Measurement Of Pulmonary Artery Pressure Research Articles

Management of pulmonary hypertension: physiological and pharmacological considerations for anesthesiologists.

For decades the pulmonary circulation was not considered as important as the systemic (“greater”) circulation. However, pulmonary hypertension can arise because of many diseases of the heart and lung. Therefore, increasing efforts in research have been undertaken leading to a profound increase in un

Significance of pulmonary artery pressure in emphysema patients with mild-to-moderate hypoxemia

The guidelines of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) do not recommend the measurement of pulmonary artery pressure in patients with chronic obstructive pulmonary disease (COPD). This is on the basis that the mean pulmonary artery pressure (mPAP) does not provide more clinical information than measurement of the oxygen tension in arterial blood ( PaO 2). The mPAP correlates well with PaO 2 in emphysema patients with severe hypoxemia ( PaO 2⩽7.3 kPa (55 mmHg)). However, the occurrence and significance of mPAP is unclear in patients without severe hypoxemia ( PaO 2>7.3 kPa (55 mmHg)). In order to evaluate the usefulness of measurement of mPAP in emphysema patients without severe hypoxemia, we performed right heart catheterization and investigated the pulmonary hemodynamics of 53 patients without severe hypoxemia. In addition, we identified long-term prognostic factors with a mean follow-up term of 77 months after right heart catheterization. Seventeen of 27 patients with mild-to-moderate hypoxemia exhibited pulmonary hypertension (mPAP⩾2.7 kPa (20 mmHg)) and the classification according to severity in GOLD exhibited a greater correlation to mPAP than PaO 2. Moreover, only mPAP was found to be a significant prognostic factor according to multivariate proportional hazards analysis ( P=0.01). We conclude that mPAP is more informative about the severity of emphysema than PaO 2 in patients with mild-to-moderate hypoxemia.

Degree of pulmonary hypertension predicts the severity of functional tricuspid regurgitation: New findings based on invasive measurements of pulmonary artery pressure

Degree of pulmonary hypertension predicts the severity of functional tricuspid regurgitation: New findings based on invasive measurements of pulmonary artery pressure

Relation of pulmonary venous wedge pressures to pulmonary artery pressures in patients with single ventricle physiology

Accurate assessment of pulmonary artery pressures (PAP) is important in determining the indication for Fontan procedure in patients with single ventricle physiology. However, it is sometimes difficult to measure PAP directly. Pulmonary vein wedge pressure (PVWP) may be used as an alternative to PAP in such cases. Several studies have demonstrated that PVWP correlates with PAP 1 Rao S. Sissman N.J. The relationship of pulmonary venous wedge to pulmonary arterial pressures. Circulation. 1971; 44: 565-574 Crossref PubMed Scopus (13) Google Scholar , 2 Hawker R.E. Celermajor J.M. Comparison of pulmonary artery and pulmonary venous pressures in congenital heart disease. Br Heart J. 1973; 35: 386-391 Crossref PubMed Google Scholar , 3 Waldman J.D. LaCorte M. Dick M. John S.A. Miettinen O.S. LaFarge C.G. The pulmonary venous wedge pressure in pulmonary artery hypertension. Cathet Cardiovasc Diagn. 1977; 3: 231-239 Crossref PubMed Scopus (8) Google Scholar , 4 Chern M.S. Yeh S.J. Lin F.C. Wu D. Hung J.S. Estimation of pulmonary artery pressure from pulmonary vein wedge pressure. Cathet Cardiovasc Diagn. 1994; 31: 277-282 Crossref PubMed Scopus (6) Google Scholar since a technique of catheterization for obtaining PVWP was introduced by Hellems et al. 5 Hellems H.K. Haynes F.W. Dexter L. Kinney T.D. Pulmonary capillary pressure in animals estimated by venous and arterial catheterization. Am J Physiol. 1948; 155: 98-105 PubMed Google Scholar However, these studies were based on patients with simple heart disease, and little is known about patients with complex heart disease. Accurate measurements of PAP and pulmonary vascular resistance (Rp) are critical in the selection of patients with complex heart disease for the Fontan procedure. If PVWP is used as an alternative to PAP, a small difference between PAP and PVWP could produce a big difference in the Rp, resulting in misinterpretation in determining the indication for the Fontan procedure. Thus, it is necessary to know not only the correlation between PVWP and PAP, but also to know how closely PVWP estimates PAP in patients with single ventricle physiology. The purpose of this report was to evaluate how accurately PVWP estimates PAP and to assess the relation focusing on the clinical use of PVWP as an alternative to PAP in patients who are being evaluated as Fontan candidates.

