Biomedical subjects

R Duranti

Publications and source records attributed to R Duranti.

At least 73 records · Page 4Linked to original sources

PubMed1990

Inspiratory muscle strength and respiratory drive in patients with rheumatoid arthritis.

In 15 patients with rheumatoid arthritis (RA) and in 12 age- and sex-matched normal subjects, we evaluated inspiratory muscle strength and respiratory control system. Inspiratory muscle strength was assessed by measuring maximal inspiratory pressure (MIP). Respiratory drive was assessed by evaluating surface electromyographic activity of the diaphragm (EMGd) during both room-air breathing and hypercapnic rebreathing. Compared to the predicted value (mean +/- 1.65 SD), MIP was significantly reduced in nine patients (60%). All told, we noticed a significant inverse relationship in the patients between MIP and duration of steroid therapy (p less than 0.01). During room-air breathing, both EMGd and mouth occlusion pressure (P0.1), expressed both in actual values and as percentage of MIP, were significantly greater in patients than in the normal control group (p less than 0.001 for both). Both EMGd and P0.1 (%MIP) response slopes to CO2 were significantly greater in patients than in the normal control group (p less than 0.01 and p less than 0.001, respectively) and significantly related to the functional stage of disease. During quiet breathing and for a PETCO2 of 60 mm Hg, both EMGd (p less than 0.01 and p less than 0.05, respectively) and P0.1 (%MIP) (p less than 0.01 and p = 0.001, respectively) were inversely related to MIP. These results indicate that RA patients may exhibit inspiratory muscle weakness and increased respiratory drive. Steroid myopathy and rheumatoid myositis could explain the reduction in MIP, whereas neural afferents arising from respiratory muscle, lung, or joint receptors could be involved in the observed increase in neural drive.

Arthritis, Rheumatoid↗

PubMed1990

Changes in ventilatory muscle function with negative pressure ventilation in patients with severe COPD.

Patients with severe COPD may be in a state of ventilatory muscle (VM) fatigue. In these patients, rapid and shallow breathing has been hypothesized to be a compensatory mechanism that prevents more severe fatigue from taking place. To test these hypotheses, we studied the effects of VM resting in a group of patients with severe COPD. Eleven clinically stable patients with COPD and chronic hypercapnia were studied. Six of them (group A) had a seven-day period of negative pressure-assisted ventilation (NPV), and five (group B) with similar functional characteristics served as a control group. Compared with a normal age-matched control group, both A and B groups exhibited significantly lower tidal volume (VT), inspiratory time (TI), total time of the respiratory cycle (Ttot) and Ti/Ttot ratio, decrease in muscle strength, and greater electromyographic activity of diaphragm (EMGd) and parasternal muscles, but similar ventilation and VT/TI. After the study period, group A exhibited significant increase in VT, Ti, and TI/Ttot (p less than 0.05), and decrease in PaCO2 (p less than 0.05), EMGd, and EMGint (p less than 0.05 for both), and a slight but significant increase in maximal inspiratory pressure (MIP) (p less than 0.05). These data suggest that NPV rests VM, increases their strength, and reduces hypercapnia in patients with severe COPD.

Aged↗

PubMed1990

Neural respiratory drive and neuromuscular coupling in patients with chronic obstructive pulmonary disease (COPD).

In 15 spontaneously breathing patients with chronic obstructive pulmonary disease (COPD) divided into two groups, one with normocapnia (A) and one with chronic hypercapnia (B), we evaluated the maximal voluntary inspiratory muscle strength (MIP), the pattern of breathing, the mouth occlusion pressure (Po.1), the neural respiratory drive (NRD), assessed by surface electromyographic (EMG) activity of the diaphragm (EMGd) and EMG activity of intercostal muscles (EMGint), and the chest wall neuromuscular coupling, assessed in terms of Po.1/EMGd ratio. Compared with an age-matched normal control group, both A and B groups exhibited lower MIP, significantly greater EMGd and EMGint, and lower Po.1/EMGd ratio. However, a similar pattern, along with a rapid and shallow breathing, differentiated group B from group A. In group B we found a significant direct relationship between Po.1/EMGd ratio and MIP, and an inverse relationship between PaCO2 and Po.1/EMGd ratio. These data seem to indicate the following: (1) EMG is a more precise method than Po.1 in assessing the magnitude of the NRD; (2) NRD is increased in these patients; and (3) clinical manifestations probably associated with inspiratory muscle fatigue (marked decrease in muscle strength, rapid and shallow breathing, and alveolar hypoventilation) may be accompanied by a greater NRD and a more marked derangement in chest wall neuromuscular coupling in COPD.

