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Biomedical subjects

R Rodriguez-Roisin

Publications and source records attributed to R Rodriguez-Roisin.

At least 19 recordsLinked to original sources

Evaluation of CD30 as a marker for th2 lymphocytes in bronchoalveolar lavage in interstitial lung diseases.

Several studies have been carried out to clarify the relationship between CD30 expression and Th2 lymphocytes, although the results have been controversial. To investigate whether CD30 is a useful marker for Th2 lymphocytes in bronchoalveolar lavage (BAL) in interstitial lung diseases (ILD), we studied six control subjects and 31 patients with ILD (12 with idiopathic pulmonary fibrosis, seven with hypersensitivity pneumonitis, three with chronic eosinophilic pneumonia and nine with sarcoidosis). The levels of interleukin-5 (IL-5) (secreted by Th2 cells), interferon-gamma (IFNgamma) (secreted by Th1 cells) and the expression of CD30 on lymphocytes were determined in BAL fluid. There were no differences in the percentage of CD30+ lymphocytes between controls and patients with ILD (0.8+0.4% vs. 2+/-0.4%). In order to determine the relationship between Th2 cells and CD30 expression, we divided the patients into two groups according to BAL IL-5 levels. Group I consisted of eight patients (three chronic eosinophilic pneumonia, three hypersensitivity pneumonitis, two idiopathic pulmonary fibrosis) with high IL-5 levels (298+/-138 pg ml(-1)). Group II consisted of the remaining 23 ILD patients with normal IL-5 levels (0.9+/-0.6 pg ml(-1)). The percentage of eosinophils in BAL fluid was significantly higher in group I compared with group 11 (34+/-16% vs. 3+/-1%, P < 0.05). A correlation between CD30+ lymphocytes and IL-5 in group 1 was not shown. There were no differences in the number of CD30+ I we found a significant correlation between IL-5 levels and the percentage of eosinophils (r = 0.95, P < 0.0001). Our results suggest that CD30 does not appear to be a useful marker for Th2 lymphocytes in BAL from patients with ILD.

Adult↗

Pulmonary gas exchange response to oxygen breathing in acute lung injury.

The mechanisms and time course of the pulmonary gas exchange response to 100% O(2) breathing in acute respiratory failure needing mechanical ventilation were studied in eight patients with acute lung injury (ALI) (48 +/- 18 yr [mean +/- SD]) and in four patients (66 +/- 2 yr) with chronic obstructive pulmonary disease (COPD). We postulated that, in patients with ALI while breathing 100% O(2), the primary mechanism of hypoxemia, i.e., increased intrapulmonary shunt, would further worsen (increase) as a result of reabsorption atelectasis. Respiratory and inert gases, and systemic and pulmonary hemodynamics were measured at maintenance fraction of inspired oxygen (FI(O(2))-m), at 30 and 60 min while breathing 100% O(2), and then at 30 min of resuming FI(O(2))-m. During 100% O(2) breathing, in patients with ALI, Pa(O(2)) (by 207 and 204 mm Hg; p < 0.01 each), Pa(CO(2)) (by 4 mm Hg each) (p < 0.05 each), and intrapulmonary shunt (from 16 +/- 10% to 22 +/- 11% and 23 +/- 11%) (p < 0.05 each) increased respectively. By contrast, in patients with COPD, Pa(O(2)) (by 387 and 393 mm Hg; p < 0.001 each), Pa(CO(2)) (by 4 and 5 mm Hg) and the dispersion of pulmonary blood flow (log SDQ) (from 1.33 +/- 0.10 to 1.60 +/- 0.20 and 1.80 +/- 0.30 [p < 0.05]) increased, respectively. In patients with ALI, the breathing of 100% O(2) deteriorates intrapulmonary shunt owing to collapse of unstable alveolar units with very low ventilation-perfusion (V A/Q) ratios, as opposed to patients with COPD, in whom only the dispersion of the blood flow distribution is disturbed, suggesting release of hypoxic pulmonary vasoconstriction.

Aged↗

Capnometric recirculation gas tonometry and weaning from mechanical ventilation.