The role of tissue reperfusion in the reexpansion injury of the lungs

The aim was to discuss the balance between free radical damage and body defense mechanisms that occurred in reexpansed pulmonary tissue and to evaluate the relationship between the changes in the pulmonary circulation and the mentioned balance. Twenty male Wistar Albino rats were used for these study results. Pneumothorax was created in the left hemithorax by percutaneous route in all the rats. After 7 days, the first group (n = 10) had a sternotomy under ketamine anesthesia. Following invasive measurement of pulmonary artery pressure, tissue samples were obtained from the lower lobes of the right and left lungs before reexpansion occurred. Tracheotomies were opened in the second group (n = 10) with a 16 gauge cannula. Following sternotomy, invasive mean pulmonary artery pressure measurements were obtained by the support of non-invasive cardiac monitorization. The lungs were aerated with 4 cmH(2)O oxygen and fixed volume support and 1 h of reexpansion was obtained. Invasive mean pulmonary artery pressure measurements were repeated after reexpansion and tissue samples were obtained from the lower lobes of left and right lungs. Nitric oxide (NO), malondialdehyde (MDA) and superoxide dismutase (SOD) levels were measured in tissue samples, surfactant staining and light microscopic evaluations were performed. At the end of the reexpansion, there was a decrease in mean pulmonary artery pressure (P < 0.01), MDA (P < 0.01) and SOD (P < 0.05) levels and an increase in NO (P < 0.05) levels. Under the light microscopic examination, in the samples that were provided with reexpansion, the alveolo-capillary membrane was thickened due to increasing edema, increase in the number of lymphocytes and return of the neutrophil leukocytes to the area. There was no significant difference between the groups in terms of surfactant staining. The tissue reperfusion that is achieved with the restoration of blood flow during the reexpansion of collapsed lungs, can be the initial pathology in the chain of events that result in reexpansion injury.

Adenosine A2A receptor activation decreases reperfusion injury associated with high-flow reperfusion

Introduction: High pulmonary artery flow rates can result in severe reperfusion injury after lung transplantation. Our hypothesis was that selective activation of the adenosine A2A receptor with a highly specific analog (ATL-146e) would inhibit leukocyte activation and decrease reperfusion injury after high-flow reperfusion. Methods: Using our isolated, ventilated, blood-perfused rabbit lung model, all groups (n = 8 per group) underwent lung harvest, 4 hours of cold storage, and blood reperfusion for 30 minutes. Measurements of pulmonary artery pressure (in millimeters of mercury), arterial oxygenation (in millimeters of mercury), myeloperoxidase, peak inspiratory pressure, and wet/dry weight ratio were obtained. Groups 1 (high flow) and 2 (high flow ATL-146e) underwent reperfusion at 120 mL/min for 30 minutes. Groups 3 (controlled high flow) and 4 (controlled high flow ATL-146e) underwent controlled reperfusion with an initial reperfusion of 60 mL/min for the first 5 minutes, followed by a rate of 120 mL/min for 25 minutes. During reperfusion, groups 2 and 4 received ATL-146e at 4 μg · kg−1 · min−1. Results: ATL-146e significantly improved lung physiologic measurements under both high-flow (group 1 vs group 2) and controlled high-flow (group 3 vs group 4) conditions after 30 minutes. Conclusions: The adenosine A2A receptor analogue ATL-146e significantly decreases the severity of reperfusion injury in the setting of both high-flow and controlled high-flow reperfusion.J Thorac Cardiovasc Surg 2002;124:973-8

Defects in caveolin-1 cause dilated cardiomyopathy and pulmonary hypertension in knockout mice.

