Biomedical subjects
G Rolla
Publications and source records attributed to G Rolla.
Exhaled NO in diffuse alveolar haemorrhage.
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Hepatopulmonary syndrome: role of nitric oxide and clinical aspects.
Hepatopulmonary syndrome is defined by oxygenation impairment due to abnormal intrapulmonary vascular dilatations in patients with liver disease. The implication of enhanced pulmonary production of nitric oxide in the pathogenesis of intrapulmonary vascular dilatations has been demonstrated both in murine models and in human hepatopulmonary syndrome. The diagnosis of hepatopulmonary syndrome in chronic liver disease is of paramount importance, considering the fact that severe hypoxemia related to hepatopulmonary syndrome may occur in patients with well compensated liver disease and that survival is reduced in patients with hepatopulmonary syndrome relative to non hepatopulmonary syndrome patients. Priority for liver transplantation, which is presently the only cure, has been recently increased in patients with advanced hepatopulmonary syndrome.
Effect of inhalation aspirin challenge on exhaled nitric oxide in patients with aspirin-inducible asthma.
BACKGROUND: A complex relationship between arachidonic acid metabolites and nitric oxide (NO) synthesis has been reported in asthma. The effects of inhaled aspirin on fractional exhaled NO (FENO) in patients with aspirin-tolerant (ATA) and aspirin-inducible (AIA) asthma compared with normal controls have been investigated. METHODS: The FENO was measured baseline, after saline and lysine-aspirin (L-ASA) bronchial challenge in 10 patients with ATA and in 10 patients with AIA [mean (PD(20)FEV(1) L-ASA): 14.7 +/- 12.7 mg], who had comparable age and baseline FEV(1). Ten healthy subjects served as controls. Sputum eosinophils were counted after saline and after L-ASA challenge in the two groups of asthmatics. RESULTS: Asthmatic patients had baseline FENO significantly higher than controls (29.7 +/- 6.8 vs 9.8 +/- 2.05 p.p.b. respectively, P < 0.0001). No difference was observed in methacholine PD(20)FEV(1) and baseline FENO between ATA and AIA patients. After L-ASA inhalation, FENO increased significantly only in patients with AIA, reaching the peak value 4 h after bronchoconstriction (from 31.1 +/- 6 to 43 +/- 4.8 p.p.b., P < 0.001), while no change was observed in patients with ATA and in controls. Sputum eosinophils increased significantly after L-ASA inhalation only in patients with AIA (from 8.1 +/- 2.7 to 11.1 +/- 2.8%, P < 0.005) and there was a significant relationship between the increase in sputum eosinophils and the increase in FENO after ASA challenge. CONCLUSION: Exhaled NO may indicate eosinophilic airway inflammation during ASA exposure in patients with ASA inducible asthma.
Cardiopulmonary exercise testing and exhaled nitric oxide in the assessment of patients with mitral stenosis.
AIM: In patients with mitral stenosis, symptoms do not always correlate with echocardiographic data. The aims of the study were to evaluate the role of cardiopulmonary exercise testing in the assessment of patients with mitral stenosis and to quantify nitric oxide production at rest and at the end of exercise. METHODS: We evaluated 43 patients with moderate to severe mitral stenosis with a discrepancy between echocardiographic data and symptoms. Nitric oxide output was calculated by measuring nitric oxide concentration in the exhaled air at rest and at the end of exercise test. RESULTS: Patients were divided in 2 groups: group 1 with a functional capacity <75% at cardiopulmonary exercise test (VO2max in % of the predicted one) and group 2 with functional capacity >75%. Transvalvular gradient and pulmonary artery pressure were significantly higher in group 1 than in group 2 (respectively 9.07 +/- 2.11 mmHg vs 6.01 +/- 1.08 mmHg, p<0.001 and 42.8 +/- 7.2 mmHg vs 33.1 +/- 4.7 mmHg, p<0.001). Patients of group 1 had a lower nitric oxide output at the end of exercise compared to group 2 (231.4 +/- 96.6 nl/min vs 326.3 +/- 74.0 ml/min, p=0.01) and to normal subjects (511.15 +/- 180.1 nl/min, p<0.001). CONCLUSION: Cardiopulmonary exercise testing provides objective non invasive information in the evaluation of patients with discrepancy between symptoms and echocardiographic data. Different levels of nitric oxide output during exercise suggest the role of nitric oxide in regulating pulmonary vascular tone.
