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Biomedical subjects

R Duranti

Publications and source records attributed to R Duranti.

At least 55 records · Page 3Linked to original sources
PubMed1996

Role of sputum differential cell count in detecting airway inflammation in patients with chronic bronchial asthma or COPD.

BACKGROUND: Sputum may provide an alternative source of bronchial cells to investigate characteristics of airway inflammation and its functional correlates in patients with asthma or chronic obstructive pulmonary disease (COPD). METHODS: Two groups of clinically stable patients were studied: a group of 43 patients with mild or moderate asthma and a group of 18 patients with COPD. Twenty normal subjects formed a control group. Sputum production was either spontaneous or induced with inhaled hypertonic saline for five minute periods for up to 20 minutes. The concentration of saline was increased at intervals of 10 minutes from 3% to 4%. Plugs from the lower respiratory tract were selected for differential counting in cytocentrifugation preparations. Bronchial provocation tests were performed by inhaling progressive concentrations of histamine from a DeVilbiss 646 nebuliser and the concentration of histamine which caused a 20% fall in the forced expiratory volume in one second (FEV1) was calculated (PC20FEV1). RESULTS: Neutrophils predominated in the sputum of subjects with COPD while eosinophils predominated in the sputum of those with chronic asthma. However, in 28% of asthmatic subjects an increased percentage of neutrophils was found. In asthmatic patients the differential count of eosinophils was inversely related to the FEV1, FEV1/VC, and bronchial hyperresponsiveness, and directly related to clinical scores. CONCLUSIONS: The cellular profile of sputum in normal subjects and in patients with asthma and COPD is different. The concentration of eosinophils in the sputum correlates with the severity of asthma.

Adolescent↗
PubMed1996

Breathing pattern and carbon dioxide retention in severe chronic obstructive pulmonary disease.

BACKGROUND: The factors leading to chronic hypercapnia and rapid shallow breathing in patients with severe chronic obstructive pulmonary disease (COPD) are not completely understood. In this study the interrelations between chronic carbon dioxide retention, breathing pattern, dyspnoea, and the pressure required for breathing relative to inspiratory muscle strength in stable COPD patients with severe airflow obstruction were studied. METHODS: Thirty patients with COPD in a clinically stable condition with forced expiratory volume in one second (FEV1) of < 1 litre were studied. In each patient the following parameters were assessed: (1) dyspnoea scale rating, (2) inspiratory muscle strength by measuring minimal pleural pressure (PPLmin), and (3) tidal volume (VT), flow, pleural pressure swing (PPLsw), total lung resistance (RL), dynamic lung elastance (ELdyn), and positive end expiratory alveolar pressure (PEEPi) during resting breathing. RESULTS: Arterial carbon dioxide tension (PaCO2) related directly to RL/PPLmin, and ELdyn/PPLmin, and inversely to VT and PPLmin. There was no relationship between PaCO2 and functional residual capacity (FRC), total lung capacity (TLC), or minute ventilation. PEEPi was similar in eucapnic and hypercapnic patients. Expressing PaCO2 as a combined function of VT and PPLmin (stepwise multiple regression analysis) explained 71% of the variance in PaCO2. Tidal volume was directly related to inspiratory time (TI), and TI was inversely related to the pressure required for breathing relative to inspiratory muscle strength (PPLsw, %PPLmin). There was an association between the severity of dyspnoea and both the increase in PPLsw (%PPLmin) and the shortening in TI. CONCLUSIONS: The results indicate that, in stable patients with COPD with severe airflow obstruction, hypercapnia is associated with shallow breathing and inspiratory muscle weakness, and rapid and shallow breathing appears to be linked to both a marked increase in the pressure required for breathing relative to inspiratory muscle strength and to the severity of the breathlessness.

Aged↗
PubMed1995

Comparative effects of plasma exchange and pyridostigmine on respiratory muscle strength and breathing pattern in patients with myasthenia gravis.