Caveolins are important components of caveolae, which have been implicated in vesicular trafficking and signal transduction. To investigate the in vivo significance of Caveolins in mammals, we generated mice deficient in the caveolin-1 (cav-1) gene and have shown that, in the absence of Cav-1, no caveolae structures were observed in several nonmuscle cell types. Although cav-1(-/-) mice are viable, histological examination and echocardiography identified a spectrum of characteristics of dilated cardiomyopathy in the left ventricular chamber of the cav-1-deficient hearts, including an enlarged ventricular chamber diameter, thin posterior wall, and decreased contractility. These animals also have marked right ventricular hypertrophy, suggesting a chronic increase in pulmonary artery pressure. Direct measurement of pulmonary artery pressure and histological analysis revealed that the cav-1(-/-) mice exhibit pulmonary hypertension, which may contribute to the right ventricle hypertrophy. In addition, the loss of Cav-1 leads to a dramatic increase in systemic NO levels. Our studies provided in vivo evidence that cav-1 is essential for the control of systemic NO levels and normal cardiopulmonary function.

Pulmonary Artery Rupture After Attempted Removal of a Pulmonary Artery Catheter

Pulmonary Artery Rupture After Attempted Removal of a Pulmonary Artery Catheter

Pulmonary perfusion patterns and pulmonary arterial pressure.

To use artificial intelligence methods to determine whether quantitative parameters describing the perfusion image can be synthesized to make a reasonable estimate of the pulmonary arterial (PA) pressure measured at angiography. Radionuclide perfusion images were obtained in 120 patients with normal chest radiographs who also underwent angiographic PA pressure measurement within 3 days of the radionuclide study. An artificial neural network (ANN) was constructed from several image parameters describing statistical and boundary characteristics of the perfusion images. With use of a leave-one-out cross-validation technique, this method was used to predict the PA systolic pressure in cases on which the ANN had not been trained. A Pearson correlation coefficient was determined between the predicted and measured PA systolic pressures. ANN predictions correlated with measured pulmonary systolic pressures (r = 0.846, P <.001). The accuracy of the predictions was not influenced by the presence of pulmonary embolism. None of the 51 patients with predicted PA pressures of less than 29 mm Hg had pulmonary hypertension at angiography. All 13 patients with predicted PA pressures greater than 48 mm Hg had pulmonary hypertension at angiography. Meaningful information regarding PA pressure can be derived from noninvasive radionuclide perfusion scanning. The use of image analysis in concert with artificial intelligence methods helps to reveal physiologic information not readily apparent at visual image inspection.

Serial noninvasive assessment of progressive pulmonary hypertension in a rat model

Current methods used to investigate pulmonary hypertension in rat models of the disease allow for only one to two measurements of pulmonary artery (PA) pressure in the life of a rat. We investigated whether transthoracic echocardiography can be used to assess the progression of pulmonary hypertension in rats at multiple time points. Serial echocardiographic measurements were performed over a 6-wk period on rats injected with monocrotaline (MCT) or placebo. Development of a midsystolic notch in the PA waveform, a decrease in the PA flow acceleration time (PAAT), an increase in right ventricular (RV) free-wall thickness, and the development of tricuspid regurgitation (TR) were observed as pulmonary hypertension developed. Changes in the PA waveform and PAAT began in week 3 of disease development as the PA systolic pressure (PASP) reached 25-30 mmHg according to right heart catheterization. The RV free-wall thickness increased significantly by week 5 (PASPs 40-50 mmHg). Development of quantifiable TR occurred in week 6 or at PASPs > 65 mmHg. A linear correlation was found between the PAAT and PASP in the range of 30-65 mmHg and between the RV-right atrial pressure gradient (derived from TR velocity) and PASP at pressures >65 mmHg, which enabled a noninvasive estimate of the PASP over a wide range of pressures based on these parameters. These data indicate that transthoracic echocardiography can be used for monitoring the progress of pulmonary hypertension in a rat model.