Effect on dyspnoea and hypoxaemia of inhaled N(G)-nitro-L-arginine methyl ester in hepatopulmonary syndrome.
Hepatopulmonary syndrome--a complication of chronic liver disease-is characterised by hypoxaemia, which results from widespread intrapulmonary vascular dilatations. Amplified production of pulmonary nitric oxide is thought to be important in development of this disorder in patients with liver cirrhosis. Here, we report a 64-year-old man with hepatopulmonary syndrome associated with hepatitis-C-virus-related cirrhosis. We gave the patient nebulised N(G)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthesis, which enhanced oxygenation (arterial oxygen pressure increased from 6.98 to 9.45 kPa). After L-NAME, the distance the patient could walk in 6 min rose by 92 m. Administration of L-NAME by aerosol might offer a new approach to treatment of hepatopulmonary syndrome.
Immunohistochemical characterisation of the lymph node reaction in pig post-weaning multisystemic wasting syndrome (PMWS).
The superficial inguinal lymph nodes of 10 piglets which had died spontaneously of post-weaning multisystemic wasting syndrome (PMWS), in which the porcine circovirus type II (PCV-II) genome was revealed by PCR, were submitted to immunohistochemical investigation for CD4, CD8, IgM, MAC387, S-100 protein, vimentin and F-VIII-RA and compared with three normal cases. The lymph node reaction was graded as initial, intermediate and end stage according to histological criteria. In the initial and intermediate stages, absence of follicles and depletion of lymphocytes were evident. Associated with this was a reduction in numbers of interfollicular dendritic cells and interdigitating cells and a reduction/absence of B cells and mainly CD4+ T lymphocytes. In the end stage the reduced expression of high endothelial venules and the prevalence of the stromal component of the lymph node was prominent, as well as the above changes. It is concluded that more than one mechanism is involved in the immunosuppressive ability of PCV-II: reduction of the antigen presenting ability and reduction of B cells and CD4+ T cell function.
Oral nitric oxide during plaque deposition.
BACKGROUND: Nitric oxide (NO) is one of the most powerful antibacterial compounds. We investigated if NO oral production increases during dental plaque deposition. MATERIALS AND METHODS: Oral NO and salivary nitrite were measured in 31 healthy subjects - 11 smokers and 20 nonsmokers - with natural healthy teeth, in the morning after tooth cleaning (baseline), after withdrawal of oral hygiene for 24 h and again after tooth cleaning. RESULTS: NO and nitrite were significantly higher during plaque deposition than with clean teeth: mean NO values +/- SEM were 44.3 +/- 4.9 parts per billion (ppb) at baseline, 58.8 +/- 3.7 ppb with plaque and 43.6 +/- 3.7 ppb after tooth cleaning, P < 0.05; nitrite values were 32.9 +/- 5.5 microm at baseline, 66.4 +/- 8.2 with plaque and 37.5 +/- 5.5 after tooth cleaning, P < 0.01. During plaque deposition, oral NO was significantly directly related to salivary nitrite (r = 0.497, P = 0.002) and so were their respective changes after tooth cleaning (r = 0.577, P < 0.001). Smokers had significantly lower oral NO than nonsmokers, with both clean and dirty teeth (P < 0.001), and higher bacteria counts in the plaque (38.6 +/- 11.5 vs. 19.9 +/- 2.3, P = 0.046). CONCLUSIONS: Oral NO production increases during de novo deposition of dental plaque. NO might be an early host defence mechanism against bacterial proliferation in the plaque. Such a mechanism is inhibited by cigarette smoking.
