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Biomedical subjects

G Rolla

Publications and source records attributed to G Rolla.

At least 19 recordsLinked to original sources
PubMed1992

Bronchial responsiveness, oscillations of peak flow rate and symptoms in patients with mitral stenosis.

To better characterize airway hyperresponsiveness reported in cardiac patients questionnaire-recorded symptoms, bronchial responsiveness to methacholine (Mch) and to ultrasonically nebulized distilled water (UNDW), diurnal oscillations of peak expiratory flow (PEF) rate were evaluated in 32 patients with moderate mitral stenosis. Twenty patients were responsive to Mch (defined as provocative dose producing a 20% fall in forced expiratory volume in one second (PD20 FEV1) less than 3.2 mg) (geometric mean PD20 FEV1 851 +/- 154 micrograms SE). Only two patients showed a fall in FEV1 greater than 20% after UNDW challenge. Patients responsive to Mch challenge had lower FEV1 as percentage of vital capacity (FEV1/VC) (80 +/- 4.8 vs 83 +/- 3.8%, p less than 0.05), higher coefficient of variation of PEF (CV-PEF) (7.1 +/- 2.8 vs 5 +/- 2.4, p less than 0.05) and higher prevalence of wheeze (70 vs 25%, p less than 0.05) in comparison with patients non-responsive to Mch challenge. CV-PEF was significantly related to FEV1 (r = 0.347, p less than 0.05) and maximal expiratory flow at 50% expired volume (MEF50) (r = 0.405, p less than 0.05). The probability of responding to Mch bronchial challenge increased proportionally with the increase in CV-PEF and the decrease in FEV1, FEV1/VC and MEF50. Airway hyperresponsiveness of patients with mitral stenosis seems to be more similar to that reported in bronchitic than in asthmatic patients.

Adult↗
PubMed1991

Histamine hyperresponsiveness of the extrathoracic airway in patients with asthmatic symptoms.

Functional abnormalities of the extrathoracic airway (EA) may produce symptoms mimicking bronchial asthma. We assessed the bronchial (B) and EA responsiveness to inhaled histamine in 40 patients with asthmatic symptoms and in nine asymptomatic controls. FEV1 and maximal mid-inspiratory flow (MIF50) were used as index of bronchial and EA narrowing. Hyperresponsiveness of the intra-(BHR) or extra-(EA-HR) thoracic airway was diagnosed when the provocative concentrations of histamine (PC20FEV1 or PC25MIF50) were less than 8 mg/ml. Fiberoptic laryngoscopy was performed in nine patients and three controls. The glottal region was measured at mid-volume of maximal inspiration (AgMI) and expiration (AgME) before and after histamine. Predominant EA-HR was found in 13 patients, predominant BHR in 12, equivalent BHR and EA-HR in another 12; no significant airway narrowing was observed in three patients and in the nine controls. EA-HR was significantly associated with female sex, sinusitis, post-nasal drip, dysphonia; BHR with atopy, wheezing and lower MEF50. The percent change in AgMI after histamine was closely related to the PC25MIF50 (r = 0.87, P less than 0.001), that of AgME to the PC20FEV1 (r = 0.78, P less than 0.01). These findings suggest that the assessment of EA responsiveness may be useful in the evaluation of asthmatic symptoms, especially in patients with no BHR.

Asthma↗
PubMed1991

Reduction of bronchial responsiveness to methacholine after mitral valve replacement.

Sixteen patients with mitral valve disease, in whom bronchial hyperresponsiveness to methacholine had been detected shortly before mitral valve replacement (MVR), were reevaluated 35 +/- 1.5 months after MVR. In 9/16 patients there was a significant (greater than 1.5 fold) increase in bronchial provocation dose of methacholine (PD20FEV1) after MVR. In the same patients there was a significant increase in vital capacity (from 69.6 +/- 5 to 75.8 +/- 5.2% of predicted, p less than 0.01), a significant decrease in cardiothoracic ratio and in radiologic score for lung edema (from 64.3 +/- 2.9 to 56 +/- 2.1, p less than 0.01 and from 38 +/- 4.5 to 14.6 +/- 2, p less than 0.001, respectively). In all the patients the increase in PD20FEV1 was not related to any change in spirometric values but it was related to the decrease in cardiothoracic index (r = 0.72, p less than 0.01) and in radiologic score for lung edema (r = 0.61, p less than 0.05) observed after cardiosurgery.

Bronchial Provocation Tests↗
PubMed1990

Hyperresponsiveness of the extrathoracic airway in patients with captopril-induced cough.

