Diaphragm muscle fiber injury after inspiratory resistive breathing.

Zhu, Ercheng; Petrof, Basil J.; Gea, J; Comtois, Norman; Grassino, A.

doi:10.1164/ajrccm.155.3.9116995

Cited by 80 publications

(69 citation statements)

References 27 publications

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“…When faced with an elevated mechanical load, increased muscle activation predisposes to diaphragmatic muscle injury [30]. Downregulation of respiratory motoneuronal output has been postulated as a useful adaptive strategy to avoid structural injury in the face of an elevated load [9,13], and such disfacilitation has even been termed "central wisdom".…”

Section: Discussionmentioning

confidence: 99%

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

2001

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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.

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Section: Discussionmentioning

confidence: 99%

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

2001

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“…Finally, growth may be indirectly affected following increased expression of oxygen-derived free radicals and cytokines as a result of respiratory muscles' strenuous contraction (26,32,38). Muscle strenuous contraction induces protein loss and cachexia (25).…”

Section: The Experimental Modelmentioning

confidence: 99%

Chronic upper airway resistive loading induces growth retardation via the GH/IGF-I axis in prepubescent rats

Tarasiuk¹,

Segev²

2007

Journal of Applied Physiology

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Tarasiuk A, Segev Y. Chronic upper airway resistive loading induces growth retardation via the GH/IGF-I axis in prepubescent rats. J Appl Physiol 102: [913][914][915][916][917][918] 2007. First published November 30, 2006; doi:10.1152/japplphysiol.00838.2006.-The effect of upper airway loading on longitudinal bone growth and various components of the growth hormone (GH)/insulin-like growth factor I (IGF-I) axis has not been fully elucidated. In the present study, the effect of chronic resistive airway loading (CAL) in a prepubescent rat model on linear bone growth and weight gain was investigated. We hypothesize that CAL induced in prepubescent rats will lead to impaired longitudinal growth due to impairment in circulating and liver GH/IGF-I parameters. The tracheae of 22-day-old rats were obstructed by tracheal banding to increase inspiratory esophageal pressure. The GH/IGF-I markers were analyzed using ELISA, RT-PCR, and Western immunoblot analysis 14 days after surgery. Animals exhibited impaired longitudinal growth as demonstrated by reduction of tibia and tail length gains by 40% (P Ͻ 0.0001) and body weight gain by 24% (P Ͻ 0.0001). No differences were seen in total body energy balance, i.e., oxygen consumption, daily food intake, or arterial blood gases. Circulating GH, IGF-I, and IGF binding protein-3 (IGFBP-3) levels were reduced by 40% (P ϭ 0.037), 30% (P Ͻ 0.006), and 27% (P ϭ 0.02), respectively, in the CAL group. Liver IGF-I mRNA level decreased by 20% (P Ͻ 0.0002), whereas GH receptor mRNA and protein expression were unchanged. We conclude that impaired longitudinal growth in prepubescent CAL rats is related to a decrease in GH, IGF-I, and IGFBP-3 levels. chronic resistive loading; growth hormone; insulin-like growth factor I; insulin-like growth factor binding protein-3; prepuberty ONE OF THE CONSEQUENCES OF chronic resistive airway loading (CAL) in adult rats is malfunction in body weight gain (12, 27) without effect on longitudinal bone growth (35). The failure to gain weight was not related to decreased caloric intake (12) and was recently attributed to a decline in serum insulin-like growth factor I (IGF-I) levels (35). The endocrine effect of pituitary-secreted growth hormone (GH) is induction of IGF-I and IGF binding protein-3 (IGFBP-3) synthesis in various organs, including the liver; both are highly correlated with the 24-h mean GH levels (3, 7). This effect is mediated via activation of GH receptor (GHR), which is extensively distributed throughout many tissues (9). Impairment of the GH/IGF-I axis in prepubescent rats, before bone growth is completed, leads to skeletal growth retardation (31). The effect of CAL on the GH/IGF-I axis and longitudinal growth in prepuberty rats is not known.In the present study, the effect of CAL on longitudinal growth and weight gain was studied using the prepubescent rat model. We hypothesize that CAL will impair the GH/IGF-I axis, consequently leading to longitudinal growth retardation. We explored the effect of CAL on linear growth, serum GH, IGF-I, and ...

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“…Ultimately, the most pertinent clinical measures are the power of breathing (WOB per minute) and PTP, which relate to respiratory muscle perfusion/oxygen consumption, and probably signify the potential for oxidative stress, inflammation, and structural damage [71][72][73][74] to the muscles from excessive exertion. Paradoxically, unrestricted spontaneous breathing during severe respiratory failure may promote ventilator-dependence.…”

Section: Concluding Observationsmentioning

confidence: 99%

Patient-Ventilator Interaction During Acute Lung Injury, and the Role of Spontaneous Breathing: Part 2: Airway Pressure Release Ventilation

Kallet

2011

Respir Care

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Airway pressure release ventilation (APRV) and bi-level positive airway pressure (BIPAP) are proposed to reduce patient work of breathing (WOB) sufficiently and to obviate issues related to patient-ventilator synchrony, so that spontaneous breathing can be maintained throughout the course of acute lung injury (ALI). Thus, APRV/BIPAP should reduce requirements for sedation and muscle paralysis, and thereby reduce the duration of mechanical ventilation. Only 17 human, animal, or lung-model studies have examined these claims, either directly or indirectly. Most did not target patients with ALI. Studies on sedation use have serious methodological limitations. Other studies found that APRV/BIPAP either increased WOB and asynchrony, or had no effect on energy expenditure. To supplement the discussion of patient WOB during APRV/BIPAP in ALI, 4 clinical examples showed marked elevation and wide variation in patient WOB. One plausible explanation is that spontaneous breathing is superimposed upon the mechanical ventilation pattern. Thus a variety of "breathing environments" exist during APRV/BIPAP that affect patient WOB and respiratory drive differently and perhaps unpredictably. This characteristic of APRV/BIPAP makes WOB comparisons with traditional modes problematic. Furthermore, the theoretical benefits of APRV, in terms of controlling patient WOB, appear particularly limited when lung-protective 190RESPIRATORY CARE

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Diaphragm muscle fiber injury after inspiratory resistive breathing.

Cited by 80 publications

References 27 publications

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

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

Chronic upper airway resistive loading induces growth retardation via the GH/IGF-I axis in prepubescent rats

Patient-Ventilator Interaction During Acute Lung Injury, and the Role of Spontaneous Breathing: Part 2: Airway Pressure Release Ventilation

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