The aim of this study was to describe changes in regional intramucosal PCO(2) (Pr(CO(2)) measured with capnometric recirculation gas tonometry [CRGT]) in patients with acute respiratory failure, who proceed from mechanical ventilation to weaning. In addition, we compared the predictive power for the weaning outcome of CRGT measurements obtained during mechanical ventilation to the frequency/ tidal volume (f/VT) ratio. A total of 24 patients (31 weaning trials) were included in the study, but four of the 24 patients (17%) were excluded because of extubation failure. Of the remaining 27 weaning trials in 20 patients, 12 (44%) were unsuccessful. Changes observed in patients with weaning failure (increase in Pr(CO(2)) from 60.4 +/- 15.0 mm Hg in mechanical ventilation to 67.4 +/- 21.0 mm Hg, in weaning) were significantly different (p = 0.046) from those observed in patients with weaning success (fall in Pr(CO(2)) from 61.5 +/- 15.0 mm Hg in mechanical ventilation to 56.3 +/- 16.7 mm Hg in weaning). However, absolute values of Pr(CO(2)) were not significantly different between patients with weaning success and failure, neither during mechanical ventilation (success, 61.5 +/- 15.0 versus failure, 60.4 +/- 15.0 mm Hg, p = 0.848) nor during weaning (success, 56.3 +/- 16.7 versus failure, 67.4 +/- 21.0 mm Hg, p = 0.135). The best single predictor for weaning outcome was the f/VT ratio measured early during weaning (area under the curve: 0.844 +/- 0.081; adjusted odds ratio for threshold value </= 105: 42.0, 95% CI 3.8 to 469.1, p = 0.002). CRGT could confirm a significant increase in Pr(CO(2)) during weaning in patients who finally failed the weaning trial. However, differences between patients with weaning success and failure were small and CRGT did not replace or improve the predictive power of the f/VT ratio for weaning outcome.

Acute Disease↗

Toward a consensus definition for COPD exacerbations.

In patients with COPD, an acute worsening of respiratory symptoms is often described as an exacerbation. Exacerbations are associated with a significant increase in mortality, hospitalization, and health-care utilization, but there is currently no widely accepted definition of what constitutes an exacerbation of COPD. This paper summarizes the discussions of the workshop, "COPD: Working Towards a Greater Understanding," in which the participants proposed the following working definition of an exacerbation of COPD: a sustained worsening of the patient's condition, from the stable state and beyond normal day-to-day variations, that is acute in onset and necessitates a change in regular medication in a patient with underlying COPD.

Diagnosis, Differential↗

Hepatopulmonary syndrome associated with cardiorespiratory disease.

BACKGROUND/AIMS: Hepatopulmonary syndrome is defined as a clinical triad including chronic liver disease, abnormal pulmonary gas exchange resulting ultimately in profound arterial hypoxaemia, and evidence of intrapulmonary vascular dilatations. We report five patients with liver cirrhosis diagnosed with hepatopulmonary syndrome who had associated chronic obstructive or restrictive respiratory diseases. METHODS: Clinical, radiographic and constrast-enhanced echocardiographic findings, and systemic and pulmonary haemodynamic and gas exchange, including ventilation-perfusion distributions, measurements were assessed in all five patients. RESULTS: Echocardiography was consistent with the presence of intrapulmonary vasodilation without intracardiac abnormalities, and high resolution computed tomographic scan features were compatible with clinical (3 cases) or histopathological diagnoses (2 cases) of associated respiratory disorders. The most common prominent functional findings were moderate to severe arterial hypoxaemia, caused by moderately to severely increased intrapulmonary shunting and/or mild to moderate low ventilation-perfusion areas, and hypocarbia along with an increased cardiac output and a low pulmonary artery pressure and vascular resistance. CONCLUSIONS: These functional characteristics, classically reported in the setting of clinically stable, uncomplicated hepatopulmonary syndrome, conform to a distinctively unique, chronic gas exchange pattern. Equally important, these pulmonary haemodynamic-gas exchange hallmarks are not influenced by the co-existence of chronic cardiorespiratory disease states. These data may have clinical relevance for elective indication of hepatic transplantation in patients with life-threatening hepatopulmonary syndrome.

Adult↗

Severe portopulmonary hypertension after liver transplantation in a patient with preexisting hepatopulmonary syndrome.