Aged↗

PubMed1989

Control of breathing in patients with short-term primary hypothyroidism.

In 8 patients (3 men and 5 women) with short-term primary hypothyroidism before and during replacement therapy, and in an age-matched control group (9 men and 7 women), we assessed maximal inspiratory muscle force (Pimax) and the ventilatory control system at neural (EMG), muscular (P0.1), and ventilatory (VE and Vt/Ti) levels. While hypothyroid, patients exhibited a significantly lower Pimax. During a CO2 rebreathing test, hypothyroid patients exhibited similar diaphragmatic electromyographic (EMGd) and ventilatory (VE) response slopes to increasing end-tidal CO2 tension (delta EMGd/delta Pet CO2 and delta VE/delta PetCO2), but significantly less delta P0.1/delta PetCO2 (p less than 0.05) and delta(Vt/Ti)/delta PetCO2 (p less than 0.05) response slopes. During replacement therapy with L-triiodothyronine (L-T3), Pimax (p less than 0.05), delta P0.1/delta PetCO2, and delta(Vt/Ti)/delta PetCO2 response slopes were found to be significantly increased (p less than 0.05 for both) while neither EMGd nor VE response changed significantly. We concluded that short-term hypothyroidism does not seem to be associated with blunted neural inspiratory output (EMGd), the respiratory control system seems to be affected mostly at a peripheral (muscular) level, and L-T3 increases both force (P0.1 and Pimax) and velocity (Vt/Ti) of inspiratory muscle contraction.

Adult↗

PubMed1989

Neural respiratory drive and neuromuscular coupling during CO2 rebreathing in patients with chronic interstitial lung disease.

In 12 patients with CILD and 18 age-matched normal subjects we assessed the ventilatory control system at three levels: (a) neural, as assessed by EMGd (XP/Ti) and EMGint muscles via surface electrodes; (b) muscular, as assessed by mouth occlusion pressure (P0.1); and (c) ventilatory, as assessed by both ventilation (VE) and the related parameters, tidal volume (VT) and respiratory frequency (f). Compared with a normal control group, patients exhibited a significant decrease in lung volumes and in MIP; VT and inspiratory time (Ti) were significantly lower, while VT/Ti, P0.1, and both EMGd and EMGint were significantly greater in patients. During a CO2 rebreathing test, patients exhibited significantly greater EMGd, EMGint, and P0.1 responses to increasing PETCO2 than the control group. VE response slopes were similar in the two groups. For a given EMGd response slope (delta XP/Ti/delta PETCO2), the average P0.1 response slope (delta P0.1/delta PETCO2) was found to be significantly lower in patients than in the normal control group. Compared with normal subjects, CILD patients have a normal or increased neural component of respiratory activity and relatively low neuromuscular coupling (delta P0.1/delta XP/Ti). The decreased neuromuscular coupling could be explained in these patients by a reduced inspiratory muscle strength.

Aged↗

PubMed1988

Increase in muscular pain threshold following low frequency-high intensity peripheral conditioning stimulation in humans.

The effects of low frequency-high intensity transcutaneous and intramuscular electrical nerve stimulation (TENS and IENS, respectively) on ipsilateral muscular pain threshold were studied in healthy volunteers. The combined effects of TENS (or IENS) and vibration as well as the effects of TENS applied to contralateral regions were also investigated. Muscular pain threshold was evaluated by the subjects' verbal reports in response to electrical stimulation (wire electrodes) of the vastus medialis muscle and by the appearance of blink response (startle reaction) without habituation. TENS was generally applied to the skin overlying the same muscle, and in some instances to the skin overlying the contralateral vastus medialis or triceps muscle. IENS was performed through the same electrodes used for inducing muscular pain. Vibration was applied to the tendon of ipsilateral quadriceps femoris muscle. TENS consistently induced marked and long-lasting elevations of ipsilateral muscular pain threshold. Comparable results were obtained by IENS. TENS and vibration performed simultaneously induced increases in muscular pain threshold, which were greater than those obtained with each individual conditioning stimulation. TENS proved to be capable of enhancing muscular pain threshold even when applied to contralateral regions; however, these effects were smaller and of shorter duration. The results provide evidence that low frequency-high intensity TENS (or IENS) are effective in raising muscular pain threshold and support the hypothesis that this type of stimulation brings supraspinal control systems into action through the activation of group III afferent fibres.