How common is severe pulmonary hypertension after pediatric cardiac surgery?

Pulmonary hypertension may result in significant morbidity and mortality after pediatric cardiac surgery. The objective of this study was to determine the incidence and outcome of severe pulmonary hypertension, defined as a ratio of pulmonary to systemic arterial pressure equal to or greater than 1.0, after cardiac surgery in children. Data from all children younger than 18 years who had undergone cardiothoracic surgery from January 1, 1994, to December 31, 1998, were examined. To find children with severe pulmonary hypertension, we reviewed intensive care unit charts from patients who had been monitored with a pulmonary artery catheter after the operation (n = 151), had received mechanical ventilation for more than 4 days after the operation (n = 124), or had died in the operating room or the intensive care unit (n = 22). Intraoperative and postoperative measurements of mean pulmonary arterial pressure and postoperative echocardiographic studies during the first 3 postoperative days were used to select the children. During the study period, 1349 children (including 164 neonates and 511 infants, median age 12 months) underwent cardiac operations with an overall perioperative mortality of 22 patients (1.6%). Twenty-seven children (2%, median age 4.2 months) had severe pulmonary hypertension. Of these, 2 (7.4%) died within 30 days of the operation, and 3 others (11%) died within a year (median follow-up 53 months). Nitric oxide inhalation was used in 5 of the 27 cases, and it probably saved the life of 1 patient, may have helped in 1 case, and had no discernible effect in 3 cases. Severe pulmonary hypertension was most common after correction of complete atrioventricular septal defects (14%, n = 12/85). Thirteen of 131 children with Down syndrome (9.9%) had severe pulmonary hypertension. Severe postoperative pulmonary hypertension occurred after 2% of the cardiac procedures and in most cases was managed successfully with conventional treatment and had a favorable postoperative outcome. The low incidence relative to previous reports may reflect the benefits of early correction and improved intraoperative and postoperative care.

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.

Cardiovascular and subjective evaluations of oxymorphone/diazepam and hydromorphone/diazepam induction in experimentally induced hypovolemic dogs

The purpose of this study was to assess neuroleptanalgesic induction in experimentally induced hypovolemic dogs (removal of 30 mL kg−1 of blood over 30 minutes). Six healthy dogs (17.5–31 kg) were randomly assigned in a crossover design to receive oxymorphone/diazepam (OD) or hydromorphone/diazepam (HD) with at least 3 weeks between trials. Dogs were anesthetized with isoflurane (ISO) in 33% oxygen (+N2O) by mask, maintained using controlled ventilation (CV) with ISO in 100% O2 for instrumentation [tracheal end-tidal gases (Criticare1100), HR, BP, thermodilution CI, CVP, pulmonary artery pressure (PAP), temperature (T) and blood gas measurements]. Normovolemic (NV) values were obtained following this and equilibration of 15 minutes at 1.8% end-tidal ISO (1.5 MAC). The percentage ISO was reduced as hypovolemia was induced and then the dogs were allowed to recover. Measurements were repeated after the dog was walking (HV) – at least 15 minutes after recovery. The dogs received IV oxymorphone 0.05 mg kg followed by diazepam (0.2 mg kg) (OD) or hydromorphone 0.1 mg kg−1 followed by diazepam (0.2 mg kg−1) (HD) and were reassessed, including subjective evaluation for depth. The opioid dose (OpD) was repeated after 5 minutes. A person, blind to the treatment, evaluated depth and ease of intubation (after 5 minutes). Other measurements were taken, endotracheal intubation performed, and 0.9% end-tidal ISO provided with CV. After 15 minutes equilibration, measurements were repeated. Glycopyrrolate (GL) 0.01 mg kg−1 was given IV and the last measurements taken 10 minutes later. Dogs received half of the blood removed + remaining volume × 3 as crystalloid during recovery. Opioid/diazepam effect occurred by 1 minute in all dogs. Intubation would not have been possible in 1/6 (HD, OD) with initial dose. All dogs were intubated after whole opioid dose (3/6 HD and 2/6 OD were more difficult). An anova for repeated measures was performed on changes produced with different interventions over time (e.g. HV–OpD) with significance if p ≤ 0.015. The OpD resulted in a significant change (mean difference ± SE) in HR (HD − 41 ± 10 b.p.m.; OD, 30 ± 12 b.p.m.), diastolic BP (HD − 5 ± 5 mm Hg), pH (HD − 0.10 ± 0; OD − 0.09 ± 0), PaCO2 (HD + 13 ± 0.8 mm Hg, OD + 15 ± 1.5 mm Hg) compared to HV. Transfer of HV dogs to ISO resulted in changed CI (HD − 30 ± 6 mL kg−1 minute−1), BE (HD − 2.5 ± 0.6 mEq L−1; OD − 2.7 ± 0.5 mEq L−1) and T (OD 1.0 ± 0.25 °C) compared to NV. Administration of GL changed HR (HD + 50 ± 9 b.p.m.; OD + 42 ± 13 b.p.m.), systolic BP (HD, −23 ± 5 mm Hg) and SV index (HD, −0.4 mL kg−1 minute−1). The PAP values were difficult to interpret but tended to be lower in OD following HV. The HD and OD provide comparable induction following hypovolemia. The GL reversal of opioid bradycardia provides no advantage in hypovolemic dogs.

