A Study of Gastric Secretions in Chronic Obstructive Pulmonary Emphysema

The severity of respiratory distress occurring prior to loss of posture during exposure to: 20, 30, 40, 50, 60, 70, 80 or 90 per cent carbon dioxide in air; 2 or 5 per cent residual oxygen in argon; 30 per cent carbon dioxide in argon with either 2 or 5 per cent residual oxygen; or 40 per cent carbon dioxide in argon with either 2 or 5 per cent residual oxygen, was subjectively determined in pigs from their behaviour. The results indicated that exposure to 2 per cent oxygen in argon (anoxia) induced minimal respiratory distress, 30 per cent carbon dioxide in argon with 2 per cent residual oxygen induced a moderate distress and exposure to all the concentrations of carbon dioxide in air induced severe respiratory distress in the pigs. From the animal welfare point of view, using 2 per cent oxygen in argon (anoxia) appears to be the optimum choice for gas stunning pigs. Secondly, a mixture of 30 per cent carbon dioxide in argon with 2 per cent residual oxygen is preferred to 90 per cent carbon dioxide in air.

The aversive effects of 90 per cent argon in air, 30 per cent carbon dioxide in air or 90 per cent carbon dioxide in air were investigated in slaughter weight pigs. Aversion was assessed from their reluctance to enter the three gaseous atmospheres to obtain a reward (apples). The pigs did not show any aversion to the inhalation of 90 per cent argon in air. The majority of the pigs did not show aversion to the presence of 30 per cent carbon dioxide in air. By contrast, the inhalation of 90 per cent carbon dioxide was aversive to the majority of the pigs. Fasting them for up to 24h prior to testing did not overcome the pigs ‘ reluctance to enter an atmosphere containing 90 per cent carbon dioxide.

The reactions of turkeys to the presence of either 90 per cent argon in air (anoxia), 72 per cent carbon dioxide in air or a mixture of 30 per cent carbon dioxide and 60 per cent argon in air with 3 per cent residual oxygen were tested. The majority of the turkeys did not avoid a feeding chamber containing either argon or the mixture of carbon dioxide and argon, but 50 per cent of the turkeys avoided a feeding chamber containing 72 per cent carbon dioxide in air. It is concluded that from the point of view of welfare, either 90 per cent argon in air or a mixture of 30 per cent carbon dioxide and 60 per cent argon in air, would be preferable to a high concentration of carbon dioxide for stunning/killing turkeys.