Adult↗

PubMed1988

Effects of heterotopic ischemic pain on muscular pain threshold and blink reflex in humans.

Ischemic pain was induced in the left arm of 6 healthy volunteers using a modification of the submaximal effort tourniquet test. Its effects on both muscular pain threshold (determined in the vastus medialis muscle by means of electrical stimulation) and on the 2nd component of the blink reflex (R2) were investigated in the contralateral body side. Muscular pain threshold increased (peak value during ischemic pain) and maintained significantly higher values for 60 min. R2 response decreased while its latency increased; these variations appeared during ischemic pain and reached a maximum soon after the end of ischemia, still remaining significant for 15 min. The results support the suggestion that the analgesic effects of heterotopic noxious stimulation in humans are subserved by supraspinal inhibitory mechanisms.

Adult↗

PubMed1988

Changes in neural drive (EMGd) and neuromuscular coupling during histamine-induced bronchoconstriction in patients with asthma.

This study was undertaken in order to assess the neural drive to the respiratory muscles and the inspiratory neuromuscular coupling in patients with bronchial asthma during histamine-induced bronchoconstriction. Bronchoconstriction was produced in a graded fashion, with histamine phosphate aerosol of increasing dose, in twelve asymptomatic asthmatic patients and was measured by FEV1. Inspiratory drive was measured by electromyographic activity of the diaphragm (EMGd) and the coupling of the neural drive to the respiratory muscles was assessed by the relationship of mouth occlusion pressure (P0.1) to EMGd. During the test we also measured electromyographic activity of the inspiratory intercostal (EMGint), sternomastoid (EMGsm) and expiratory abdominal (EMGab) muscles. Histamine caused a significant decrease in FEV1, a significant increase in P0.1, EMGd, EMGint, and a relevant increase in EMGsm, with no substantial increase in EMGab. An inverse significant relationship between the change in FEV1 and changes in P0.1, EMGd and EMGint and a significant correlation between the change in FEV1 and in the P0.1/EMGd ratio were observed. We conclude that a progressive increase in bronchospasm is accompanied by a progressive increase in respiratory neural drive and decrease in neuromuscular coupling. This could be caused both by an increase in lung volume and a lack of abdominal expiratory muscle recruitment.

Adult↗

PubMed1987

Effects of aminophylline on respiratory drive and neuromuscular coupling in normal man and in patients with chronic airflow obstruction.

In order to evaluate the separate effects of aminophylline on the neural and muscular components of the respiratory control system, assessed by electromyographic activity of the diaphragm (EMGd) and mouth occlusion pressure (P0.1), respectively, 6 normal subjects and 14 patients with mild or moderate chronic airflow obstruction (8 asthmatics and 6 COPD) were studied during CO2 rebreathing, before and after administration of a therapeutic dose of aminophylline 5.6 mg/kg. Compared to normal subjects, before aminophylline administration both asthmatic and COPD patients exhibited a significantly greater value in EMGd response slope to CO2. In no group did aminophylline modify P0.1 or EMGd activity response slope to CO2, nor did it significantly affect neuromuscular coupling, assessed by plotting change in P0.1 against change in EMGd activity with increasing CO2. The data appear to indicate that aminophylline in therapeutic concentrations does not modify respiratory drive or neuromuscular coupling in normal subjects, or in patients with mild or moderate chronic airflow obstruction.

Action Potentials↗

PubMed1987

Effect of inhaled histamine on occlusion pressure and breathing pattern in asthmatic patients.

In animals, histamine inhalation is known to increase either respiratory frequency or respiratory drive by stimulation of airway vagal sensitive endings. However, it is not well known whether these changes are concomitant in man. In order to elucidate this point, we carried out the present investigation in thirty-five asthmatic patients who underwent bronchial provocation test by progressively doubling the dose of inhaled histamine. Bronchial reactivity to histamine allowed two populations of patients to be defined: group I with moderate and group II with mild, increased reactivity. In the twenty-three group I patients, neuromuscular inspiratory drive, assessed by mouth occlusion pressure (P0.1), was found to be significantly increased while no significant changes in breathing pattern were noted. In the twelve group II patients histamine did not modify P0.1 or breathing pattern. However, we were able to separate in group I a sub-group of ten patients, as with atopic asthma, in which histamine-induced increase in P0.1 was paralleled by rapid and shallow breathing (RSB). Changes in P0.1 and breathing pattern did not depend on baseline airway calibre. In group I, after bronchoconstriction had been reversed by inhaling a beta 2-agonist bronchodilator agent (fenoterol), P0.1 decreased significantly and RSB was found to be reversed; however, these changes were not interrelated. We concluded that: in asthmatics, histamine-induced increase in P0.1 is not necessarily paralleled by, nor related with, change in breathing pattern and in atopics a 'sensitization' of vagal receptors could account for the concomitance of enhanced P0.1 with RSB.