BACKGROUND: Pyridostigmine, an acetylcholinesterase antagonist, is useful in improving respiratory function in patients with myasthenia gravis. More recently, plasma exchange has been employed in myasthenia gravis because it acts presumably by removal of circulating antibodies against acetylcholine receptors. Surprisingly, comparative data on the effects of pyridostigmine and plasma exchange on lung volumes, respiratory muscle strength, and ventilatory control system in patients with myasthenia gravis are lacking. METHODS: Nine consecutive patients with grade IIb myasthenia gravis were studied under control conditions and after a therapeutic dose of pyridostigmine. In a second study the patients were re-evaluated a few days after a cycle of plasma exchange, before taking pyridostigmine. In each subject pulmonary volumes, inspiratory (MIP) and expiratory (MEP) muscle force, and respiratory muscle strength, calculated as average MIP and MEP as percentages of their predicted values, were measured. The ventilatory control system was evaluated in terms of volume (tidal volume, VT) and time (inspiratory time, TI, and total time, TTOT) components of the respiratory cycle. Mean inspiratory flow (VT/TI)--that is, the "driving"--and TI/TTOT: that is, the "timing"--components of ventilation were also measured. RESULTS: In each patient treatment relieved weakness and tiredness, and dyspnoea grade was reduced with plasma exchange. Following treatment, vital capacity (VC) increased on average by 9.7% with pyridostigmine and by 14% with plasma exchange, and MIP increased by 18% and 26%, respectively. In addition, with plasma exchange but not with pyridostigmine forced expiratory volume in one second (FEV1) increased by 16% and MEP increased by 24.5%, while functional residual capacity (FRC) decreased a little (6.8%). The change in respiratory muscle strength was related to change in VC (r2 = 0.48). With plasma exchange, VT increased by 18.6% and VT/TI increased by 13.5%, while neither TI nor TI/TTOT changed. CONCLUSIONS: Plasma exchange can be used in patients with myasthenia gravis when symptoms are not adequately controlled by anticholinesterase agents. Plasma exchange increases respiratory muscle force and tidal volume due to changes in "driving" but not "timing" of the respiratory cycle.

Adult↗
PubMed1995

Mechanical loading and control of breathing in patients with severe chronic obstructive pulmonary disease.

BACKGROUND: High neural drive to the respiratory muscles and rapid and shallow breathing are frequently observed in patients with chronic obstructive pulmonary disease (COPD), and both mechanical and chemical factors are thought to play a part. However, the interrelation between these factors and the modifications in the control of breathing are not clearly defined. The effects of an acute decrease in mechanical load by the administration of a high dose of a beta 2 agonist were studied. METHODS: Nine spontaneously breathing patients with severe COPD took part in the study. Criteria for entry were FEV1 of < 40% of predicted and an improvement in FEV1 of < 200 ml after inhalation of 400 micrograms fenoterol. The following parameters were measured: lung volumes, tidal volume (VT), respiratory frequency (Rf), maximal pleural pressure during a sniff manoeuvre (PPLmax), pleural pressure swings (PPLsw), lung resistance (RL), RL/PPLmax ratio, and surface electromyographic activity (EMG) of diaphragm (EDI) and parasternal (EPS) muscles. Arterial oxygen saturation (SaO2), end tidal carbon dioxide pressure (PETCO2), and the electrocardiogram were also monitored. Each variable was measured under control conditions and 20 and 40 minutes after the inhalation of 800 micrograms fenoterol. In five patients the effects of placebo were also studied. RESULTS: Fenoterol resulted in an increase in FEV1 and decrease in FRC. SaO2 did not change, while PETCO2 fell and heart rate increased. The VT increased, and Rf decreased, PPLsw fell and PPLmax increased, thus the PPLsw/PPLmax ratio fell. Both RL and RL/PPLmax also fell, and a substantial decrease in EDI and EPS was observed. Changes in PPLsw were related to changes in FEV1 and RL. Changes in VT and Rf, and EDI/TI and EPS/TI were also related to changes in PPLsw and RL/PPLmax ratio, but not to changes in FEV1. No variation was observed with placebo. CONCLUSIONS: In patients with severe COPD a decrease in inspiratory muscle loading relative to the maximal available strength, as expressed by the RL/PPLmax and PPLsw/PPLmax ratios, appears to be the major determinant of changes in breathing pattern and inspiratory muscle activity (decrease in EMG).

Aged↗
PubMed1995

Control of breathing in patients with limb girdle dystrophy: a controlled study.

