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Biomedical subjects

G Rolla

Publications and source records attributed to G Rolla.

At least 37 records · Page 2Linked to original sources
PubMed1997

Exhaled nitric oxide and oxygenation abnormalities in hepatic cirrhosis.

Impaired arterial oxygenation, ranging from increased alveolar-arterial oxygen gradient (AaDo2) to hypoxemia, is commonly present in patients with cirrhosis. Nitric oxide (NO), through pulmonary vasodilatation, may play a major role in the oxygen abnormalities of cirrhosis. Our aim was to study the relationship between NO production and O2 abnormalities in 45 nonsmoking patients with cirrhosis and without major cardiovascular and respiratory diseases. Intrapulmonary shunting was detected by contrast-enhanced (CE) echocardiography. Lung volumes and diffusion, arterial blood gas analysis, serum NO2-/NO3-, NO output in the exhaled air, and cardiac index by the echocardiographic method were determined in all patients. Twenty-seven (60%) patients had an abnormally increased (> 15 mm Hg) AaDo2. The mean values of exhaled NO output and serum NO2-/NO3- were significantly higher in cirrhotic patients than in controls (252 +/- 117 vs. 75.2 +/- 19 nL/min/m2, P < .0001; and 47.5 +/- 29.4 vs. 32.9 +/- 10.1 micromol/L, P < .02, respectively). In all patients, there was a significant correlation between exhaled NO and AaDo2 (r = .78, P < .0001). Twelve patients (26.6%) were found to have CE-echocardiographic evidence of intrapulmonary shunting (positive CE-echo). Nine patients were considered to have hepatopulmonary syndrome (HPS) on the basis of an AaDo2 > 15 mm Hg and positive CE-echo. These 9 patients had a mean value of exhaled NO significantly higher than patients without HPS (331 +/- 73.2 vs. 223 +/- 118.4 nL/min/m2, P < .05). In all patients, cardiac index was positively correlated with exhaled NO (r = .47, P < .001) and with serum NO2-/NO3- (r = .43, P < .01). The results suggest an important role of NO in the oxygenation and circulatory abnormalities of patients with cirrhosis.

Adult↗
PubMed1997

Pentoxifylline attenuates LPS-induced bronchial hyperresponsiveness but not the increase in exhaled nitric oxide.

BACKGROUND: Inhaled endotoxin (LPS) may cause a transient increase in airway responsiveness, possibly through a cytokine-mediated airway inflammation, which is associated with an increase in nitric oxide synthesis and release. OBJECTIVE: We wondered whether pentoxifylline (PTX), which may attenuate cytokine release induced by LPS, could inhibit LPS-induced increase in airway responsiveness. METHODS: Methacholine (Mch) bronchial responsiveness was assessed 2 and 24 h after saline or LPS inhalation in eight subjects with bronchial hyperresponsiveness (PD20FEV1 610 +/- 53 micrograms), treated with iv saline or PTX, in a double-blind crossover design. Nitric oxide (NO) in the exhaled air, which was expected to increase after LPS inhalation, and PEFR values were also measured at baseline, hourly for 6 h and 24 h later. RESULTS: After LPS inhalation PEFR decreased significantly compared with placebo inhalation, reaching a maximum decrease of 11.25 +/- 1.05 and 4.5 +/- 0.84% of baseline, at 2 h, respectively during saline and PTX infusion, P < 0.001. Exhaled NO were elevated after LPS compared with placebo inhalation at 1 h (35.6 +/- 4.8 vs 18 +/- 2.8 ppb, P < 0.001), with no difference during saline or PTX infusion. Exhaled NO remained elevated until the 6th hour. PD20FEV1 2h after LPS inhalation was significantly lower than after placebo inhalation both during saline infusion (234 +/- 29 vs 625 +/- 62 micrograms, P < 0.001) and during PTX infusion (441 +/- 47 vs 616 +/- 48 micrograms, P < 0.001), the difference between saline and PTX being significant (P < 0.01). At 24 h no difference in PEFR, PD20FEV1 and exhaled NO was observed in comparison with pre-study values. CONCLUSION: PTX attenuates both the decrease in airway patency and the increase in bronchial responsiveness induced by LPS inhalation, without any significant change in exhaled NO, which is increased by LPS inhalation.

