations. The mean value of left ventricle ejection fraction significantly increased (p < 0.05) and mean values of central venous pressure, pulmonary artery systolic and diastolic pressure, pulmonary capillary wedge pressure and pulmonary vascular resistance significantly decreased (p < 0.05) in the PGI(2) group. The mean value of pulmonary capillary wedge pressure significantly decreased (p < 0.05) and the mean value of central venous pressure significantly increased (p < 0.05) in the control group. In conclusion, prostacyclin (PGI(2)) is effective in the treatment of protamine-mediated acute pulmonary hypertension and right ventricular failure in the perioperative period in isolated CABG operations. This finding may be an important contribution to the treatment of severe protamine complications during open-heart operations.     

Dilation of the coronary sinus on echocardiogram: prevalence and significance in patients with chronic pulmonary hypertension.

BACKGROUND: Although rarely seen in healthy patients, the coronary sinus (CS) is often visualized on echocardiography in patients with right-sided heart disease. However, the prevalence of this finding and its relation to right-sided heart structure and pressure remains undefined. METHODS: We examined the transthoracic echocardiograms of 43 consecutive patients referred for the evaluation of pulmonary hypertension (26 men, 17 women) with a mean age of 53 +/- 15 years (range 21 to 82 years). Structural abnormalities of the tricuspid valve were absent. All patients underwent right heart catheterization within 48 hours of their echocardiogram, which revealed the following pressures: mean pulmonary artery (50 mm Hg, range 31 to 84 mm Hg) and right atrial (RA) (mean 10, range 1 to 24 mm Hg). Echocardiograms were analyzed for CS size (identified as the smallest diameter of a circular structure in the left atrioventricular groove in the parasternal long-axis view), as well as RA and right ventricular (RV) sizes. The presence and severity (grades 1 through 3) of tricuspid regurgitation (TR) were also recorded. RESULTS: The CS was visualized in 35 (81%) of 43 patients, and measurements ranged from 0.4 to 1.6 cm (mean 0.8 cm). No difference in RA size, RV size, TR grade, RA pressure (RAP), RV pressure (RVP), mean pulmonary artery pressure (PAP), or pulmonary vascular resistance (PVR) was observed between patients with a visualized and nonvisualized CS. Coronary sinus size correlated significantly with RA size (r = 0.60, P <.001) and pressure (r = 0.59, P <.001), but not with RV size, degree of TR, RVP, PAP, or PVR. Nineteen of 35 patients with a visualized CS underwent pulmonary artery thromboendarterectomy (PTE), and their CS size and RAP were unchanged (0.8 cm and 12 mm Hg, respectively, preand post-PTE; both P = NS [not significant]), though a decrease was observed in other measurements: RA size (4.2 versus 4.8 cm, P =.02), RV size (4.2 versus 5.1 cm, P =.0004), mean PAP (37 versus 72 mm Hg, P <.0001), and PVR (230 versus 899 mm Hg, P <.0001). CONCLUSIONS: Coronary sinus dilation was observed in 81% of a selected group of patients with pulmonary hypertension in the absence of structural disease of the tricuspid valve. Coronary sinus dilation is related to RAP and RA size, but not to RV size, degree of TR, RVP, PA pressure, or PVR. Once dilated, CS size does not change shortly after decreases of RA size, RV size, or PA pressure produced by PTE.     

Dyspnoea and diffuse pulmonary nodules in a patient with pulmonary veno-occlusive disease: a case report and literature review

Pulmonary veno-occlusive disease (PVOD) is a rare type of pulmonary hypertension characterized by capillary damage or arterial pulmonary hypertension. Early lung transplantation is the only effective treatment for PVOD because of the lack of specificity in its clinical manifestations and its rapid progression and poor prognosis. A 28-year-old woman presented with exertional dyspnoea. A chest computed tomography scan revealed diffuse centrilobular ground glass opacities in both lungs, a ratio of the transverse diameter of the main pulmonary trunk to the ascending aorta of >1, and enlargement of the right ventricle and right atrium. A right atrial floating catheter test showed right ventricular pressure of 82/0/4 mmHg, mean pulmonary artery pressure of 83/34/53 mmHg, and pulmonary artery wedge pressure of 15/8/12 mmHg. A mutation was found in the eukaryotic translation initiation factor 2 alpha kinase 4 (EIF2AK4) gene. Thus, the patient was diagnosed with PVOD and subsequently given standard bosentan treatment (62.5 mg twice a day). However, after 6 months of follow-up, there was no significant improvement in the pulmonary artery pressure or activity tolerance (6-minute walking test). Therefore, cardiopulmonary transplantation was performed. Early diagnosis and timely treatment of PVOD may improve the patient’s prognosis.     