BACKGROUND: In patients with limb girdle dystrophy the relative contribution of peripheral factors (respiratory muscle weakness, and lung and/or airway involvement) and central factors (blunted and/or inadequate chemoresponsiveness) in respiratory insufficiency has not yet been established. To resolve this, lung volumes, arterial blood gas tensions, respiratory muscle strength, breathing pattern and neural respiratory drive were investigated in a group of 15 patients with limb girdle dystrophy. An age-matched normal group was studied as a control. METHODS: Respiratory muscle strength was assessed as an arithmetic mean of maximal inspiratory (MIP) and expiratory (MEP) pressures. Breathing pattern was evaluated in terms of volume (ventilation VE, tidal volume VT) and time (respiratory frequency Rf, inspiratory time TI, expiratory time TE) components of the respiratory cycle. Neural respiratory drive was assessed as the mean inspiratory flow (VT/TI), mouth occlusion pressure (P0.1) and electromyographic activity (EMG) of the diaphragm (EMGd) and the intercostal parasternal (EMGp) muscles. In 10 of the 15 patients the responses to carbon dioxide (PCO2) stimulation were also evaluated. RESULTS: Most patients exhibited a moderate decrease in vital capacity (VC) (range 37-87% of predicted), MIP (range 23-84% of predicted), and/or MEP (range 13-41% of predicted). The arterial carbon dioxide tension (PaCO2) was increased in three patients breathing room air, while PaO2 was normal in all. Compared with the control group Rf was higher, and VT, TI and TE were lower in the patients. EMGd and EMGp were higher whilst VT/TI and P0.1 were normal in the patients. Respiratory muscle strength was inversely related to EMGd and EMGp. PaCO2 was found to relate primarily to VC and duration of illness, but not to respiratory muscle strength. During hypercapnic rebreathing delta VE/delta PCO2, delta VT/delta PCO2, and delta P0.1/delta PCO2 were lower than normal, whilst delta EMGd/delta PCO2 and delta EMGp/delta PCO2 were normal in most patients. A direct relation between respiratory muscle strength and delta VT/delta PCO2 was found. CONCLUSIONS: The respiratory muscles, especially expiratory ones, are weak in patients with limb girdle dystrophy. Reductions in respiratory muscle strength are associated with increased neural drive and decreased ventilatory output (delta VT/delta PCO2). The decrease in VC, together with the duration of disease, influence PaCO2. VC is a more useful test than respiratory muscle strength for following the course of limb girdle dystrophy.

Adult↗
PubMed1995

Carbon dioxide responsiveness in COPD patients with and without chronic hypercapnia.

To ascertain whether and to what extent the reduced ventilatory response to a hypercapnic stimulus in chronic obstructive pulmonary disease (COPD) patients depends on a blunted chemoresponsiveness of central origin or to mechanical impairment, we studied two groups of COPD patients without (group A) and with (group B) chronic hypercapnia, but with similar degrees of airway obstruction and hyperinflation. The study was performed on 17 patients (9 normocapnic and 8 hypercapnic). Six age-matched normal subjects (group C) were also studied as a control. During a CO2 rebreathing test, ventilation (VE), mouth occlusion pressure (P0.1), and the electromyographic activity of diaphragm (Edi) were recorded and then plotted against end-tidal carbon dioxide tension (PCO2). Inspiratory muscle strength was significantly lower in the hypercapnic group (group B) compared to normocapnic group (A), and in these groups compared to the control group (C). Both patient groups exhibited significantly lower delta VE/delta PCO2 than the control group. In hypercapnics, delta P0.1/delta PCO2 was significantly lower than in normocapnics and control group, whilst mouth occlusion pressure as % of maximal inspiratory pressure delta P0.1 (% MIP)/delta PCO2 did not differ significantly among the three groups. delta Edi/delta PCO2 increased from C to A. At a PCO2 of 8.65 kPa, VE was similar in the normocapnic and control group, but lower in hypercapnics; Edi was similar in hypercapnic and control group; but greater in normocapnics. P0.1(% MIP) did not differ significantly among groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Control of breathing in a subset of patients with systemic lupus erythematosus.