Smoking and hypoxemia caused by hepatopulmonary syndrome before and after liver transplantation.
Severe hypoxemia may occur in patients with liver disease as a result of abnormal intrapulmonary vasodilatations (hepatopulmonary syndrome, HPS). Liver transplantation (LT) is the only effective treatment of HPS, with a quite variable delay of improvement of oxygenation. Smoking, by decreasing respiratory nitric oxide (NO), apparently contributed to improved oxygenation in a 44-year-old man with alcohol-induced cirrhosis, complicated by HPS, who underwent LT. The patient quit smoking just before LT, when his PaO(2) was 29 mm Hg and exhaled NO (eNO) 28 ppb, a value far above the normal limits (9.6 +/- 3.2 ppb). After LT, oxygenation remained poor and eNO remained high for more than 4 months, when the patient started to smoke again (blood HbCO going up to 5%). At that time eNO decreased to 6 ppb and PaO(2) increased to 67 mm Hg. The strict relationship between eNO and oxygenation observed in this case reinforces the hypothesis that NO is the most important vasodilating mediator in HPS. Smoking may have hastened the resolution of HPS after LT by inhibiting respiratory NO and/or through a generalized impairment of endothelium-dependent vasodilation.
Effect of edentulism on spirometric tests.
The impact of denture wear in edentulous subjects while performing routine spirometric measurements has never been systematically investigated. We compared the values of FVC, FEV(1), PEFR, FEF(50%), FIV(1), and FIF(50%) recorded with and without dentures in three groups of edentulous subjects: 36 asymptomatic subjects with normal spirometry (N), 22 patients with chronic obstructive pulmonary disease (COPD), and 18 with interstitial lung disease (ILD). In 14 subjects retropharyngeal space with and without dentures was assessed by cephalometry. Subjects with N and ILD had significantly lower airflow rates without dentures, whereas subjects with COPD had no significant difference in spirometric values recorded with or without dentures. The retropharyngeal space was significantly decreased by removing dentures (from 1.52 +/- 0.07 to 1.16 +/- 0.09 cm, SEM, p < 0.0001). These findings indicate that in edentulous subjects with a normal or restrictive pattern, the recording of flow-volume curves with or without dentures produces small but significant differences. Although such differences do not appear to have clinical significance, the fact that when dentures are used some respiratory flows are higher would favor the use of dentures in edentulous subjects during spirometric evaluation.
Hypertension and ascorbic acid.
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Changes in airway responsiveness following mantle radiotherapy for Hodgkin's disease.
UNLABELLED: STUDY OBJECTIVES To investigate whether mantle radiotherapy (MRT) for the lung, through its proinflammatory effects, can induce an increase in airway responsiveness. DESIGN: Follow-up of the changes in lung function and methacholine responsiveness in patients 1, 6, 12, and 24 months after they underwent MRT. PATIENTS: Thirteen nonasthmatic patients with bulky Hodgkin's lymphoma who were scheduled for MRT. MEASUREMENTS AND RESULTS: Chest radiographs, lung function tests, methacholine thresholds of the bronchi (the provocative dose of methacholine causing a 10% fall in FEV(1) [PD(10)]) and central airway (the provocative dose of methacholine causing a 25% fall in the maximal mid-inspiratory flow [PD(25)MIF(50)]), and the provocative dose of methacholine causing five or more coughs (PDcough) were serially assessed. One month after patients underwent MRT, there were significant decreases in PD(10) (mean [+/- SEM], 2,583 +/- 414 microg to 1,512 +/- 422 microg, respectively; p < 0.05), PD(25)MIF(50) (mean 2,898 +/- 372 microg to 1,340 +/- 356 microg, respectively; p < 0.05), and PDcough (mean 3,127 +/- 415 microg to 1,751 +/- 447 microg; p < 0.05), which were independent of the decrease in FEV(1) and reversed within 6 months in all patients but three. Six months after undergoing MRT, four patients showed radiation-induced lung injury (RI) on chest radiographs, which subsequently evolved into fibrosis. These patients had greater decreases in vital capacity, FEV(1), MIF(50), and methacholine thresholds than those without RI, and this persisted up to 2 years after they had undergone MRT. One year after the patients underwent MRT, a close relationship was found overall between the change in FEV(1) and those in both PD(10) (r = 0.733; p = 0.004) and PD(25)MIF(50) (r = 0.712; p = 0.006). CONCLUSIONS: : MRT triggers an early transient increase in airway responsiveness, which reverses spontaneously. In patients with RI, the persistence of airway dysfunction long after undergoing MRT may depend on airway remodeling from radiation fibrosis.