Adult↗
PubMed1997

Increased nitric oxide in exhaled air of patients with systemic lupus erythematosus.

OBJECTIVE: In experimental animals, elevated nitric oxide (NO) production has been implicated in the pathogenesis of a lupus-like syndrome. Abnormalities of lung function tests are reported in a high proportion of patients with systemic lupus erythematosus (SLE). We investigated whether NO output in exhaled air might be increased in patients with SLE and whether it is related to disease activity and to respiratory function abnormalities. METHODS: Lung volume, maximal expiratory flow at 50 and 25% of vital capacity (MEF50 and MEF25), diffusion coefficient for carbon monoxide (KCO), and NO in the exhaled air were measured in 27 outpatients with SLE (23 women, age 39.2 +/- 16.3). NO in exhaled air was also measured in 30 healthy control subjects. Disease activity was assessed by the European Consensus Lupus Activity Measurement (ECLAM) scoring system. RESULTS: Mean values of peak concentrations of NO exhaled air were 64.8 +/- 27.9 parts per billion (ppb) in patients and 31.6 +/- 7.7 ppb in controls, p < 0.001. Peak NO concentration was directly related to ECLAM activity score (p < 0.05) and inversely related to MEF25 (p < 0.05). CONCLUSION: NO in exhaled air is significantly increased and correlated with disease activity in patients with SLE. Whether increased NO output depends on respiratory tract inflammation, as the relationship with MEF25 may suggest, or on circulating cytokines produced elsewhere remains to be investigated.

Adolescent↗
PubMed1996

Respiratory function in systemic lupus erythematosus: relation with activity and severity.

The objective of this study was to examine the relation between respiratory function tests, disease activity and disease severity in ambulatory patients with systemic lupus erythematosus (SLE) who did not present with overt respiratory problems. Lung volumes, maximal expiratory flows at 50% and 25% of vital capacity (MEF50 and MEF25), bronchial threshold to methacholine (PD15FEV1), transfer factor CO (KCO) were measured in 24 consecutive SLE outpatients (22 women, age 41 +/- 14.8 years) and in 24 healthy controls matched for age and sex. In SLE patients alveolar-arterial oxygen gradient (AaO2) was also measured. Disease activity was assessed by European Consensus Lupus Activity Measurement (ECLAM) scoring system and disease severity by Lupus Severity of Disease Index. In comparison to controls SLE patients showed a significant decrease of total lung capacity (TLC) (91.7 +/- 16.5 vs 102.7 +/- 12.9% predicted, P < 0.01), MEF25 (58.4 +/- 25.2 vs 73.5 +/- 19.5% predicted, P < 0.005) PD15FEV1 (2164 +/- 1122 vs 4230 +/- 1014 micrograms methacholine, P < 0.0001) and KCO (77.1 +/- 20.5 vs 96.3 +/- 12.4% predicted, P < 0.001). AaO2 (mean value 13.2 +/- 8.4) was abnormally high (> 20 mmHg) in 12 patients. The ECLAM score of activity was inversely related with KCO (r = 0.48, P < 0.02). The severity index was significantly related with FEV1/VC ratio (r = 0.43, P < 0.05), MEF50 (r = 0.51, P < 0.01), MEF25 (r = 0.40, P < 0.05) and PD15FEV1 (r = 0.51, P < 0.01). In eight patients, evaluated also after treatment intensification, there was a significant increase in KCO (from 71.8 +/- 24.7 to 84.9 +/- 22.3% predicted, P < 0.01) along with a decrease in ECLAM score (from 3.0 +/- 1.34 to 0.69 +/- 0.75, P < 0.01). The relation between disease activity and KCO suggests a relation between systemic and alveolar inflammation whereas the relation between severity index, airway patency and reactivity indices suggests a cumulative damage to the airways in SLE patients, even in the absence of overt respiratory manifestations.

Adult↗
PubMed1995

Are asthma-like symptoms due to bronchial or extrathoracic airway dysfunction?