BACKGROUND: Inspiratory muscle weakness and abnormalities in breathing pattern and in respiratory drive have been reported in patients with multisystem disorders. In patients with systemic lupus erythematosus (SLE), data on respiratory muscle strength and control of breathing are scarce. METHODS: We studied a subset of nine female patients with SLE with no major findings of cardiovascular, renal, or neurologic involvement, and with a normal routine chest radiograph. An age- and sex-matched normal group was also studied as a control. We evaluated lung volumes, diffusing lung properties (TLCO, TLCO/VA), maximal inspiratory (MIP) and expiratory (MEP) pressures, end-tidal carbon dioxide tension (PCO2), and breathing pattern: ventilation (VE), tidal volume (VT), inspiratory time (TI), and respiratory frequency (Rf). Neural respiratory drive, assessed in terms of mean inspiratory flow (VT/TI), mouth occlusion pressure (P0.1), and surface electromyographic activity of the diaphragm (Edi) and intercostal (Eps) muscles was also evaluated. RESULTS: As a whole, patients exhibited mild decrease in MIP; vital capacity was slightly reduced in two patients and TLCO/VA was moderately reduced in three. During a hypercapnic rebreathing test, delta VT/delta PCO2 was lower, delta P0.1/delta PCO2 was normal, while delta Edi/delta PCO2 and delta Eps/delta PCO2 were higher in patients compared with normal control subjects. delta VT/delta PCO2 significantly related to MIP. At 60 mm Hg of PCO2 patients maintained the rapid and shallow pattern of breathing (RSB) exhibited during room-air breathing: lower VT, shorter TI, and greater Rf, with VE, VT/TI, and Edi being greater compared with the normal control subjects. CONCLUSIONS: These data seem to indicate that in this SLE subset, mild decrease in respiratory muscle strength may accompany an increased respiratory drive, and contribute to a qualitatively abnormal ventilatory response (RSB) to carbon dioxide stimulation.

Adult↗
PubMed1995

Effects of the iron lung on respiratory function in chronic hypercapnic COPD patients.

Whether or not short-term negative pressure ventilation (NPV) improves respiratory function by decreasing the drive to the respiratory muscles in hypercapnic chronic obstructive pulmonary disease (COPD) patients remains to be defined. In six severely obstructed hypercapnic COPD patients (Group A) with grade IV dyspnoea (modified Medical Research Council (MRC) dyspnoea scale), we evaluated pulmonary volumes, arterial blood gases, the pattern of breathing (tidal volume (VT) and respiratory frequency (Rf)) and the neuromuscular respiratory drive (NMRD), before and immediately after a 7 day period with the iron lung (IL). NMRD was assessed by expressing mouth occlusion pressure (P0.1) recorded during quiet breathing as a percentage of maximal P0.1 recorded during exogenous CO2 stimulation (P0.1 max,CO2). A group of six hypercapnic, less dyspnoeic (grade II to III) COPD patients (Group B), with similar mechanical characteristics, and another less obstructed historically normocapnic control group (Group C) were also considered. Before IL, in Group A VT was lower than in C, and P0.1 (%P0.1 max,CO2) was greater than in Group B and C. After a 7 day period with IL, VT increased, Rf decreased, and arterial blood gases and dyspnoea grade improved; P0.1 (%P0.1 max,CO2) significantly decreased remaining, however, greater than in Group C. In Group A the time course of arterial carbon dioxide tension (Pa,CO2) and P0.1 (%P0.1 max,CO2) were significantly related to each other. These data seem to indicate that IL is effective in improving respiratory function and symptoms in chronic hypercapnic severely dyspnoeic COPD patients. The observation that these effects were associated with a decrease in NMRD reflects an improved efficiency of the respiratory system. After IL, respiratory function in Group A was similar or even better than that in Group B. This study also considers the possibility of putting severely dyspnoeic hypercapnic COPD patients into an IL trial before starting a traditional rehabilitation programme.

Aged↗
PubMed1994

Histamine induced changes in breathing pattern may precede bronchoconstriction in selected patients with bronchial asthma.