BACKGROUND: Portopulmonary hypertension and hepatopulmonary syndrome have been considered mutually exclusive pulmonary vascular disorders in liver disease states. METHODS: This current report describes a middle-aged patient, a candidate for liver transplantation, diagnosed with hepatopulmonary syndrome on the basis of clinical, echocardiographic and gas exchange criteria. Unusually high pulmonary pressures were observed at liver transplantation, performed 6 months after the initial diagnosis of hepatopulmonary syndrome. Three months later, the patient developed severe pulmonary hypertension and died of right ventricular failure during a second attempted liver transplantation. Postmortem histologic findings in the lung confirmed the presence of plexogenic pulmonary arteriopathy. CONCLUSION: This case illustrates the potential occurrence of hepatopulmonary syndrome and portopulmonary hypertension in the same patient, suggesting that the presence of hepatopulmonary syndrome may not preclude the development of portopulmonary hypertension.

Hepatopulmonary Syndrome↗

Isosorbide-5-mononitrate in the treatment of pulmonary hypertension associated with portal hypertension.

Pulmonary hypertension is uncommonly associated with portal hypertension. The current approach for the management of pulmonary hypertension involves the use of vasodilators in patients who show vascular responsiveness during an acute challenge. Since the association of portal hypertension with pulmonary hypertension is very seldomly presented, its optimal therapy has not been defined. Moreover, calcium-channel blockers, which are usually used in pulmonary hypertension treatment, may exert a deleterious effect on portal hypertension. Therefore, the search for drugs that may be active under both conditions has important clinical implications. This report presents the case of a patient with portal hypertension-associated pulmonary artery hypertension that was effectively treated with isosorbide-5-mononitrate (Is-5-Mn). The patient had severe portal hypertension (hepatic venous pressure gradient=14.5 mmHg) and pulmonary hypertension (mean pulmonary artery pressure (PAP)=50 mmHg). Acute administration of prostacyclin and nitric oxide elicited a significant reduction in both PAP and pulmonary vascular resistance (PVR), an effect that was also achieved with Is-5-Mn. The patient was treated with 40 mg Is-5-Mn twice daily and a haemodynamic study performed 6 months later showed that the reduction in both PAP and PVR persisted.

Female↗

Effects of inhaled furosemide on platelet-activating factor challenge in mild asthma.

Furosemide (Fur) may have an anti-inflammatory effect on airways in patients with asthma although its intrinsic mechanism remains elusive. Platelet-activating factor (PAF) is a potent proinflammatory mediator that induces systemic and respiratory effects in normal control subjects and asthmatics. The aim of this study was to assess whether pretreatment with nebulized Fur (40 mg) was able to modulate PAF-induced systemic and respiratory effects in asthma. Eleven patients were studied (mean+/-sem 22+/-0.8 yrs) with mild asthma (forced expiratory volume in one second, 95+/-4%) in a randomized, double-blind, placebo-controlled, cross-over fashion, one week apart. PAF challenge (18 microg) was carried out 15 min after administration of Fur or placebo. Peripheral blood neutrophils, respiratory system resistance, and arterial blood gases were measured at baseline, and 5, 15 and 45 min after PAF; urinary cysteinyl leukotriene E4 (uLTE4) was also measured, at baseline and 120 min after PAF challenge. Although Fur did not alter PAF-induced systemic and respiratory effects, it did partially inhibit (63%; p<0.04) the increments of uLTE4 levels shown after PAF inhalation. It is concluded that furosemide is not effective in protecting against platelet-activating factor challenge in patients with asthma despite its potential inhibition of leukotriene synthesis. These findings reinforce the view that the pulmonary effects of platelet-activating factor are mediated through different pathways.

Administration, Inhalation↗

Evidence of the effectiveness of continuous positive airway pressure in the treatment of sleep apnea/hypopnea syndrome.