Patients with asthma-like symptoms may not have asthma but obstruction of the extrathoracic airway (EA). To evaluate if dysfunction of the EA causes asthma-like symptoms, we assessed bronchial and EA responsiveness to inhaled histamine in 441 patients who presented with at least one of three key symptoms--cough, wheeze, dyspnoea--but had neither documented asthma nor bronchial obstruction. The histamine concentrations causing a 20% fall in forced expiratory volume in 1 s (PC20FEV1) and a 25% fall in maximal mid-inspiratory flow (PC25MIF50) were used as respective thresholds of bronchial and EA responsiveness. Values 8 mg/mL or less indicated bronchial (B-HR) or EA hyper-responsiveness (EA-HR). The influence of concurrent upper respiratory tract diseases, such as post-nasal drip (PND), pharyngitis, laryngitis and sinusitis, was also assessed. We found four response patterns to the histamine challenge: EA-HR in 26.5% of the patients, B-HR in 11.1%, combined EA-HR and B-HR in 40.6%, and no-HR in 21.8%. Cough was reported by 79% of the patients, wheeze by 53%, and dyspnoea by 40%. Patients with cough as the sole presenting symptom (34.2%), as compared with those with wheeze and/or dyspnoea (20%), had significantly greater probability of having EA-HR (OR 5.35, 95% CI 3.25-8.82) and lower probability of having B-HR (OR 0.45, CI 0.28-0.70); patients with cough plus wheeze and/or dyspnoea (45.8%) had significantly greater probability of having both EA-HR and B-HR than either those with cough alone (OR 2.48, CI 1.49-4.13), or those with wheeze and/or dyspnoea but not cough (OR 1.74, CI 1.36-2.22). EA-HR alone or combined with B-HR was strongly associated with EA diseases, particularly pharyngitis and PND. Cough was significantly associated with PND, either when it was the sole symptom (OR 2.16, CI 1.14-4.09) or when it was combined with wheeze and/or dyspnoea (OR 3.53, CI 1.97-6.33). Our results suggest that extrathoracic airway dysfunction may account for asthma-like symptoms, particularly chronic cough. This abnormality seems to be sustained by chronic diseases of the upper respiratory tract.

Adult↗
PubMed1995

Extrathoracic and intrathoracic airway responsiveness in sinusitis.

BACKGROUND: Asthma associated with sinusitis is supposed to be sustained by bronchoconstrictive reflexes originating in extrathoracic airway (EA) receptors. OBJECTIVE: The study was designed to evaluate the relationship between EA responsiveness and bronchial responsiveness in sinusitis. METHODS: We performed histamine inhalation challenge in 106 patients with chronic sinusitis, during disease exacerbation and after treatment with antimicrobials and nasal flunisolide (100 micrograms daily) for 2 weeks. Forced expiratory volume in 1 second (FEV1) and maximal mid-inspiratory flow (MIF50) were the respective indexes of bronchial and EA narrowing; the histamine concentrations causing a 20% fall in FEV1 (PC20) and 25% drop in MIF50 (PC25MIF50) were used as thresholds of bronchial and EA responsiveness. Thresholds of 8 mg/ml or less were assumed to indicate bronchial hyperresponsiveness (B-HR) or EA hyperresponsiveness (EA-HR). RESULTS: During sinusitis exacerbation 76 patients had EA-HR, which in 46 was associated with B-HR. The values of PC20 were closely related with those of PC25MIF50 (p < 0.001). EA-HR and B-HR were strongly associated with pharyngitis. After treatment, mean PC25MIF50 and PC20 were significantly increased (p < 0.001). The improvement of PC25MIF50 was closely related to that of PC20 (p < 0.001) and to the decrease in neutrophils in nasal lavage (p < 0.05). EA-HR reversed in 58 patients and improved in 10; B-HR reversed in 29 and improved in 12. CONCLUSIONS: Our findings suggest that in sinusitis, B-HR may be sustained by constrictive reflexes originating in pharyngeal receptors, made hypersensitive by seeding of the inflammatory process.

