Neural Respiratory Drive and Neuromuscular Coupling in Patients with Chronic Obstructive Pulmonary Disease (COPD)

Gorini, Massimo; Spinelli, Andrea; Ginanni, Roberta; Duranti, Roberto; Gigliotti, Francesco; Scano, Giorgio

doi:10.1378/chest.98.5.1179

Cited by 65 publications

(57 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Second, as compared to FA-exposed mice, the greatest change of ventilation in CS-exposed mice was the rapid breathing, leading to an increase of V̇E. Actually, a rapid breathing rate has often been observed in hypercapnic COPD patients (Altose et al 1977;Fahey et al 1983;Gorini et al 1990;van de Ven et al 2002), although the baseline ventilation has been reported to be increased (Gorini et al 1990;Topeli et al 2001), decreased (Altose et al 1977), or unchanged (Sorli et al 1978;Montes de Oca et al 1998;van de Ven et al 2002). Additionally, we also found a slightly, but significantly higher HR in CSexposed mice as compared to FA-exposed mice (Fig.…”

Section: It Is Novel That the Major Symptoms Of Anesthetized C3h/hen mentioning

confidence: 99%

“…They are hypercapnia (Pa CO 2 > 50 torr) coupled with hypoxemia (Pa O 2 < 60 torr) (Pauwels et al 2001); rapid breathing (Altose et al 1977;Fahey et al 1983;Gorini et al 1990;van de Ven et al 2002); and an attenuated ventilatory response (AVR) to hypercapnia/hypoxia (Schaefer 1949;Fahey et al 1983;Franciosi et al 2006;Ucgun et al 2006). It is generally accepted that the AVR is correlated with mechanical limitation of ventilatory capacity (Cherniack et al 1956;Pauwels et al 2001).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Blunted ventilatory response to hypoxia/hypercapnia in mice with cigarette smoke-induced emphysema

Zhuang

Wang

et al. 2007

Respiratory Physiology & Neurobiology

View full text Add to dashboard Cite

It has been reported that the degree of emphysema induced by chronic cigarette smoke (CS) is greater in female C3H/HeN mice as compared to other mouse strains. We hypothesized that these mice would develop the similar major characteristics seen in hypercapnic patients with chronic obstructive pulmonary disease (COPD), including emphysema, pulmonary inflammation, hypercapnia/ hypoxemia, rapid breathing, and attenuated ventilatory response (AVR). Mice were exposed either to CS or filtered air (FA) for 16 wk. After exposure, arterial blood gases and minute ventilation were measured before and during chemical challenges in anesthetized and spontaneously breathing mice. We found that as compared to FA, CS exposure caused emphysema and pulmonary inflammation associated with: (1) hypercapnia and hypoxemia, (2) rapid breathing, and (3) AVR to 25 breaths of pure N 2 , 5% CO 2 alone, and 5% CO 2 coupled with 10% O 2 . The similarity of these pathophysiological characteristics between our mouse model and COPD patients suggests that this model could be effectively applied to study COPD pathophysiology, especially central mechanisms of the AVR genesis.

show abstract

Section: It Is Novel That the Major Symptoms Of Anesthetized C3h/hen mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Blunted ventilatory response to hypoxia/hypercapnia in mice with cigarette smoke-induced emphysema

Zhuang

Wang

et al. 2007

Respiratory Physiology & Neurobiology

View full text Add to dashboard Cite

show abstract

“…An inability to maintain a normal respiratory motor response during an exacerbation of COPD could lead to critical hypoventilation, respiratory failure, and death. Unfortunately, investigations have yielded inconsistent results, with reports of increased [4], decreased [5,6], and equivalent [7,8] respiratory motor output in hypercapnic and normocapnic patients. These conflicting findings stem, in part, from limitations of techniques used to measure respiratory motor output, such as the diaphragmatic electromyogram and airway occlusion pressure [9].…”

mentioning

confidence: 99%

The voluntary drive to breathe is not decreased in hypercapnic patients with severe COPD