Administration, Inhalation↗

PubMed1987

D-Arg1, D-Trp7,9, Leu11-substance P (spantide) does not antagonize substance P-induced hyperexcitability of the nociceptive flexion withdrawal reflex in the rat.

The effect of D-Arg1, D-Trp7,9, Leu11-substance P (SP) (spantide), a putative SP antagonist, on SP-induced facilitation of the flexion reflex was examined. The drugs were injected intrathecally (i.t.) in decerebrate, spinalized, unanaesthetized rats. Substance P (10 ng) caused an increase in reflex magnitude for about 5 min. Spantide (10 ng and 100 ng) also caused a facilitation of the reflex that was similar to SP. Spantide (10 ng) plus SP (10 ng) also had a similar excitatory effect. One microgram of spantide totally blocked the flexion reflex, which could not be reversed by SP, L-glutamate, L-aspartate or naloxone. It is concluded that spantide does not have an antagonistic effect on SP-induced changes in spinal reflex excitability. Some of the effects of i.t. spantide observed in behavioural studies may be due to a non-specific spinal motor block. It is suggested that the flexion reflex in the decerebrate, spinalized rat is a useful physiological model in studies of the effects of algesic and analgesic drugs at spinal level.

Afferent Pathways↗

PubMed1987

Inspiratory impedance during histamine-induced bronchoconstriction in patients with bronchial asthma.

Histamine inhalation provocation tests were performed in 18 asymptomatic asthmatic patients with progressively increasing doses of a pressurized aerosol of histamine phosphate. Forced expiratory volume in 1 s (FEV1), total neuromuscular output, assessed by mouth occlusion pressure (P0.1), mean inspiratory flow (VT/Ti), and the P0.1/(VT/Ti) ratio, which represents an index of effective inspiratory impedance of the respiratory system, were measured. With histamine, compared to control, FEV1 decreased and P0.1/(VT/Ti) increased (p less than 0.01 for both). After bronchoconstriction was reversed by administration of a beta 2-agonist bronchodilator (fenoterol), a significant decrease in P0.1/(VT/Ti) (p less than 0.001) and a significant increase in FEV1 (p less than 0.01) were noted as compared to histamine. With histamine, change in P0.1/(VT/Ti) was found to be related to its pre-histamine value (p less than 0.01). Furthermore, with histamine and fenoterol, changes in P0.1/(VT/Ti) and concurrent changes in FEV1 were found to be significantly related (p less than 0.001). From these data we calculated that the P0.1/(VT/Ti) ratio provides a useful tool in the clinical assessment of histamine-induced bronchospasm.

Adult↗

PubMed1986

Percutaneous microneurography in man does not cause pressure block of almost all axons in the impaled nerve fascicle.

Neural activity from the median nerve was recorded in 5 volunteers with a concentric needle electrode that has two recording surfaces in very close proximity at the tip. The aim of this study was to establish the probability of recording activity in the nerve from both surfaces simultaneously. We wanted to test one aspect of a recent critique of the microneurographic technique (Wall and McMahon, Pain, 21 (1985) 209-229), namely the suggestion that the recording electrode in these types of studies causes pressure block of almost all fibers in the impaled nerve fascicle. In 80% of our experiments it was possible to record neural activity at both surfaces simultaneously. These results indicate that the physiological state of the peripheral nerves during microneurographic explorations is not necessarily highly abnormal due to pressure block of nearly 100% of the nerve fibers close to the recording electrode tip. Our results thus speak against this aspect of the criticism of the microneurographic technique.

Adult↗

PubMed1986

Effects of histamine and reproterol inhalation on mouth occlusion pressure in patients with bronchial asthma.