Analysis of Variance↗
PubMed1995

Reversible bronchial hyperresponsiveness induced by OK-T3/IL-2 administration in a patient with multiple myeloma.

Severe bronchial hyperresponsiveness to methacholine developed after intravenous therapy with OK-T3 and IL-2 in a patient with multiple myeloma, in whom no factors known to be associated with bronchial hyperresponsiveness were present. A substantial increase and activation of peripheral T-lymphocytes was observed after immunotherapy. Bronchial responsiveness and lymphocyte subsets both returned to normal baseline values 2 months after the patient was shifted to subcutaneous low dose administration of IL-2. The strict association between peripheral T-lymphocytes activation and the development of bronchial hyperresponsiveness suggests a causal relationship.

Antibodies, Monoclonal↗
PubMed1995

Effect of inhaled norepinephrine on the nitroglycerin-induced bronchodilatation in asthmatics.

Previous studies on the bronchodilating effect of nitrates yielded conflicting results. We hypothesized that the concomitant bronchial vasodilatation induced by nitrates may limit the increase of airway patency due to bronchial smooth muscle relaxation. To test this hypothesis, we evaluated the bronchodilating effect of nebulized nitroglycerine (NTG), 0.2 mg, in 12 patients with reversible airway obstruction (FEV1 64.3 +/- 8.2% predicted, > 15% increase after salbutamol 200 micrograms by metered-dose inhaler), pretreated with aerosolized norepinephrine (NE) (0.04 mg) or placebo (PL), in a randomized double-blind crossover design, in two separate days. Baseline FEV1 values of the two test days and FEV1 after NE or PL inhalations were not significantly different. After NTG inhalation, FEV1 was 73.8 +/- 7.9% predicted, with NE pretreatment, and 70 +/- 8.2% predicted with PL pretreatment (p < 0.01). The maximal percent increases of FEV1 above baseline were 14.9 +/- 4.8% and 9.2 +/- 2.4%, respectively, after NE and PL pretreatment (p < 0.01). In conclusion, NTG produces a better bronchodilatation when the concomitant vasodilatation is attenuated by a vasocostrictive agent.

Administration, Inhalation↗
PubMed1994

Effect of pleurotomy on pulmonary function after coronary artery bypass grafting with internal mammary artery.

Coronary artery by-pass grafting with internal mammary artery (IMA) has become the graft conduit of choice, due to improved survival and its long term patency rate. However, some studies have shown that, in comparison with saphenous vein grafts, after IMA grafting, there is increased postoperative impairment of pulmonary function, possibly due to the frequent performance of pleurotomy. In 57 consecutive patients, admitted for elective CABG with IMA, we prospectively evaluated the early (2nd and 6th day) postoperative chest X-ray complications and the late (2 months) respiratory function tests changes. Thirty-two patients had been subjected to pleurotomy (group 1) and 25 not (group 2). The incidence of pulmonary atelectasis and pleural effusion in 2nd and in 6th postoperative days was not different in the two groups: 22 vs. 19%, 74 vs. 52% in 2nd, and 29 vs. 19%, 48 vs. 38% in 6th postoperative day respectively. The incidence of elevated hemidiaphragm in 6th postoperative day was not different in the two groups (18.5 vs. 14%). Two months after surgery the mean values of spirometric tests were significantly lower than the preoperative values: VC from 88.5 +/- 1.26 to 80 +/- 1.65% of predicted, P < 0.001, FEV1 from 96.1 +/- 1.27 to 84.7 +/- 1.73% of predicted, P < 0.001, MEF50 from 84.9 +/- 3.14 to 69.2 +/- 3.18% of predicted, P < 0.001. No significant changes were detected in RV and in AaPO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Artery Bypass↗
PubMed1994

Intercellular adhesion molecule-1 is upregulated on peripheral blood T lymphocyte subsets in dual asthmatic responders.

