Action of intercostal muscle afferents on the respiratory rhythm of anesthetized cats

Remmers, John E.; Marttila, Irja

doi:10.1016/0034-5687(75)90119-x

Cited by 85 publications

(20 citation statements)

References 19 publications

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“…A similar response was also reported for patients with chronic interstitial lung dis-ease (6,21). Since our plaque group was normo xemic , chemical humoral factors can be ruled out as the cau se; thu s the pos sible mechanisms of resting hyperventilation are mechanical adaptation to the increased ela stic work of breathing or a reflex-mediated increase in breathing frequency originating from the che st wall receptors (22). Quantitative support for the hypothesis that pleural plaques provoke resting hyperventilation is the observed significant linear correlation between the pleural score and Pa C02 (correla tion coefficient -0.70).…”

Section: Discussionsupporting

confidence: 80%

Association between asbestos-related pleural plaques and resting hyperventilation.

Dujić

Eterović²,

Tocilj³

1993

Scand J Work Environ Health

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Section: Discussionsupporting

confidence: 80%

Association between asbestos-related pleural plaques and resting hyperventilation.

Dujić

Eterović²,

Tocilj³

1993

Scand J Work Environ Health

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“…In type B patients bronchial disease may predominate, and as both stretch and irritant receptors are located in the airways, chronic bronchitis may well cause increased ac tivity on their part. In the absence of any direct evidence, however, abnormal reflexes originating from the chest wall and intrinsic changes in rhythmicity of the respiratory centres due to chronic hypercapnia and hypoxia cannot be ex cluded as possible mechanisms causing a shorter Γ, and a fall in V T (Remmers & Martilla, 1975). In addition, in type B patients the lungs tend to be oedematous, a fact that may well stimulate pul monary J-receptors, leading again to rapid, shallow breathing (Paintal, 1973).…”

Section: Respiratory Patternmentioning

confidence: 97%

Control of Breathing in Patients with Chronic Obstructive Lung Disease

et al. 1978

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1. Using the mouth occlusion pressure technique, we have studied the control of breathing in seven hypercapnic and eight non-hypercapnic patients with chronic obstructive lung disease. 2. When breathing room air, pulmonary ventilation, mean inspiratory flow and P0.1 (mouth occlusion pressure developed 0.1 s after the onset of occluded inspiration at functional residual capacity) were not significantly different between the two groups of patients. Tidal volume, however, was significantly lower in the hypercapnic than in the non-hypercapnic patients, as a result of a significantly lower duration of inspiration. 3. The lower tidal volume in the hypercapnic patients leads to decreased alveolar ventilation, and appears to be the main cause of retention of carbon dioxide.

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“…The lower maximum inspiratory pressure of group II patients was probably the result of their higher FRC. However, poor nutrition, which has been shown to impair respiratory muscle function and is a common problem in patients with COPD, could also have decreased inspiratory muscle strength (14)(15)(16) (20,21). Similar effects have been demonstrated recently in man in response to chest wall vibration that selectively increases muscle spindle afferent activity (22).…”

Section: Discussionmentioning

confidence: 52%

Mechanisms underlying CO2 retention during flow-resistive loading in patients with chronic obstructive pulmonary disease.

Oliven¹,

Kelsen²,

Deal³

et al. 1983

J. Clin. Invest.

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A B S T R A C T The present study examined the respiratory responses involved in the maintenance of eucapnea during acute airway obstruction in 12 patients with chronic obstructive disease (COPD) and 3 agematched normal subjects. Acute airway obstruction was produced by application of external flow-resistive loads (2.5 to 30 cm H20/liter per s) throughout inspiration and expiration while subjects breathed 100% 02. Application of loads of increasing severity caused progressive increases in Pco2 in the patients, but the magnitude of the increase in Pco2 varied substantially between subjects. On a resistance of 10 cm H2O/liter per s, the highest load that could be tolerated by all COPD patients, the increase in Pco2 ranged from 1 to 11 mm Hg, while none of the normal subjects retained CO2. Based on the magnitude of the increase in Pco2 the patients could be divided into two groups: seven subjects whose Pco2 increased by <3 mm Hg (group I) and five subjects whose Pco2 increased by >6 mm Hg (group II). Base-line ventilation and the pattern of breathing were similar in the two groups. During loading group I subjects maintained or increased tidal volume while all group II patients decreased tidal volume (VT). The smaller tidal volume in group II subjects was mainly the result of their shorter inspiratory time as the changes in mean inspiratory flow were similar in the two groups. The magnitude of CO2 retention during loading was inversely related to the magnitude of the change in VT (r = -0.91) and inspiratory time (T,) (r = -0.87) but only weakly related to the change in ventilation (r = -0.53). The changes in PCO2, VT, and T, during loading correlated with the subjects' maximum static

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Action of intercostal muscle afferents on the respiratory rhythm of anesthetized cats

Cited by 85 publications

References 19 publications

Association between asbestos-related pleural plaques and resting hyperventilation.

Association between asbestos-related pleural plaques and resting hyperventilation.

Control of Breathing in Patients with Chronic Obstructive Lung Disease

Mechanisms underlying CO2 retention during flow-resistive loading in patients with chronic obstructive pulmonary disease.

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