Continuous positive airway pressure (CPAP) is worldwide considered as the standard treatment of sleep apnea/hypopnea syndrome (SAHS) although studies on the effectiveness of this treatment are limited. The aim of our study was to evaluate the effectiveness of CPAP in improving SAHS-related symptoms, daytime function, perceived health status, and quality of life in patients with moderate to severe SAHS. The effect of conservative treatment (CT) measures-sleep hygiene and weight loss- was compared with CT + CPAP. We included 105 consecutive patients (13 females, age 53 +/- 10 yr, body mass index [BMI] = 32 +/- 6 kg/m2, apnea/hypopnea index [AHI] = 56 +/- 20, Epworth sleepiness scale [ESS] = 12 +/- 5) who met our criteria for CPAP treatment. Patients were randomly allocated in two groups of similar characteristics. Group 1 (n = 37) was asked to improve sleep hygiene and started a weight loss program. Group 2 (n = 68) received, in addition, treatment with CPAP. Both groups were followed through weekly telephone calls and appointments. Sleepiness, other symptoms related to SAHS, daytime function, perceived health status, and quality of life were assessed through questionnaires at inclusion and after 3 mo of treatment. The relief of sleepiness and other SAHS-related clinical symptoms and improvement in perceived health status was much greater in Group 2 receiving CT + CPAP compared with Group 1, only receiving CT. The odds of experiencing a treatment response with CPAP + CT compared with CT alone was 6.52 (odds ratio [OR] = 2.51 to 17.6, 95% confidence interval [95% CI]). CPAP is currently the treatment of choice. At this time, the indication of CPAP treatment in moderate to severe SAHS is adequately supported.

Body Mass Index↗

Inflammatory reaction in pulmonary muscular arteries of patients with mild chronic obstructive pulmonary disease.

Endothelial dysfunction and intimal thickening have been shown in pulmonary arteries (PA) of patients with mild chronic obstructive pulmonary disease (COPD). To investigate whether an inflammatory process related to tobacco smoking might be involved in the development of pulmonary vascular abnormalities in COPD, we characterized the inflammatory cell infiltrate and the endothelium-dependent relaxation in PA of 39 patients who underwent lung resection, divided into three groups: "nonsmokers" (n = 7); "smokers," with normal lung function (n = 12); and "COPD" (n = 20). Endothelium-dependent relaxation was assessed in vitro by exposing PA rings to adenosine diphosphate (ADP). Inflammatory cell types were identified by immunohistochemistry. PA of COPD patients developed lower relaxation in response to ADP than nonsmokers and smokers. The number of inflammatory cells was increased in PA of COPD compared with the other two groups. This cell infiltrate was largely constituted by T lymphocytes. The CD8(+) T-cell subset was increased in both smokers and COPD compared with nonsmokers, yielding a reduction of the CD4(+)/CD8(+) ratio. The intensity of the inflammatory infiltrate correlated with both the endothelium-dependent relaxation and the intimal thickness. We conclude that cigarette smoking induces a CD8(+) T-lymphocyte infiltrate in PA, which is associated with the impairment of the vessel's structure and function, suggesting the potential involvement of an inflammatory process in the pathogenesis of pulmonary vascular abnormalities in the early stage of COPD.

Aged↗

Effects of endurance training on skeletal muscle bioenergetics in chronic obstructive pulmonary disease.

Physiologic adaptations after an 8-wk endurance training program were examined in 13 patients with chronic obstructive pulmonary disease (COPD) (age, 64 +/- 4 [SD] yr; FEV1, 43 +/- 9% pred; PaO2, 72 +/- 8 mm Hg; and PaCO2, 36 +/- 2 mm Hg) and in eight healthy sedentary control subjects (61 +/- 4 yr). Both pre- and post-training studies included: (1) whole-body oxygen consumption (V O2) and one-leg O2 uptake (V O2leg) during exercise; and (2) intracellular pH (pHi) and inorganic phosphate to phosphocreatine ratio ([Pi]/[PCr]) during exercise; and half-time of [PCr] recovery. After training, the two groups increased peak V O2 (p < 0.05 each) and showed a similar fall in submaximal femoral venous lactate levels (p < 0.05 each). However, control subjects increased peak V E (p < 0.01) and raised peak O2 delivery (p = 0.05), not shown in patients with COPD. Both groups increased post-training O2 extraction ratio (p < 0.05). The most consistent finding, however, was in patients with COPD, who had a substantial improvement in cellular bioenergetics: (1) half-time of [PCr] recovery fell from 50 +/- 8 to 34 +/- 7 s (p = 0.02); and (2) at a given submaximal work rate, [Pi]/[PCr] ratio decreased and pHi increased (p < 0.05 each). We conclude that beneficial effects of training in patients with COPD essentially occurred at muscle level during submaximal exercise.