Noninvasive monitoring of hemodynamic stress using quantitative near-infrared frequency-domain photon migration spectroscopy.

Hemorrhagic hypovolemia and inotropic agent administration were used to manipulate cardiac output (CO) and oxygen delivery in rabbits to investigate the correlation between noninvasive frequency domain photon migration (FDPM) spectroscopy and invasive hemodynamic monitoring parameters. Frequency-domain photon migration provides quantitative measurements of light absorption and reduced scattering (mu(a) and mu(s)(prime prime or minute), respectively) in tissue. Wavelength dependent mu(a) values were used to calculate in vivo tissue concentration of deoxyhemoglobin [Hb], oxyhemoglobin [HbO(2)], total hemoglobin [TotHb], and water [H(2)O] as well as mixed arterial-venous oxygen saturation (S(t)O(2)) in tissue. FDPM-derived physiologic properties were correlated with invasive measurements of CO and mean pulmonary artery pressure (mPAP), FDPM-derived [TotHb] and S(t) O(2) correlated significantly with hemorrhaged volume (HV), mPAP, and CO. Correlation coefficients for [TotHb] vs HV, mPAP, and CO were -0.77, 0.86, and 0.70, respectively. Correlation coefficients of S(t)O( 2) vs HV, mPAP, and CO were -0.71, 0.55, and 0.61, respectively. Dobutamine induced changes resulted in correlation coefficients between FDPM-derived and invasively measured physiologic parameters that are comparable to those induced by hypovolemia. FDPM spectroscopy is sensitive to changes in mPAP and CO of as little as 15%. These results suggest that FDPM spectroscopy may be used in clinical settings to noninvasively monitor central hemodynamic parameters and to directly assess oxygenation of tissues.

Mechanical Thrombolysis of Venous Thrombosis in an Animal Model with Use of Temporary Caval Filtration