2001

View full text Add to dashboard Cite

The voluntary drive to breathe is not decreased in hypercapnic patients with severe COPD. A. Topeli, F. Laghi, M.J. Tobin. #ERS Journals Ltd 2001. ABSTRACT: How do the respiratory centres of patients with chronic obstructive pulmonary disease (COPD) and hypercapnia respond to acute increases in inspiratory load? A depressed respiratory motor output has long been postulated, but studies on this issue have yielded inconsistent results, partly due to limitations of investigative techniques. Many of these limitations can be overcome by the twitch interpolation technique, which is capable of accurately quantifying the degree of diaphragmatic activation, termed the voluntary drive to breathe. The hypothesis that patients with COPD and hypercapnia compensate for an acute increase in mechanical load on the inspiratory muscles with a lower voluntary drive to breathe than is the case with normocapnic patients was tested.Measurements were obtained in 15 patients with COPD, six of whom displayed hypercapnia and nine normocapnia. The maximum degree of diaphragmatic activation, expressed as a voluntary activation index (mean¡SEM), was higher in hypercapnic than in normocapnic patients (98.7¡0.7 versus 94.5¡0.9% (p~0.006)), as was the mean value (94.5¡0.7 versus 88.5¡1.9% (p~0.01)). Within-patient values of the index were also less variable in the hypercapnic patients (coefficients of variation, 3.4¡0.3 versus 6.1¡0.9%, p~0.01). Multiple regression analysis revealed the ratio of dynamic elastance to maximum transdiaphragmatic pressure, an index of inspiratory muscle loading, and pH as the only variables that correlated with maximum voluntary activation index (r 2~0 .69, p~0.02 for each variable). Contrary to the hypothesis, it was concluded that voluntary activation of the diaphragm was greater and less variable in hypercapnic patients than normocapnic patients with severe chronic obstructive pulmonary disease during an acute increase in inspiratory mechanical load. Whether greater diaphragmatic recruitment during episodes of a severe exacerbation of chronic obstructive pulmonary disease provides a survival advantage for hypercapnic patients with chronic obstructive pulmonary disease remains to be determined.

show abstract

“…Mouth occlusion pressure 100 milliseconds after initiation of breath (P 0.1 ) was used to assess the central respiratory drive. It is generally recognized that P 0.1 is the best non-invasive technical index that could exclude influences generated by breathing mechanics and by consciousness in the measurement of central efferent function (11). From Table 2, maybe a higher central respiratory drive must be operated by the patients to maintain a normal breathing physiology status and regular daily activities because of hypoxaemia and/or increased respiratory resistance in Group C. This result was consistent with the information from Table 3 and Table 4 and there were negative correlations between P 0.1 and FEV1%FVC and between P 0.1 and PaO 2 , respectively (Tables 3 and 4).…”

Section: Discussionmentioning

confidence: 99%

A Study of Patients with “Interface Respiratory Failure” Due to Chronic Obstructive Pulmonary Disease

Wang¹,

Zhang²,

Feng³

et al. 2015

West Indian Med J

View full text Add to dashboard Cite

Objective: To explain a definition of "interface respiratory failure" as arterial blood gas assay with arterial oxygen partial pressure in the range of [60][61][62][63][64][65][66][67][68][69][70][71][72][73][74][75] Sujetos y métodos: Comparamos la gasometría arterial (ABG, por sus siglas en inglés), la dinámica respiratoria de descanso y sus derivados, la mecánica de los músculos respiratorios, la resistencia y compliancia (distensibilidad) de las vías respiratorias y algunas importantes citoquinas (Interleuquina-4 y el interferón-γ) de subgrupos estables de enfermedad pulmonar obstructiva crónica (EPOC) (total 50 casos) y grupo control (25 casos

show abstract

Neural Respiratory Drive and Neuromuscular Coupling in Patients with Chronic Obstructive Pulmonary Disease (COPD)

Cited by 65 publications

References 23 publications

Blunted ventilatory response to hypoxia/hypercapnia in mice with cigarette smoke-induced emphysema

Blunted ventilatory response to hypoxia/hypercapnia in mice with cigarette smoke-induced emphysema

The voluntary drive to breathe is not decreased in hypercapnic patients with severe COPD

A Study of Patients with “Interface Respiratory Failure” Due to Chronic Obstructive Pulmonary Disease

Contact Info

Product

Resources

About