Exhaled nitric oxide in systemic sclerosis: relationships with lung involvement and pulmonary hypertension.
OBJECTIVE: To measure nitric oxide (NO) concentration in exhaled air of patients with systemic sclerosis (SSc) and to investigate its relationships with lung involvement, complicated or not by pulmonary hypertension (PH). METHODS: Exhaled NO was measured by chemiluminescence in 47 patients with SSc (16 with PH) and in 30 controls. All the patients underwent Doppler echocardiography to assess pulmonary artery pressure (PAP), lung function tests, and thin section computed tomographic scans of the lung to quantify the extent of fibrosing alveolitis. RESULTS: Exhaled NO levels were higher in patients with SSc (16.6 +/- 9.1 ppb), particularly those with interstitial lung disease (ILD) (18.3 +/- 10.4 ppb), compared to controls (9.9 +/- 2.9 ppb; p < 0.0001). In patients with PH, exhaled NO was less than in patients without PH (10.7 +/- 5.9 vs 19.6 +/- 9 ppb, respectively; p < 0.001), and patients with PH without ILD had even lower exhaled NO than patients with PH and ILD (6.6 +/- 1.1 vs 12.6 +/- 6.3 ppb; p = 0.004). There was an inverse correlation between PAP and exhaled NO (r = 04).53, p = 0.004). Exhaled NO was not correlated to age, disease duration, current therapy, or form of disease (limited or diffuse). CONCLUSION: The increased concentration of exhaled NO in patients with SSc may reflect respiratory tract inflammation. The relatively low value of exhaled NO in patients with PH and the negative correlation between PAP and exhaled NO suggest the important role of NO in regulating pulmonary vascular resistance in patients with SSc.
Edentulism and worsening of obstructive sleep apnoea.
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Exhaled nitric oxide and impaired oxygenation in cirrhotic patients before and after liver transplantation.
BACKGROUND: Nitric oxide may be involved in the impaired oxygenation of cirrhotic patients, a condition that improves in most patients after liver transplantation. OBJECTIVE: To compare oxygenation and nitric oxide concentrations before and after liver transplantation. DESIGN: Before-and-after observational study. SETTING: Academic medical center. PATIENTS: 18 patients with cirrhosis and no obvious cardiopulmonary disease who underwent successful orthotopic liver transplantation. INTERVENTION: Orthotopic liver transplantation. MEASUREMENTS: Blood gas analysis, measurement of exhaled nitric oxide, contrast-enhanced echocardiography, and pulmonary function tests. RESULTS: Before transplantation, the mean (+/- SD) exhaled nitric oxide concentration was higher in patients than in normal controls (13 +/- 4.9 parts per billion [ppb] compared with 5.75 +/- 1.9 ppb; P < 0.001). After transplantation, the alveolar-arterial oxygen gradient significantly decreased (from 17.3 +/- 7.1 mm Hg to 9 +/- 5.2 mm Hg; P < 0.001), as did the exhaled nitric oxide concentration (from 13 +/- 4.9 ppb to 6.2 +/- 2.8 ppb; P < 0.001). The decrease in the exhaled nitric oxide concentration was significantly correlated with the decrease in the alveolar-arterial oxygen gradient (r = 0.56; P = 0.014). Five patients met the criteria for the diagnosis of the hepatopulmonary syndrome before transplantation; the syndrome was cured by transplantation. CONCLUSIONS: The correlation between the decrease in exhaled nitric oxide concentration after liver transplantation and the improvement in oxygenation reinforces the hypothesis that nitric oxide is an important mediator of impaired oxygenation in patients with cirrhosis.