Aged↗

Gas exchange and pulmonary haemodynamic responses to fat emulsions in acute respiratory distress syndrome.

OBJECTIVE: To investigate the gas exchange and pulmonary haemodynamic responses to two different intravenous fat emulsions in patients with acute respiratory distress syndrome (ARDS). DESIGN: Prospective, randomized, double-blind, placebo-controlled study. SETTING: Intensive care unit in a university-affiliated hospital. PATIENTS: 21 patients with ARDS [mean age, 57 +/- 3 (SEM) years; Acute Physiology and Chronic Health Evaluation II, 20 +/- 3; Murray's score, 2.85 +/- 0.12] consecutively admitted. INTERVENTIONS: Patients were assigned to three groups (n = 7 each): group A (LCT) received long-chain triglycerides (20% LCT), group B (MCT/LCT), medium-chain triglycerides/long-chain triglycerides (20% MCT/LCT: 50/50) and group C placebo (0.9% sodium chloride, NaCl). The infusion was always given at the rate of 2 mg/kg min over a total period of 12 h, with a volume infusion of 500 ml in each group. MEASUREMENTS: Data were collected before, immediately after and 12 h after infusion ceased. Pulmonary and systemic haemodynamic and gas exchange variables were measured at each time point. Serum triglyceride cholesterol, and non-esterified fatty acids levels were measured. RESULTS: During LCT infusion, cardiac output, oxygen consumption and oxygen delivery increased (all p < 0.05), whereas pulmonary haemodynamics, arterial oxygen tension, mixed venous partial pressure of oxygen and venous admixture ratio remained essentially unaltered. No changes were observed following MCT/LCT infusion. CONCLUSIONS: The administration of LCT emulsion given at a slow rate did not alter arterial oxygenation because of the beneficial effect of a high cardiac output, hence offsetting the detrimental effect of increased O2 consumption.

Adult↗

Interleukin-8 expression in bronchoalveolar lavage cells in the evaluation of alveolitis in idiopathic pulmonary fibrosis.

Interleukin-8 (IL-8) is a neutrophilic chemotactic factor which may have a prominent role in the attraction of neutrophils to the lung in idiopathic pulmonary fibrosis (IPF). The objective of this study was to investigate the usefulness of IL-8 expression in bronchoalveolar lavage (BAL) cells in the evaluation of alveolitis in IPF. We analysed the BAL cell expression of IL-8 by immunocytochemistry in 19 patients with IPF (six smokers, three ex-smokers and ten non-smokers) and in a control group composed of 14 individuals (six smokers, eight non-smokers). In IPF, BAL was performed on both the pulmonary lobe with the most extensive involvement and the one less extensively involved on high-resolution computed tomography (HRCT) scans. The percentages and absolute numbers of BAL IL-8+ macrophages from lobes with the most extensive HRCT scan involvement (36 +/- 6% and (6 +/- 2 x 10(4) ml-1) (SE) and from those less extensively involved [26% +/- 4% and (6 +/- 1) x 10(4) ml-1] were significantly higher with respect to both those from healthy smokers [17% +/- 6% and (7 +/- 4) x 10(4) ml-1] and those from non-smokers [2% +/- 1% and (1 +/- 0.3) x 10(4) ml-1] (P = 0.005 and P = 0.001, respectively), without differences between the two lobes. In contrast, both the proportions and the absolute numbers of BAL neutrophils in IPF were significantly higher in lobes with the most extensively involved HRCT scan in comparison with lobes with the least extensive involvement [13% +/- 3%, (3 +/- 1) x 10(4) ml-1 vs. 8% +/- 2%, (1 +/- 0.3) x 10(4) ml-1, P = 0.05]. Moreover, the numbers of BAL neutrophils, but not those of IL-8+ macrophages, correlated with the extent of total pulmonary HRCT scan abnormalities in the most involved lobe (r = 0.64, P = 0.04). A correlation between neutrophils and IL-8+ cells was not observed. The results of this study suggest that, in IPF, BAL neutrophilia offers a better description of the disease inflammatory process than the expression of IL-8 in BAL cells.

Aged↗

Prediction equations for plethysmographic lung volumes.