To test the effect of temporary caval filtration on pulmonary emboli when a mechanical thrombolytic device is used to treat venous thrombosis and to test the effects of a modified device on caval patency at 30-day follow-up. In a canine model of iliocaval subacute thrombosis, mechanical thrombolysis was performed with use of an 8-F over-the-wire Arrow-Trerotola Percutaneous Thrombolytic Device (PTD) with a 9-mm (iliac) or 15-mm (inferior vena cava [IVC]) basket. In six procedures, the device was made of nitinol monofilament, and in another six, it was made of braided stainless steel. All procedures were performed with a nitinol expandable sheath (temporary filter) in the suprarenal IVC. Low-molecular-weight heparin was given daily after the procedure. Venography, pulmonary arteriography, measurement of blood gases, and pulmonary artery (PA) pressure measurement were performed before and after the procedure and at 30-day follow-up. Pulmonary arteriograms from the group treated with stainless-steel devices were compared to those from an earlier group of animals in which the identical procedure was performed without caval filtration. The IVC was examined histologically. Thrombolysis was successful in all animals. Rare segmental and subsegmental pulmonary emboli (PE) were seen arteriographically; compared to procedures without filters, there was a significant reduction in PE (P <.002). However, a mild increase in pulmonary artery pressure, decrease in pH, and increase in pCO(2) were observed postprocedurally. At 30-day follow-up (n = 11), IVC patency was preserved in 45% (n = 5) of animals overall. Caval patency was significantly better in animals in which the combination of stainless-steel devices was used (five of six = 83% vs zero with nitinol device; P =.015). Histologically, the stainless-steel device caused little intimal injury and fibrosis-less than that seen with the nitinol device. Temporary filtration reduces, but does not completely eliminate, PE during mechanical thrombolysis. The stainless-steel device results in less intimal injury and better caval patency than the nitinol device.

Usefulness of transcutaneous Doppler jugular venous echo to predict pulmonary hypertension in COPD patients.

Pulmonary hypertension is an important factor that determines the prognosis of chronic obstructive pulmonary disease (COPD) patients. Echocardiography is a noninvasive and useful bedside method for measurement of pulmonary artery pressure. However, this method is sometimes difficult because of the overinflated lungs in COPD patients. This study attempted to estimate pulmonary hypertension in COPD patients using transcutaneous Doppler jugular vein flow velocity recording. The mean pulmonary artery pressure (MPAP) of 64 COPD patients was examined using cardiac catheterization. The right jugular vein flow velocity was measured within 24 h using transcutaneous Doppler echo, after which the ratio of diastolic flow (Df) and systemic flow (Sf) velocity was calculated. Subsequently, the statistical correlation of MPAP and the Df/Sf ratio was examined. MPAP was also measured using standard cardiac echo methods and the results were compared. The Df/Sf velocity ratio showed significant correlation with MPAP in COPD patients (r=0.844, p<0.0001). The sensitivity was 71.4%, and the specificity 95.3% (cut-off ratio= 1.0). Jugular venous Doppler echo could be performed in all patients while other cardiac echo methods could not be performed in all patients. The specificity of the methods used was higher than other cardiac echo methods. Transcutaneous jugular vein flow velocity measurement may be applicable to bedside prediction of pulmonary hypertension in chronic obstructive pulmonary disease patients.

Lung transplant reperfusion injury involves pulmonary macrophages and circulating leukocytes in a biphasic response

Objective: Both donor pulmonary macrophages and recipient circulating leukocytes may be involved in reperfusion injury after lung transplantation. By using the macrophage inhibitor gadolinium chloride and leukocyte filters, we attempted to identify the roles of these two populations of cells in lung transplant reperfusion injury. Methods: With our isolated, ventilated, blood-perfused rabbit lung model, all groups underwent lung harvest followed by 18-hour cold storage and 2-hour blood reperfusion. Measurements of pulmonary artery pressure, lung compliance, and arterial oxygenation were obtained. Group I (n = 8) served as a control. Group II (n = 8) received gadolinium chloride at 14 mg/kg 24 hours before lung harvest. Group III (n = 8) received leukocyte-depleted blood reperfusion by means of a leukocyte filter. Results: The gadolinium chloride group had significantly improved arterial oxygenation and pulmonary artery pressure measurements compared with control subjects and an improved arterial oxygenation compared with the filter group after 30 minutes of reperfusion. After 120 minutes of reperfusion, however, the filter group had significantly improved arterial oxygenation and pulmonary artery pressure measurements compared with the control group and an improved arterial oxygenation compared with the gadolinium chloride group. Conclusions: Lung transplant reperfusion injury occurs in two phases. The early phase is mediated by donor pulmonary macrophages and is followed by a late injury induced by recipient circulating leukocytes. (J Thorac Cardiovasc Surg 2001;121:1069-75)

