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Biomedical subjects

L Brussino

Publications and source records attributed to L Brussino.

At least 19 recordsLinked to original sources

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.

Adult↗

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.

Adult↗

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.

Aged↗

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.

Adult↗

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.

Adult↗

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↗

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↗

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↗

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↗

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↗

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↗

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↗

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↗