Both vagal and non-vagal afferences from the lung or chest wall contribute to increasing neural drive to the respiratory muscles, but only the former are known to change the breathing pattern by increasing respiratory frequency (RF) during bronchoconstriction. In order to evaluate the relative contribution of vagal and non-vagal afferences to increasing neural drive to the respiratory muscles in 14 asymptomatic asthmatic patients known to be responsive (decrease in FEV1 greater than 20% of the control values) to previous bronchial provocation test (BPT) with aerosolized histamine, we evaluated FEV1, breathing pattern and neuromuscular drive, as assessed by mouth occlusion pressure (PO.1), under control conditions, during BPT with progressive doubling doses of inhaled histamine (H) and 5 min after inhalation of a bronchodilator agent (Reproterol) (B). During HBPT FEV1 exhibited a significant decrease (p less than 0.01) while PO.1 was found to increase significantly (p less than 0.01). However, no significant changes were noted in breathing pattern. After B FEV1 returned to control values while PO.1, even if significantly reduced (p less than 0.01), did not. Changes in PO.1 were found to be significantly related to changes in FEV1 both during HBPT and B (p less than 0.05). The data suggest that in these patients non-vagal afferences, linked to the abnormalities of thoraco-pulmonary mechanics, could play a major role in changing neural drive to the respiratory muscles.

Adult↗

PubMed1985

Electromyographic observations in patients with foot pain syndromes.

Abductor hallucis muscle EMGs were performed in control subjects and in patients with chronic foot pain (9 affected by the disease of the metatarsophalangeal joint of the big toe, 6 affected by chronic foot strain) to investigate pathophysiological mechanisms of muscle pain syndromes. Unlike control subjects, patients showed an abnormal involuntary activity when standing. All patients presented a decrease of abnormal EMG activity when postural changes were induced either by variations in body weight distribution on the feet, or by changes of position in the weight-bearing foot achieved by arch supports or by boards of variable thickness applied under the forefeet or the heels. Anaesthesia of the metatarsophalangeal joint of the hallux (injection into the joint cavity of 2-3 ml 0.50% bupivacaine) reduced the abnormal EMG activity only in patients with hallux valgus, whereas it did not affect muscular activity in the other patients. Present results support the idea of the role of abnormal muscular activity in causing and maintaining chronic pain and suggest that alterations of postural mechanisms and of afferent input, in particular that arising from joint receptors, are involved in the genesis of this abnormal muscular activity.

Adult↗

PubMed1983

[Reactivation of the allogenous component of experimental skin inflammation after exposure to ultraviolet rays].

The effects of U.V. radiation induced cutaneous erythema on an experimental inflammation focus in another part of the body have been studied. The skin inflammation caused by carbon dioxide snow was used as a model. The onset of erythema is followed by reactivation of the diminishing inflammation process. It is therefore deduced that such effects are transmitted humorally and that reactivation is caused by histamine circulation. Histamine is released locally from the U.V. induced erythema and, entering into the circulation, increased the permeability of the microvessels in the inflamed area. This sends inactive chemical mediators to the interstitial sector where the appropriate conditions for their activation exist.

Adult↗

PubMed1983

[Reactivation of the algogenic component in experimental inflammation induced by histamine administration].

The action of i.v. histamine on human skin inflammation experimentally induced with carbon dioxide snow in man is described. Histamine was injected when the skin reaction was on the wane to determine its possible reactivation of inflammation. Complete recrudescence of erythralgia was noted (reappearance of pain and of erythralgic halo, with a fresh spread of secondary hyperalgesia). It is felt that histamine was responsible. Its arrival to the reaction site through microvessels in a state of increased permeability during the remission of inflammation may be assumed to promote the passage of chemical mediators in the preactive stage from the vascular to the interstitial sector, and thus to pave the way for their activation.

Dermatitis, Contact↗

PubMed1983

Relationships between characteristics of electrical stimulation, muscle pain and blink responses in man.

The present research was undertaken in 11 healthy volunteers with the aim of investigating the relationship between blink response, a feature of the startle reaction, and muscular pain evoked by muscle electrical stimulation (train of stimuli). At a repetition rate of 0.1 Hz, a close relationship was found between the threshold for muscle pain and that for the blink response, without apparent habituation. At the same rate and with stimulation intensity maintained at pain threshold, the subject could voluntarily inhibit the blink response, but not pain. Under the same conditions both pain and blink response were inhibited during a mental task. By increasing the current intensity pain became more intense and the blink response tended to increase in amplitude and to decrease in latency. Similar effects were achieved by increasing the repetition rate with the current intensity maintained at pain threshold. Habituation of the blink response, but not of pain, was found at repetition rates of 1 Hz or more. Present results indicate that nociceptive inputs from muscle have a facilitatory effect on central mechanisms subserving the blink response. It is suggested that the comparative analysis of pain sensation and the blink response may be a useful tool for pain research in man.

Adult↗