Due to the lack of information of reference values for plethysmographic lung volumes, standardized measurements were carried out on a selected sample of 482 healthy non-smoking volunteers (300 men and 182 women), aged 20-70 years, living in the Barcelona area (Spain). Prediction equations using age, height and body surface area (BSA) as covariates were calculated for the subdivisions of lung volumes [TLC, IC, EVC, FRC, RV and RV/TLC (%)], separately for both sexes. Simple linear equations predicted lung volumes as well as more complex equational models. BSA correction was useful for FRC but not for the other parameters. Our predicted FRC was up to 10% higher (mean 256 ml) than the FRC estimated by other studies using gas dilution techniques, but showed an acceptable agreement with the plethysmographic measurements carried out in an independent sample of 94 healthy non-smokers (42 men and 52 women) from Barcelona using different equipment. The present study provides an internally consistent set of prediction equations for static lung volumes. Differences in predicted FRC between the present study and other reference values obtained using gas dilution measurements should be attributed to the method of measurement.

Adult↗

Effect of inverse I:E ratio ventilation on pulmonary gas exchange in acute respiratory distress syndrome.

BACKGROUND: It is not known whether inverse I:E ratio ventilation (IRV) offers any real benefit over conventional mechanical ventilation with positive end-expiratory pressure (CMV-PEEP) at similar levels of end-expiratory pressure. METHODS: The effects of volume-controlled and pressure-controlled IRV (VC-IRV and PC-IRV, respectively) on VA/Q inequality were compared with those of CMV-PEEP at a similar level of end-expiratory pressure and with CMV without PEEP (CMV) in eight patients in the early stages of acute respiratory distress syndrome (ARDS). Respiratory blood gases, inert gases, lung mechanics, and hemodynamics were measured 30 min after the onset of each ventilatory mode. RESULTS: Recruitment of nonventilated, poorly ventilated (or both) but well-perfused alveoli increased the partial pressure of oxygen (PaO2) during CMV-PEEP (+13 mmHg) and IRV-VC (+10 mmHg; P < 0.05) compared with CMV. In contrast, PC-IRV did not affect PaO2 but caused a decrease in PaCO2 (-7 mmHg; P < 0.05). The latter was due to a concomitant decrease in dead space (P < 0.01) and shift to the right of VA/Q distributions. During PC-IRV, the increase in the mean of blood flow distribution (mean Q; P < 0.01) without a change in the dispersion (log SD Q) did not result in an increase in PaO2, probably because it reflected redistribution of blood flow within well-ventilated areas. CONCLUSIONS: Short-term PC-IRV improved carbon dioxide clearance, but the lung became less efficient as an oxygen exchanger. Furthermore, based on mean airway and plateau pressures, the risk of barotrauma was not reduced with this type of ventilation.

Adult↗

Effects of F(I)O2 on leg VO2 during cycle ergometry in sedentary subjects.

In a recent study of completely sedentary normal young subjects, leg VO2max was reduced by hypoxia in proportion to mean capillary PO2 as F(I)O2 was reduced from 0.15 to 0.12. However, the increase in VO2max from F(I)O2 = 0.15 to 0.21 was less than expected for the increase in mean capillary PO2. This finding has led us to hypothesize that in sedentary subjects breathing room air, VO2max is not limited by O2 supply but rather by oxidative capacity of mitochondria. The present study sought to obtain further evidence for or against this hypothesis in sedentary subjects by assessing leg VO2max (VO2leg) breathing 100% O2, as well as in normoxia and hypoxia. Data from 18 subjects studied at F(I)O2 = 0.12, 0.15, and 0.21 and from six more studied at 0.12, 0.15, and 1.00 were analyzed. In all 24 we measured VO2leg by arterial and venous blood sampling and thermodilution leg blood flow during maximal cycle ergometry at each F(I)O2. VO2leg was not increased by room air or 100% O2 breathing relative to that observed at F(I)O2 = 0.15, but it was reduced while breathing 12% O2. The data at F(I)O2 = 0.12 and 0.15 conformed to the predictions of O2 supply limitation of maximal VO2 as previously. These results confirm and extend our prior observations that in sedentary, as opposed to trained subjects, muscle VO2max is O2 supply limited only in hypoxia.

Adolescent↗