To examine the role of adhesion molecules in T cell recruitment and activation during allergen-induced late asthmatic response (LAR), we evaluated the expression of lymphocyte function-associated antigen-1 alpha (LFA-1 alpha) and intercellular adhesion molecule-1 (ICAM-1) on peripheral blood T lymphocyte subsets from atopic asthmatic patients and their changes following allergen inhalation challenge. 12 atopic asthmatic patients were studied. Six patients showed only a single early response after allergen challenge, and six developed a dual response. At baseline, dual responders (DR) had a significantly higher expression of ICAM-1 on CD4+ and CD8+ T lymphocytes as compared with both single early responders (P < 0.005 and P < 0.02, respectively) and controls (P < 0.001, both comparisons). Allergen challenge was followed by a decrease of CD8+ ICAM-1+ T lymphocytes in all DR (P < 0.05) and of CD4+ ICAM-1+ T lymphocytes in four out of six DR, at the time of the LAR. At the same time, a significant rise in serum levels of the soluble form of ICAM-1 was observed in DR. These results suggest that peripheral blood immunoregulatory T lymphocytes are in a higher state of activation in DR as compared with early responders. The upregulation of ICAM-1 on these cells may be important in enhancing airway inflammation in patients with LAR.

Adolescent↗
PubMed1994

A scanning electron microscope investigation of calcium fluoride-like material deposited during topical fluoride exposure on sound human enamel in vitro.

1. The morphological aspects of globules deposited in vitro when a NaF solution is applied to sound human enamel were studied by scanning electron microscopy. 2. Particles, presumably of calcium fluoride-like material, formed on the surfaces of an unerupted tooth and consisted of subunits showing a "cauliflower" appearance, indicating agglomeration of even smaller particles. The number and size of the crystals increased with time of exposure. 3. These particles represent highly resistant fluoride reservoirs and may be of clinical significance.

Calcium Fluoride↗
PubMed1994

Effect of intravenous magnesium infusion on salbutamol-induced bronchodilatation in patients with asthma.

In vitro experimental data show that magnesium increases beta-receptor affinity to agonists. We studied the effect of a mild increase in serum magnesium level on the bronchial dose-response curve to salbutamol in six patients with asthma (age 54 +/- 3.6 years, FEV1 49.2 +/- 4.9 per cent of predicted), with a normal serum magnesium level, in a double blind placebo-controlled design. The salbutamol dose-response curve was obtained on two separate days, starting 30 min after an intravenous infusion of saline or MgSO4 (20 mg/kg over 10 min, followed by 10 mg/kg/h). The baseline FEV1 values and the values after 30 min infusion on the two test days were not significantly different. During MgSO4 infusion, the serum magnesium level increased significantly from 0.86 +/- 0.01 to 1.31 +/- 0.19 mmol/litre after 30 min and 1.29 +/- 0.17 mmol/litre at the end of the study. FEV1 values after salbutamol were significantly higher during MgSO4 than during saline infusion at the low doses of salbutamol: 1480 +/- 253 vs. 1368 +/- 212 ml, P < 0.05, after 5 micrograms, and 1596 +/- 585 vs. 1378 +/- 532 ml, P < 0.01, after 10 micrograms of salbutamol. The maximum increase in FEV1 obtained after the maximum dose of salbutamol (400 micrograms) was not significantly different during saline and MgSO4 infusion. In conclusion, a mild sustained increase in serum magnesium level increases the bronchodilating effect of low doses of salbutamol, possibly through an increased beta-receptor affinity. There was no effect on the maximum bronchodilating effect of salbutamol.

Adult↗
PubMed1993

Respiratory symptoms, lung function tests, airway responsiveness, and bronchoalveolar lymphocyte subsets in B-chronic lymphocytic leukemia.