BACKGROUND: In asthmatic patients methacholine or histamine challenge may result in more rapid and shallow breathing. Bronchoconstriction can also be associated with changes in the pattern of breathing. However, few studies, particularly in patients with asthma, have investigated the possibility that changes in the pattern of breathing may precede the onset of bronchoconstriction. METHODS: Eight subjects were selected from 34 consecutive asthmatic patients who had previously exhibited a significant increase in respiratory frequency (Rf) and decrease in tidal volume (VT) accompanying a 20% or greater fall in FEV1 during a histamine bronchial provocation test. These patients also had bronchial hyperresponsiveness (histamine PC20FEV1 0.1-0.25 mg/ml). VT, Rf, and the ratio of VT to Rf were evaluated breath by breath under control conditions and two minutes after inhalation of either saline or each of a series of progressively increasing concentrations of histamine. In each subject the coefficient of variation (CV) for each breathing pattern variable was calculated under control conditions and at each histamine concentration over at least 30-40 breaths. For FEV1, VT and Rf step by step coefficients of variation were averaged and the mean (2SD) CV was considered to represent a threshold value in each patient. RESULTS: Histamine challenge resulted in increased Rf and Rf/VT, and decreased VT and FEV1. In all but one subject change in Rf and Rf/VT beyond the threshold value preceded change in FEV1 beyond the threshold value. The threshold concentrations of histamine for Rf and Rf/VT did not correlate with the threshold value for FEV1. CONCLUSIONS: In selected asthmatic patients a change in breathing pattern occurs prior to a change in FEV1. These results suggest that narrowing of the airways, in terms of decrease in FEV1, does not play a major part in the initial change in the pattern of breathing. This may be caused by direct stimulation of vagal airway receptors.

Adult↗
PubMed1994

Aminophylline and respiratory muscle interaction in normal humans.

The effects of intravenous infusion of aminophylline on respiratory muscle interaction were examined in seven normal subjects breathing at rest. Rib cage (RC-Ap) and abdominal (AB-Ap) volume displacements, pleural (Ppl), gastric (Pg), and transdiaphragmatic (Pdi) pressure swings, and electromyographic activity of the diaphragm (Edi) and the parasternal (Eps) muscles were measured under control and during infusion of either aminophylline or placebo in a double-blind randomized manner. Compared with placebo, aminophylline induced an increase in ventilation (p < 0.01) that was mainly accounted for by an increase in tidal volume (p = 0.01). Aminophylline induced a significant and similar increase in RC-Ap and AB-Ap as associated with increased Ppl and Pg swings (p = 0.002, and p < 0.01, respectively). On the contrary, no changes in end-expiratory RC and AB volume and in Ppl and Pg at end-expiration were observed, indicating that expiratory muscles did not contribute to the increase in tidal volume. Edi and Eps increased significantly with aminophylline, whereas Pdi/Edi ratio remained unchanged. We conclude that in normal humans breathing at rest: (1) aminophylline increases ventilation, promoting larger tidal volume; (2) this effect is due to increased neural drive to inspiratory muscles; (3) aminophylline does not promote any appreciable expiratory muscle recruitment and distortion in the pattern of chest wall motion.

Adult↗
PubMed1994

Four-week negative pressure ventilation improves respiratory function in severe hypercapnic COPD patients.

Studies on respiratory muscle resting by negative pressure ventilation (NPV) in patients with stable COPD have given conflicting results. Probable explanations lie in criteria of patients' selection, method of NPV application, and lack of supervision of respiratory muscle rest. Thirteen hypercapnic patients with COPD were, therefore, randomly assigned to either a NPV group or a control group. The NPV was applied by an airtight jacket (pneumosuit), 5 h a day, 5 consecutive days a week for 4 weeks. Both NPV group and control group performed in-hospital pulmonary rehabilitation program for a 4-week period. Arterial blood gases, spirometry, maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP), breathing pattern, and electromyogram (EMG) of the diaphragm and parasternal intercostal muscles were measured on the preintervention day, and at the end of the second and fourth weeks of treatment (days 13 and 27, respectively). The short-term effect of NPV on EMG suppression was also checked throughout the ventilatory sessions in three different days (1, 12, and 26, respectively). A 6-min walking test (WT) and level of dyspnea by a modified Borg scale were evaluated on the preintervention and the last days. Negative pressure ventilation resulted in a significant reduction in EMG activity of both diaphragm and parasternal muscles, associated with significant increase in MIP, tidal volume, and ventilation, and increase in PaO2 and decrease in PaCO2. A significant relationship between change in MIP and change in PaCO2 was observed (r = 0.72, p < 0.01). Improve-ment in 6-min WT and dyspnea sensation was also observed, both being the sole changes in the control group. These data seem to indicate a beneficial role of respiratory muscle rest in improving respiratory function. Adequate supervision by personnel familiar with the equipment is likely to contribute to successful treatment.