Exhaled nitric oxide and pulmonary response to iloprost in systemic sclerosis with pulmonary hypertension.
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Extrathoracic airway dysfunction in cough associated with gastroesophageal reflux.
BACKGROUND: Cough associated with gastroesophageal reflux (GER) may originate in extrathoracic airway receptors made hypersensitive by acid-induced mucosal injury. OBJECTIVE: We investigated the role of laryngeal disease and dysfunction in the pathogenesis of GER-associated cough in nonasthmatic patients. METHODS: Seven patients with GER-associated cough were compared with 7 patients with GER but no cough. The patients underwent fiberoptic endoscopy for assessment of laryngitis and esophagitis (expressed by scores); esophageal manometry; 24-hour pH monitoring; lung function tests; and histamine inhalation challenge with assessment of bronchial threshold (concentration provoking 10% fall in FEV1 [PC10]), extrathoracic airway threshold (concentration provoking 25% fall in the maximal midinspiratory flow [PC25MIF50]), and cough threshold (concentration provoking 5 or more coughs PCcough). The patients were reevaluated after 3 months of medical treatment for GER. RESULTS: Patients with cough, compared with those without cough, had significantly higher laryngitis scores (P = .002), lower esophageal sphincter pressures, longer time with pH below 4 (P = .003), greater number of episodes of reflux longer than 5 minutes (P = .016), longer esophageal clearance time (P = .048), and significantly lower PC25MIF50 (P = .005) and PCcough (P = .008) values. Laryngitis score was significantly inversely related to either PCcough (P < .001) or PC25MIF50 (P <.01) but not to PC10. Laryngitis score, PC25MIF50, and PCcough were all closely related to GER severity. After GER treatment, laryngitis, PC25MIF50, and PCcough were all significantly improved. CONCLUSIONS: These findings suggest that GER-associated cough is strongly associated with laryngeal disease and dysfunction consequent to acid reflux injury in nonasthmatic patients.
Damage of the pharyngeal mucosa and hyperresponsiveness of airway in sinusitis.
BACKGROUND: In sinusitis bronchoconstriction is supposed to originate from pharyngobronchial reflexes triggered by seeding of the inflammatory process into the pharynx. OBJECTIVE: Our aim was to evaluate whether in sinusitis bronchial and extrathoracic airway (EA) dysfunction correlate with morphologic abnormalities of the pharyngeal mucosa. METHODS: We performed histamine inhalation challenge, nasal lavage, and nasopharyngeal biopsies in 24 nonasthmatic patients with exacerbation of chronic sinusitis. The histamine PC20 was the threshold of bronchial responsiveness, and that causing 25% fall in maximal midinspiratory flow was the threshold of EA responsiveness (PC25MIF50). Thresholds of 8 mg/ml or less were assumed to indicate bronchial hyperresponsiveness (BHR) or EA hyperresponsiveness (EAHR). PC20 and PC25MIF50 values were related to clinical data, nasal lavage fluid eosinophils, pharyngeal epithelium and basement membrane thickness, and density of submucosal vessels and nervous fibers. RESULTS: The PC20 was closely related to PC25MIF50 (p = 0.0004). Ten patients had EAHR, 9 had combined EAHR and BHR, and 5 had neither EAHR nor BHR. EAHR was strongly associated with epithelial thinning, and BHR with long-standing sinusitis, a lower PC25MIF50, increased submucosal nerve density and increased nasal lavage fluid eosinophils. CONCLUSIONS: Our findings suggest that in nonasthmatic patients with sinusitis, pharyngeal damage may contribute to airway dysfunction by favoring the access of irritants to submucosal nerve endings, with activation of constrictive reflexes to the EA. Proliferation of sensory neurons, consequent to long-lasting pharyngeal inflammation, may cause more severe EA narrowing and activate pharyngobronchial reflexes.