It has been suggested that cough from captopril may originate from an increased sensitivity of receptors in the extrathoracic airway (EA). To explore this hypothesis, we assessed the responsiveness of EA and bronchi and the cough sensitivity to inhaled histamine in nine hypertensive patients with captopril-induced cough (group 1) during treatment and one month after withdrawal of the drug treatment. Nine patients who were asymptomatic while receiving captopril (group 2) and nine patients receiving no current treatment (group 3) served as controls. The EA responsiveness was assessed by using the maximal midinspiratory flow (MIF50) as an arbitrary index of EA constriction and was expressed as the histamine concentration causing a 25 percent decrease in MIF50 (PC25MIF50). PC15FEV1 was the index of bronchial responsiveness and PCcough (dose causing five or more coughs) was that of cough sensitivity. Airway hyperresponsiveness (EA-HR or BHR) was diagnosed when PC25MIF50 or PC15FEV1 were 8 mg/ml or lower. Patients with captopril-cough, as compared with controls, had significantly lower values of PC25MIF50, PC15FEV1, and PCcough; EA-HR and BHR were found, respectively, in seven and three of these patients and in none of the control subjects. In all the patients of group 1, cough and EA-HR resolved after withdrawal of captopril treatment, while BHR persisted in one. PC25MIF50, PC15FEV1, and PCcough were all significantly improved. Our findings suggest that cough during captopril therapy may originate from receptors in the EA.

Bronchial Provocation Tests↗
PubMed1990

Hypomagnesemia in chronic obstructive lung disease: effect of therapy.

In 95 patients with severe chronic airway obstruction (FEV1 33.2 +/- 12% of predicted; mean +/- SE), we investigated whether drug therapy had any influence on serum Mg levels. 11/95 patients had a serum Mg less than 1.45 mEq/l (lower normal limit). Multiple-regression analysis showed that the use of diuretics was associated with a significantly lower serum Mg level (1.59 +/- CI 0.06 mEq/l vs. an adjusted mean of 1.71 mEq/l; F = 11, 2, p less than 0.001). There was a significant negative correlation between serum Mg and the length of oral steroid therapy (1.64 +/- CI 0.02 mEq/l for less than 24 months of therapy vs. 1.52 +/- CI 0.06 mEq/l for greater than 24 months of therapy; F = 7, 3, p less than 0.005). No effect of theophylline, inhaled steroids or beta 2-agonists on serum Mg was observed. Because of potential negative effects of hypomagnesemia on respiratory function, routine serum magnesium determination is recommended in patients with chronic obstructive lung disease taking diuretic drugs or corticosteroids.

Administration, Inhalation↗
PubMed1990

Bronchial responsiveness in patients with mitral valve disease.

Bronchial responsiveness has been evaluated in patients with chronic lung congestion secondary to mitral valve disease. Methacholine bronchial challenge was performed by intermittent aerosol generation in 31 patients with mitral valve disease, 18 in New York Heart Association (NYHA) Class II and 13 in NYHA Class III, non-atopic and with baseline forced expiratory volume in one second/vital capacity (FEV1/VC) greater than 85% of predicted and in 30 normal controls. Haemodynamic data were available in 17 patients. The methacholine bronchial provocation dose causing a 35% fall of airway conductance (PD35sGaw) was significantly lower in patients (507 +/- C.I. 205 micrograms) than in normals (2779 +/- C.I. 358 micrograms), (p less than 0.001). In patients log PD35sGaw was significantly correlated with mean pulmonary artery pressure (r = 0.53, p less than 0.05), mean pulmonary capillary wedge pressure (r = 0.67, p less than 0.01), but not with any spirometric parameters. Bronchial hyperresponsiveness seems to be common in patients with mitral valve disease and evidence of lung congestion.

Bronchial Provocation Tests↗
PubMed1989

Hypomagnesemia and bronchial hyperreactivity. A case report.

In a 37-year-old woman, a heavy smoker and an alcoholic, bronchial hyperreactivity to histamine (PC20 FEV1 0.8 mg/ml) was related to hypomagnesemia (0.55 mmol/l). After acute magnesium repletion (24 h i.v. infusion MgSO4 6 g, serum magnesium 1.05 mmol/l), histamine PC20 FEV1 increased up to 9.8 mg/ml. The role of magnesium in modulating smooth muscle contractility is discussed and the importance of checking serum magnesium in patients with airway obstruction is suggested.

Adult↗
PubMed1989

Effect of ascorbic acid on increased bronchial responsiveness during upper airway infection.

We investigated the acute effect of ascorbic acid on histamine bronchial responsiveness (PC 20: concentration causing a 20% fall in FEV1) in 9 hospital staff members with upper respiratory tract infection (URI) and cough. Subjects were examined within 5 days from the start of illness and 6 weeks after. On day 1, the reproducibility of PC20 was assessed by 2 consecutive inhalation challenges 1 h apart; the two values were closely related (r = 0.96, p less than 0.001). Five subjects had bronchial hyperresponsiveness (PC20 less than 8 mg/ml histamine). On the following day, PC20 was measured before and 1 h after oral intake of 2 g ascorbic acid. Vitamin C produced a significant increase in average PC20 (p less than 0.01) from 7.8 +/- (SE) 1.2 to 25.1 +/- (SE) 1.2 mg/ml. None had airway hyperresponsiveness after treatment. Six weeks after the onset of URI, bronchial responsiveness was normal in all the subjects but one. The mean PC20 was 15.5 +/- (SE) 1.25 mg/ml, significantly higher than during URI (p less than 0.05); after ascorbic acid it increased nonsignificantly to 25.7 +/- (SE) 1.35 mg/ml. Our results indicate that vitamin C inhibits the transient increase in bronchial responsiveness occurring in otherwise normal subjects during URI.