Action Potentials↗
PubMed1993

Control of breathing in patients with severe hypothyroidism.

PURPOSE: Hypothyroid patients have been reported to have a blunted ventilatory response to carbon dioxide stimulation. However, previous data did not clarify the localization of abnormalities responsible for that disorder. The present investigation was aimed at evaluating to what extent central (neural) and/or peripheral (muscular) factors are involved in the abnormalities of the ventilatory control system in hypothyroid patients. PATIENTS AND METHODS: We studied 13 patients with severe hypothyroidism before and after 6 to 9 months of replacement therapy; 7 age- and sex-matched normal subjects were also studied as a control. In each subject, we assessed (1) inspiratory muscle strength by measuring maximal inspiratory pressure (MIP), and (2) respiratory control system during a carbon dioxide rebreathing test by measuring minute ventilation (VE), tidal volume (VT), mean inspiratory flow (VT/TI), and electromyographic (EMG) activity of the diaphragm (Edi) and intercostal (Eint) muscles. RESULTS: Compared with the normal control group (Group C), patients exhibited similar MIP, and similar VE and EMG response slopes to carbon dioxide. However, evaluating individual VE response slopes, we were able to identify two subsets of patients: Group A (six patients) with low VE response (less than mean -SD.1.65 of Group C) and Group B (seven patients) with normal VE response. Compared with both Groups B and C, Group A exhibited significantly lower VT/TI, Edi, and Eint response slopes; the difference between Groups B and C was not significant. Six patients (two from Group A and four from Group B) exhibited low MIP values compared with that in Group C. After replacement therapy, (1) VE, VT/TI, and Edi response slopes increased significantly in Group A; and (2) MIP increased, but not significantly in patients with low MIP. CONCLUSIONS: We conclude that: (1) In patients with severe hypothyroidism, the ventilatory control system may be altered at the neural level, as indicated by a blunted chemosensitivity; (2) Impaired respiratory muscle function does not seem to play a major role in the decreased ventilatory response to carbon dioxide stimulation; (3) Replacement therapy appears to normalize the response to hypercapnic stimulation, but not respiratory muscle strength.

Adult↗
PubMed1993

Preventive effects of beclomethasone on histamine-induced changes in breathing pattern in asthma.

Bronchial mucosa inflammation is a hallmark of asthma. Epithelial damage due to inflammatory process may contribute to induce a pattern of rapid and shallow breathing (RSB). Probably due to its effects on inflammatory process, beclomethasone dipropionate (BDP) decreases bronchial hypersensitivity (BH), as assessed in terms of histamine concentration causing a 20 percent FEV1 decrease from saline solution (PC20FEV1); however, no data are available on the effect of BDP on RSB. We studied 32 asymptomatic asthmatic subjects with a severe to moderate levels of BH (PC20FEV1 0.01 to 1.7 mg/ml). After they were randomly assigned to one month of either BDP (2 mg daily, 17 patients) or placebo (15 patients), they inhaled progressively doubling concentrations of histamine phosphate by tidal breathing method. With histamine in seven BDP-treated and in five placebo-treated patients, decrease in FEV1 > or = 20 percent from saline solution was paralleled by a significant decrease in tidal volume (VT), inspiratory time (Ti), and expiratory time (Te), and increase in respiratory frequency (RF). In the remaining patients, histamine failed to change the breathing pattern. In the seven RSB patients, BDP resulted in a smaller VT decrease (p < 0.02) and a smaller RF increase (p < 0.02) with histamine. The five RSB placebo-treated patients were then given one month BDP (2 mg daily): inhaled BDP, but not placebo, resulted both in a significant increase in PC20FEV1 and modulation in histamine-induced changes in breathing pattern. We conclude that high doses of BDP seem to be able to modulate histamine-induced RSB, an effect that might be linked to reversal of airway inflammation.

Adolescent↗
PubMed1993

Effects of intravenous broxaterol on respiratory drive and neuromuscular coupling in COPD patients.