A respiratory questionnaire was completed and spirometry, tests for lung volumes, diffusion capacity for CO, and methacholine bronchial challenge were performed in 24 outpatients with B-chronic lymphocytic leukemia (B-CLL), aged 44-79, presenting in different stages of their disease. In 10 patients, bronchoalveolar lavage (BAL) fluid was also obtained. Ten of twenty-four patients had symptoms consistent with chronic bronchitis, unrelated both to smoking history and to the clinical stage. Abnormal values (< 2 SD) were found in 4 patients for total lung capacity (TLC), in 9 for vital capacity (VC), 8 for forced expiratory volume in 1 sec (FEV1), 11 for MEF50, 15 for MEF25 and in 7 for diffusing capacity for carbon monoxide. Seven of nineteen patients had PD20FEV1 at less than 1,600 micrograms of methacholine chloride. There was a significantly negative correlation between white blood cell count and VC (r = 0.41, P < 0.05). A positive correlation was found between PD20FEV1 and FEV1/VC (r = 0.61, P < 0.01). The mean and SEM for BAL cells/ml was 463 (71.8) x 10(3). No leukemic cells but a marked increase in T lymphocytes (32.5 +/- 7.8%) were found in BAL fluid. There were significantly negative correlations between the number of BAL CD3+ T lymphocytes and PD20FEV1 (r = 0.61, P < 0.05), and between the number of BAL CD8+ T lymphocytes and PD20FEV1 (r = 0.84, P < 0.01). In conclusion, patients with B-CLL have a high prevalence of respiratory symptoms, small airway dysfunction and CD8 "alveolitis" related to airway responsiveness; despite the well-known lung interstitial lymphocyte infiltration in B-CLL, leukemic cells are not found in BAL fluid.

Adult↗
PubMed1993

Atrial natriuretic peptide and bronchial hyperresponsiveness in patients with mitral stenosis.

Atrial natriuretic peptide (ANP) has been reported to have protective effects against methacholine-induced bronchoconstriction in asthmatics. The aim of the study was to evaluate the relationship between plasma ANP levels and bronchial responsiveness to methacholine in patients with mitral stenosis. In 12 patients with moderate mitral stenosis, age 35-58 years, 9 female, 8 in NYHA class 2, 4 in NYHA class 3 for symptoms, plasma ANP and bronchial threshold to methacholine (PD20FEV1) were determined. The same measurements were performed in 10 asthmatic patients, hyperresponsive to methacholine, and in 10 normal subjects, nonresponsive to methacholine. Mean +/- SE plasma ANP levels were significantly higher in patients with mitral stenosis in comparison with asthmatics and normals (159 +/- 41.8, 7.3 +/- 0.98, 7.6 +/- 1.3, respectively, p < 0.01). In patients with mitral stenosis there was a significant relationship between plasma ANP and PD20FEV1 (r = 0.81, p < 0.01). No relationship was found between ANP and PD20FEV1 in asthmatics. In conclusion, in patients with mitral stenosis ANP seems to play a protective role against bronchial hyperresponsiveness to methacholine.

Adult↗
PubMed1993

Bronchodilating effect of ipratropium bromide in heart failure.

The aim of this study was to test the hypothesis that lung oedema causes an obstructive airway impairment, due to an increase in cholinergic bronchial tone in patients with chronic heart failure (CHF). Ten patients with CHF were tested by inhalation of ipratropium bromide and placebo, given in sequential randomized order, in double-blind fashion, after assessment of baseline lung function, both during acute cardiac decompensation and after 8-10 days of adequate treatment. The decrease in lung oedema was associated with a significant increase in vital capacity (VC) (from 70 +/- 4.4 to 83 +/- 5.4% pred), forced expiratory volume in one second (FEV1) (from 59 +/- 3.6 to 72 +/- 4.6% pred), FEV1/VC (from 61 +/- 2.8 to 64 +/- 2.3%) and residual volume (RV) (from 94 +/- 7.9 to 99 +/- 6.8% pred). Ipratropium bromide produced a far better bronchodilatation during acute decompensation when FEV1 increased from 59 +/- 3.6 to 70 +/- 3.7% pred, than after intensive treatment for heart failure, when FEV1 increased from 72 +/- 4.6 to 76 +/- 4.8% pred. The maximum absolute increase in FEV1 induced by ipratropium bromide was 286 +/- 32 ml at admission and only 111 +/- 15 ml after treatment. In conclusion, in chronic heart failure, airway obstruction is partially reversible after inhalation of an anti-muscarinic drug, when lung oedema is present, supporting the hypothesis that lung oedema increases cholinergic bronchial tone.

Aged↗