Adult↗
PubMed1989

Mucosal oedema and airway hyperreactivity.

Mucosal oedema and airway hyperreactivity are common features of asthma, in which they seem to share a common pathogenesis, i.e. airway inflammation. The relationship between oedema and hyperreactivity has not yet been properly investigated. Some speculations are advanced, based on the available experimental evidence. Mucosal oedema may amplify bronchial responsiveness by increasing epithelial permeability, by altering airway mechanics, or by stimulating neural pathways. On the other hand, bronchoconstriction may contribute to oedema by increasing hydrostatic pressure in postcapillary venules.

Asthma↗
PubMed1989

Effects of vitamin C on airway responsiveness to inhaled histamine in heavy smokers.

Histamine bronchial threshold, the provocation concentration of histamine causing a 25% fall in maximal expiratory flow at 50% of forced vital capacity from the control value (PC25MEF50), was measured in seven heavy smokers and in seven sex- and age-matched nonsmokers before and one hour after ingestion, double-blind, of vitamin C (2 g) or placebo. Smokers had significantly lower baseline values of serum ascorbate, maximal expiratory flow at 50% of forced vital capacity (MEF50) and PC25MEF50: the latter was negatively related to serum ascorbate (r = -0.85; p less than 0.001). Acute treatment with vitamin C produced a significant decrease in PC25MEF50 in smokers (95% confidence limit (CL) from 4.87-3.36 to 2.91-2.01 mg.ml-1; p = 0.017), whilst it had no effect in nonsmokers. A preliminary open study on the effect of prolonged administration of vitamin C (1 g daily) was performed in smokers. One week of treatment produced a further significant decrease in PC25MEF50 (p less than 0.0001). Our results suggest that in heavy smokers histamine bronchial responsiveness may be attenuated by chronic ascorbate deficiency. In these circumstances, acute and short-term treatment with vitamin C may increase the bronchoconstrictive response to inhaled histamine.

Adult↗
PubMed1988

A freeze-fracture study of human bronchial epithelium in normal, bronchitic and asthmatic subjects.

Tight junctions (TJ) play a major role in maintaining the integrity of epithelia. Damage of conducting airway surface epithelium is commonly observed in asthma, and recent data suggest that epithelial cells modulate airway smooth muscle tone by the production of relaxant factor(s). To evaluate the ultrastructure of tight junctions (TJ) in human bronchial epithelium of normal and diseased lung, biopsy samples were obtained by fiberoptic bronchoscopy in three normal healthy subjects, four asthmatic patients with bronchial hyperreactivity to methacholine and one heavy smoker with chronic bronchitis. Specimens were examined by electron microscopy, using both thin sections and freeze-fracture techniques. In normal subjects two types of TJ were identified, based on 27 type I, 23 type II junctional areas. Epithelium from the patient with chronic bronchitis showed extensive mucous metaplasia and only junctions of the second type. Extensive epithelial damage was detected in asthmatic subjects, so that a few TJ could be found. Varying degrees of TJ abnormalities were observed and the possible role of such ultrastructural derangements was discussed.

Adult↗
PubMed1988

Acute effect of intravenous magnesium sulfate on airway obstruction of asthmatic patients.

The bronchodilating effect of magnesium sulfate (MgSO4) was studied in ten asthmatic patients with moderate to severe airway obstruction. Two grams of MgSO4 or saline in double-blind crossover design was administered IV for 20 minutes (0.40 mmol/min) and forced expiratory capacity and forced expiratory volume in one second (FEV1) were studied at intervals. Only at the end of MgSO4 infusion did FEV1 increase significantly (109% of initial values). The bronchodilating effect was short lasting and far less than that observed after salbutamol.

Adult↗
PubMed1988

Dose-related effect of inhaled magnesium sulfate on histamine bronchial challenge in asthmatics.

The effects of various doses of inhaled MgSO4 on the histamine bronchoprovocation test were studied in nine asthmatics in clinical remission (FEV1 greater than 80% of predicted). The minimal effective dose of MgSO4 was 0.20 mmol, which increased the dose of histamine which produced a 20% decrease in control FEV1 (PD20) from 2.88 +/- 1.4 to 5.62 +/- 1.38 mumol, p less than 0.05. A greater increase of histamine PD20 was observed after inhalation of MgSO4 at 0.40 mmol (6.90 +/- 1.6 mumol of histamine, p less than 0.05 in comparison with baseline PD20). The decrease in bronchial hyper-reactivity produced by MgSO4 suggests that it influences smooth muscle contractility and may prove to be clinically important in the treatment of asthma.

Adolescent↗