An initial imaging study on pulmonary artery hypertension secondary to cancerous invasion of central pulmonary artery in lung cancer

To investigate the incidence of pulmonary artery hypertension secondary to cancerous invasion of central pulmonary artery (CICPA) in lung cancer and the diagnostic value of CT on pulmonary artery hypertension. Twenty cases of lung cancer combined with CICPA underwent pulmonary artery pressure measurement through right heart catheterization and CT scanning. CT findings were blindly assessed and were compared with the results of pulmonary artery pressure measurement. Three cases (3/20, 15%) showed mild pulmonary artery hypertension in arteries proximal to CICPA segments, in which CT findings were dilation of the main pulmonary artery and increase of the diameter ratio of the main pulmonary artery to the descending aorta at the same level. CT diagnostic accuracy for pulmonary artery hypertension was 90%(18/20). Pulmonary artery hypertension occurs with low incidence in lung cancer with CICPA. CT is of great value in diagnosing pulmonary artery hypertension in lung cancer with CICPA.

Ischaemic preconditioning before lower limb ischaemia–reperfusion protects against acute lung injury

Abstract Background Ischaemic preconditioning (IPC) of skeletal muscle, by exposing it to repeated brief periods of ischaemia and reperfusion (I-R) before a subsequent longer ischaemic period, protects against local damage on reperfusion. In a large animal model of hindlimb I-R it was hypothesized that hindlimb IPC would attenuate the systemic inflammatory response syndrome and prevent acute lung injury associated with limb reperfusion injury. Methods Anaesthetized ventilated swine (six per group) were used throughout. After midline laparotomy, animals were randomized to the following three groups: bilateral external iliac artery occlusion for 120 min, followed by reperfusion for 180 min (I-R group); IPC (three cycles of 5 min ischaemia, then 5 min reperfusion of both external iliac arteries) followed by bilateral external iliac artery occlusion for 120 min and reperfusion for 180 min (I-R + IPC group); or laparotomy alone (control group). Acute lung injury was assessed by invasive pulmonary artery pressure (PAP) measurement, arterial to alveolar (A-a) oxygen gradient, lung tissue wet: dry weight ratio, and lung myeloperoxidase (MPO) concentration. Results Conclusion Lower limb I-R induces systemic inflammation and acutely impairs oxygen transport associated with lung neutrophil sequestration. IPC attenuates acute pulmonary hypertension, impairment of oxygen transport, oedema and leucosequestration in planned lower limb I-R.

Increased nitric oxide in exhaled air in patients with rheumatic heart disease.

Endogenous production of nitric oxide and its presence in exhaled air was observed in humans. Prior studies have yielded contrasting information about the production of nitric oxide in patients with heart failure. The aim of this study was to measure nitric oxide in the exhaled air of patients with chronic rheumatic heart disease with and without pulmonary hypertension. Seventy-four patients (6 patients had isolated mitral stenosis; 13 patients had combined mitral stenosis and mitral regurgitation; 1 patient had isolated mitral regurgitation; 54 patients had combined mitral and aortic valve disease) and 27 healthy subjects were entered in the study. The nitric oxide concentration in exhaled air was determined with a chemiluminescence analyser. Echocardiography was performed in all patients to assess the severity of the valve disease and for the measurement of pulmonary artery pressure. The level of exhaled nitric oxide was significantly greater in patients with rheumatic heart disease than in controls. The value of nitric oxide concentration in exhaled air was significantly increased in patients with pulmonary hypertension, as compared with patients who had normal pulmonary artery systolic pressure. We found increased nitric oxide in the exhaled air in patients with rheumatic heart disease, especially in those with pulmonary hypertension, compared with healthy patients.