Evolution of the Ventilatory Capacity in Chronic Bronchitis

Howard, P

doi:10.1136/bmj.3.5562.392

Cited by 44 publications

(16 citation statements)

References 6 publications

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“…Though ventilatory function studies were performed in the present investigation, it was not possible to correlate either the number of acute exacerbations or infections due to a particular virus with a persistent change in the maximum breathing capacity (unpublished observation). Howard (1967), studying this problem in a larger group and for a longer period, noted that the majority of acute exacerbations treated with antibiotics had very little effect on individual forced expiratory volume (F.E.V.0.75) curves.…”

Section: Discussionmentioning

confidence: 99%

Viral Antibody Levels and Clinical Status in Acute Exacerbations of Chronic Bronchitis: a Controlled Prospective Study

Stenhouse¹

1968

BMJ

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Section: Discussionmentioning

confidence: 99%

Viral Antibody Levels and Clinical Status in Acute Exacerbations of Chronic Bronchitis: a Controlled Prospective Study

Stenhouse¹

1968

BMJ

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“…In the 1950s and 1960s, the British hypothesis of the pathogenesis of COPD included as major contributors recurrent bacterial infection and mucus hypersecretion (200). With the realization of tobacco smoke exposure as the primary pathogenic mechanism of COPD and the emergence of evidence that mucus hypersecretion and worsening airway obstruction were independent, the British hypothesis fell into disfavor (28,102,145). Several longitudinal cohort studies in the 1960s and 1970s demonstrated that the incidence of bacterial isolation from sputum during exacerbations of COPD was not different from the incidence during stable COPD (123,196).…”

Section: Bacterial Pathogens As a Cause Of Acute Exacerbations Of Copdmentioning

confidence: 99%

Bacterial Infection in Chronic Obstructive Pulmonary Disease in 2000: a State-of-the-Art Review

2001

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SUMMARY Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death in the United States. The precise role of bacterial infection in the course and pathogenesis of COPD has been a source of controversy for decades. Chronic bacterial colonization of the lower airways contributes to airway inflammation; more research is needed to test the hypothesis that this bacterial colonization accelerates the progressive decline in lung function seen in COPD (the vicious circle hypothesis). The course of COPD is characterized by intermittent exacerbations of the disease. Studies of samples obtained by bronchoscopy with the protected specimen brush, analysis of the human immune response with appropriate immunoassays, and antibiotic trials reveal that approximately half of exacerbations are caused by bacteria. Nontypeable Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pneumoniae are the most common causes of exacerbations, while Chlamydia pneumoniae causes a small proportion. The role of Haemophilus parainfluenzae and gram-negative bacilli remains to be established. Recent progress in studies of the molecular mechanisms of pathogenesis of infection in the human respiratory tract and in vaccine development guided by such studies promises to lead to novel ways to treat and prevent bacterial infections in COPD.

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“…A mobile collapse point would accommodate for resistance changes in small airways and prevent the increased resistance of bronchiolar disease from reducing the FEV. The deterioration of the FEV is a very noticeable feature of the progress of chronic obstructive airways disease (Howard, 1967;Fletcher, 1967). A study of patients with this disorder was made to examine the relative importance of resistance, recoil pressure and collapsibility to the deterioration of the FEV.…”

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confidence: 98%

Peripheral Airways Resistance, Static Recoil and the Forced Expiratory Volume

Cayton

Howard

1972

Clinical Science

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1. The forced expiratory volume (FEV0·75) was measured at increasing mouth pressures in twenty-seven patients with obstructive airways disease. Attempts were made to divide the patients on clinical grounds into emphysematous, bronchitic or asthmatic categories; there was no evidence from the (FEV/mouth pressure) plots that their airways functioned differently during forced expiration. 2. Static elastic recoil was measured in twelve patients. There was no evidence that this factor alone caused the loss of FEV in any patient. 3. It is suggested that the use of the FEV as a test of respiratory function during the natural history of obstructive airways disease should be considered in three stages. There is an initial phase when peripheral airways disease develops with little or no alteration of the FEV. In the second phase the FEV decreases from normal values to below 1·0 litre, and at this stage is considered a sensitive indicator of peripheral airways resistance. In stage 3 the FEV is low and further changes can only be small. But airways resistance continues to increase and could be a more sensitive measurement of further airways disease.

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Evolution of the Ventilatory Capacity in Chronic Bronchitis

Cited by 44 publications

References 6 publications

Viral Antibody Levels and Clinical Status in Acute Exacerbations of Chronic Bronchitis: a Controlled Prospective Study

Viral Antibody Levels and Clinical Status in Acute Exacerbations of Chronic Bronchitis: a Controlled Prospective Study

Bacterial Infection in Chronic Obstructive Pulmonary Disease in 2000: a State-of-the-Art Review

Peripheral Airways Resistance, Static Recoil and the Forced Expiratory Volume

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