右心室流出道多普勒血流频谱和肺毛嵌压对老年肺心病的临床诊断价值

为了评价脉冲多普勒记录右心室流出道（ＲＶＯＴ）及左室流入道（ＬＶＩＴ）血流频谱以检测肺动脉压（ＰＡＰ）和肺毛嵌压（ＰＣＷＰ）对老年肺心病的临床意义。研究老年肺心病（ＣＰ）２１例、老年慢性支气管炎（ＣＢ）２２例、健康老人（Ｈ）１５名。结果和结论：１）在ＲＶＯＴ比在肺动脉主干内记录血流图容易成功，在ＬＶＩＴ测定左室等容舒张时间比心机图容易；２）ＲＶＯＴ血流频谱可将ＣＰ与ＣＢ及Ｈ区别开来（Ｐ＜０．０１）。ＣＰ的ＲＶＯＴ血流图的特点是，加速时间缩短，＜１００ｍｓ；右心室收缩时间间期异常，ＲＰＥＰ／ＲＶＥＴ＞０．４；由血流曲线计算的肺动脉压及即血管总阻力增高；３）有气短和肺湿性罗音，如ＰＣＷＰ不高，则不支持左心功能不全或舒张型心力衰竭；４）ＣＰ患者的血浆心钠素（ＡＮＰ）显著升高。这反映肺动脉压和右心房压力升高；５）本文ＲＶＯＴ血流图诊断ＣＰ的敏感性为９０．５％，特异性９４．６％。     

Continuous inhalation of nitric oxide protects against development of pulmonary hypertension in chronically hypoxic rats.

Exposure to hypoxia and subsequent development of pulmonary hypertension is associated with an impairment of the nitric oxide (NO) mediated response to endothelium-dependent vasodilators. Inhaled NO may reach resistive pulmonary vessels through an abluminal route. The aim of this study was to investigate if continuous inhalation of NO would attenuate the development of pulmonary hypertension in rats exposed to chronic hypoxia. In conscious rats previously exposed to 10% O2 for 3 wk, short-term inhalation of NO caused a dose-dependent decrease in pulmonary artery pressure (PAP) from 44 +/- 1 to 32 +/- 1 mmHg at 40 ppm with no changes in systemic arterial pressure, cardiac output, or heart rate. In normoxic rats, acute NO inhalation did not cause changes in PAP. In rats simultaneously exposed to 10% O2 and 10 ppm NO during 2 wk, right ventricular hypertrophy was less severe (P < 0.01), and the degree of muscularization of pulmonary vessels at both alveolar duct and alveolar wall levels was lower (P < 0.01) than in rats exposed to hypoxia alone. Tolerance to the pulmonary vasodilator effect of NO did not develop after prolonged inhalation. Brief discontinuation of NO after 2 wk of hypoxia plus NO caused a rapid increase in PAP. These data demonstrate that prolonged inhalation of low concentrations of NO induces sustained pulmonary vasodilation and reduces pulmonary vascular remodeling in response to chronic hypoxia.     

PAC-1、CD62P检测在慢性阻塞性肺疾病患者防治中的应用价值

目的探讨慢性阻塞性肺疾病(COPD)患者PAC-1、CD62P水平在肺心病发生发展过程中的意义。方法病例来自江苏省苏北人民医院呼吸科确诊的COPD患者60例,按有无肺心病分为肺心病组30例,单纯COPD组30例,另设20名健康体检者为对照组。应用流式细胞术检测全血活化血小板标记物PAC-1、CD62P的水平,以及与肺动脉压、血氧分压关系的分析。结果单纯COPD组,肺心病组PAC-1、CD62P表达水平均高于正常对照组(P0.01),肺心病组PAC-1C、D62P表达水平又高于单纯COPD组(P0.01)。PAC-1、CD62P的表达水平重度肺动脉高压组(45 mmHg)轻度肺动脉高压组(45mmHg)(P0.01)。PAC-1、CD62P的表达水平重度缺氧组(60 mmHg)轻度缺氧组(60 mmHg)(P0.01)。结论 COPD患者尤为合并肺心病患者存在血小板活化,PAC-1、CD62P可作为判断病情严重性及抗血小板药物治疗的依据。     