Broxaterol, a new selective beta 2-agonist, has been shown to exert inotropic effects on both fresh and fatigued canine diaphragm. We evaluated the effect of broxaterol on the activation and force output of the respiratory muscles in patients with chronic obstructive pulmonary disease (COPD). We studied 9 patients with moderate to severe COPD. Each patient was infused with saline and Broxaterol (200 micrograms) in saline alternately. We measured lung volumes, maximal inspiratory pressure (MIP), maximal expiratory pressure (MEP), breathing pattern, P0.1, respiratory muscle EMG (diaphragm, EMGd, and parasternal, EMGp) and P0.1/EMGd ratio. Measurements were made under control conditions and at 15, 30, 60, and 120 min after each infusion. Broxaterol, but not saline, resulted in a slight but significant increase in vital capacity (VC), forced expiratory volume in one second (FEV1) and MIP, and a decrease in functional residual capacity (FRC). Breathing pattern did not change, while EMG significantly decreased, and P0.1/EMGd significantly increased in 5 of the 9 patients after broxaterol. These data seem to indicate that by partially unloading the respiratory muscles, broxaterol results in decreased muscle activation (EMG). Increase in chest wall neuromuscular coupling (P0.1/EMGd) may also be observed.

Adrenergic beta-Agonists↗
PubMed1993

Control of breathing in patients with neuromuscular diseases.

We reviewed the studies devoted to investigate the control of breathing in patients with neuromuscular diseases. Neural respiratory drive has been assessed in terms of minute ventilation and mouth occlusion pressure (P0.1) in patients with several types of neuromuscular affections (amyotrophic lateral sclerosis, poliomyelitis and post-polio syndrome, Guillain Barré syndrome, muscular dystrophies, inflammatory muscle diseases). More recently we have used electromyographic activity of diaphragm to evaluate neural drive in patients with myasthenia gravis and muscular dystrophies. The results of these studies seem to indicate that patients with myasthenia gravis are not likely to have a decreased respiratory drive, the disorder in neuromuscular transmission being probably the reason for the apparent decrease in diaphragmatic neural activation during hypercapnic stimulation. Increase in neural afferent information from lung and/or rib cage might explain both the increased neural respiratory drive and the faster breathing observed in patients with neuromuscular disease.

Humans↗
PubMed1991

Respiratory responses induced by the activation of somatic nociceptive afferents in humans.

To further investigate the role of somatic nociceptive afferents in the neural control of breathing, we studied the respiratory effects of their activation by means of either electrical stimulation or ischemic pain in 14 healthy volunteers. Painful electrical cutaneous stimulation increased respiratory frequency (f), mean inspiratory flow (VT/TI), and rate of rise (XP/TI) of integrated electromyographic activity of diaphragm (IEMGdi). Painful muscular electrical stimulation caused similar but larger changes accompanied by increases in tidal volume (VT), peak XP of IEMGdi, and ventilation (VE); it also entrained respiratory rhythm. Ischemic pain, which was characterized by a progressively increasing intensity, caused augmentation in respiratory activity that displayed an increasing trend: VE, f, VT, XP, VT/TI, and XP/TI increased. In the light of available literature, it seems conceivable to suggest that respiratory responses to painful electrical stimulation are mediated through the activation of cutaneous (A delta) and muscular (group III) fine-myelinated afferents, and responses to ischemic pain are mediated by the activation of both fine myelinated (group III) and unmyelinated (group IV) muscular afferents. The input conveyed by these afferents may constitute an effective stimulus to respiration in humans.

Adult↗
PubMed1991

Suppression of ventilatory muscle activity in healthy subjects and COPD patients with negative pressure ventilation.

We evaluated the ability of NPV to suppress EMGd and EMGint in seven patients with severe COPD and five normal subjects. Subjects were studied either without (A) or with mouthpiece and nose clip (B). Electromyographic suppression was assessed comparing EMG activity during NPV with the control activity without a mouthpiece and prior to the initiation of the NPV run. In normal subjects, in A, NPV resulted in a partial suppression of EMGd; in B, prior to NPV, EMGd rose compared with A prior to NPV. In patients, in A, NPV resulted in a suppression of both EMGd and EMGint. In B, prior to NPV, both EMGd and EMGint rose compared with A prior to NPV. Thus, it seems that NPV is able to produce a consistent reduction in inspiratory muscle EMG activity. This variable NPV ability would have to be assessed for better selection criteria for patient candidates in a rehabilitation program.

Adult↗