超声心动图在窒患儿和早产儿肺动脉高压治疗中的价值

目的 探讨超声心动图在窒息儿和早产儿肺动脉高压治疗中的诊断价值.方法 选取超声心动图首诊为肺动脉高压的窒息儿和早产儿175例,轻度肺动脉高压组60例,中度组97例,重度组18例,排除先天性心脏病诊断,治疗后复查超声心电图,对比分析治疗前后的肺动脉压力及右心系统参数变化.结果 各组肺动脉高压患儿治疗后肺动脉压力均低于治疗前（P〈0.01）,其中重度肺动脉高压组下降明显,治疗前后对比为（72.89±2.61） mmHg vs （35.2±2.98） mmHg,各组肺动脉收缩压均降至正常范围（〈40 mmHg）,降压效果显著,主肺动脉内径及右心室前后径较治疗前减小（P〈0.01）,其中中度肺动脉高压组减小明显,主肺动脉内径治疗前后的对比为（8.57±0.52） mm vs （6.86±0.60） mm,右心室前后径治疗前后对比为（9.38±0.57） mm vs （7.40±0.50） mm,临床治疗效果满意,各组间差异有统计学意义.结论 超声心动图能够对窒息儿和早产儿治疗前后的肺动脉压力进行客观评价,为临床早期治疗、防止肺动脉高压的进一步发展及改善预后提供指导.     

Neither nitroglycerin nor nitroprusside selectively reduces sepsis-induced pulmonary hypertension in piglets

No therapeutic agent consistently decreases pulmonary arterial pressure (PAP) more than aortic pressure in neonates with persistent pulmonary hypertension of the newborn. We have investigated whether nitroglycerin (NG) or nitroprusside (NP) selectively decreases PAP in an animal model of sepsis-induced pulmonary hypertension. Piglets were anesthetized, intubated, and ventilated. Pulmonary hypertension was induced by an iv infusion of group B Streptococci. Piglets were then divided into three groups with group B Streptococci infusion ongoing. Neither PAP nor the pulmonary vascular resistance index was decreased significantly by either NP or NG. NP decreased significantly both mean aortic pressure and the systemic vascular resistance index. Cardiac index decreased significantly during both NG and placebo infusion. These data suggest that neither NP nor NG is likely to be beneficial in sepsis-induced pulmonary hypertension in newborns.     

Decrease in pulmonary artery pressure after administration of thoracic epidural anesthesia in a patient with Marfan syndrome awaiting aortic valve replacement procedure

Thoracic epidural anesthesia is an adjunct to general anesthesia in cardiac surgery. Decrease in heart rate and blood pressure are frequently seen beneficial effects. There are several other hemodynamic effects of thoracic epidural anesthesia such as decrease in systemic vascular resistance, cardiac index, left ventricular stroke work index among others. However, the effect of thoracic epidural anesthesia on pulmonary artery pressure (PAP) has not been studied extensively in humans. Thoracic epidural anes-thesia decreased pulmonary artery pressure in experimen-tally induced pulmonary hypertension in animals. The mechanisms involved in such reduction are ill understood. We describe in this report, a significant reduction in PAP in a patient with Marfan’s syndrome scheduled to under-go aortic valve replacement. The possible mechanisms of decrease in pulmonary artery pressure in the described case are, decrease in the venous return to the heart, decrease in the systemic vascular resistance, decrease in the right ventric-ular function and finally, improvement in myocardial contraction secondary to all the above. The possibility of Marfan’s syndrome contributing to the decrease in PAP appears remote. The authors present this case to generate discussion about the possible mechanisms involved in thoracic epidural anesthesia producing beneficial effects in patients with secondary pulmonary hypertension. Thoracic epidural anesthesia appears to decrease pulmonary artery pressure by a combination of several mechanisms, some unknown to us. This occurrence, if studied and understood well could be put to clinical use in pulmonary hypertensives.