Article1 June 1961THE DIFFUSE OBSTRUCTIVE PULMONARY SYNDROME IN A TUBERCULOSIS SANATORIUM. I. ETIOLOGIC FACTORSW. Y. HALLETT, M.D., C. J. MARTIN, M.D., F.A.C.P.W. Y. HALLETT, M.D.Search for more papers by this author, C. J. MARTIN, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-54-6-1146 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptMore than a hundred years ago Laennec described both tuberculosis and chronic obstructive emphysema, but without relating them to each other.1-2 Subsequently, a relationship between these disorders has been suggested by Anno and Tomashefski,3 who showed a high incidence of pulmonary emphysema in selected tuberculosis patients, and by Gaensler and Lindgren,4 who found obstructive pulmonary disease in 42.6% of 780 tuberculous patients who were being considered for surgery. The present study of a general tuberculosis population was initiated to define any relationship between the two diseases and to evaluate other factors of etiologic importance.METHODThe maximal expiratory flow rate5...Bibliography1. FreundMiddlebrook JG: The mycobacteria in bacterial and mycotic infections of man, Dubos, R. J., Ed., J. P. Lippincott Company, Philadelphia, 1948, p. 295. Google Scholar2. Laennec RT: A treatise on diseases of the chest, 3rd Ed., (translated by J. Forbes), S. & W. Wood, New York, 1838, in Pulmonary emphysema, Barach, A. L. and Bickerman, H. A, Eds., Williams and Wilkins Company, Baltimore, 1956. Google Scholar3. AnnoTomashefski HJF: Studies on the impairment of respiratory function in pulmonary tuberculosis. Amer. Rev. Tuberc. 71: 333, 1955. Google Scholar4. GaenslerLindgren EAI: Chronic bronchitis as an etiologic factor in obstructive emphysema, preliminary report. Amer. Rev. Resp. Dis. 80 (no. 1, part 2): 185, 1959. MedlineGoogle Scholar5. Goldsmith JR: A simple test of maximal expiratory flow for detecting ventilatory obstruction. Amer. Rev. Tuberc. 78: 180, 1958. Google Scholar6. MartinHallett CJWY: The diffuse obstructive pulmonary syndrome in a tuberculosis sanatorium. II. Incidence and symptoms. Ann. Intern. Med. 54: 1156, 1961. LinkGoogle Scholar7. DrinkerHatch PT: Industrial dusts. McGraw-Hill Book Company, Inc., New York, 1954. Google Scholar8. MayerRappaport EI: Bronchitis and emphysema. J. A. M. A. 165: 1227, 1957. CrossrefMedlineGoogle Scholar9. SpainKaufman DMG: The basic lesion in chronic pulmonary emphsema. Amer. Rev. Tuberc. 68: 24, 1953. Google Scholar10. Mitchell RS: Theories of the pathogenesis of emphysema. Amer. Rev. Resp. Dis. 80 (no. 1, part 2): 2, 1959. MedlineGoogle Scholar11. Bell J.: Experimental pulmonary emphysema. Production of emphysematous bullae in the rabbit by infection with tuberculosis. Amer. Rev. Tuberc. 78: 848, 1958. Google Scholar12. SteenkenWolinsky WE: Formation of bullae or cystlike cavities during chemotherapy in rabbits with pulmonary tuberculosis. Amer. Rev. Tuberc. 75: 965, 1957. Google Scholar13. Alarcon DG: Regressive giant bullous emphysema in tuberculosis of adults. Dis. Chest 27: 31, 1955. CrossrefMedlineGoogle Scholar14. McLean KH: The histology of generalized pulmonary emphysema. II. Diffuse emphysema. Aust. Ann. Med. 6: 203, 1957. CrossrefMedlineGoogle Scholar15. Fletcher CM: Chronic bronchitis. Amer. Rev. Resp. Dis. 80: 483, 1959. MedlineGoogle Scholar16. Higgins IT: Respiratory symptoms, bronchitis and ventilatory capacity in random sample of an agricultural population. Brit. Med. J. 2: 1198, 1957. CrossrefMedlineGoogle Scholar17. McLean KH: The macroscopic anatomy of pulmonary emphysema. Aust. Ann. Med. 5: 73, 1956. MedlineGoogle Scholar18. Pemberton J: Chronic bronchitis, emphysema, and bronchial spasm in bituminous coal workers. An epidemiologic study. Arch. Industr. Health 13: 529, 1956. MedlineGoogle Scholar19. Motley HL: Pulmonary function impairment in pneumoconiosis. J. A. M. A. 172: 1591, 1960. CrossrefMedlineGoogle Scholar20. GreenDundee PTJC: The association of chronic pulmonary emphysema with chronic peptic ulceration. Canad. Med. Ass. J. 67: 438, 1952. MedlineGoogle Scholar21. BaumKalserKathe GLMHJH: The association of chronic peptic ulcer and chronic pulmonary emphysema. Abstract of papers, Annual Meeting, National Tuberculosis Association, Los Angeles, Calif., May 15-20, 1960. Google Scholar22. LowellFranklinMichelsonSchiller FCWALIW: Chronic obstructive pulmonary emphysema: a disease of smokers. Ann. Intern. Med. 45: 268, 1956. LinkGoogle Scholar23. FlickPaton ALRR: Obstructive emphysema in cigarette smokers. Arch. Intern. Med. 104: 518, 1959. CrossrefMedlineGoogle Scholar24. WilsonMeadorJayHiggins RHRSBEE: The pulmonary pathologic physiology of persons who smoke cigarettes. New Engl. J. Med. 262: 956, 1960. CrossrefMedlineGoogle Scholar25. WoodFishmanReemtsmaBarkerdi Sant' Agnese JAAPKHGPA: A comparison of sweat chlorides and intestinal fat absorption in chronic obstructive pulmonary emphysema and fibrocystic disease of the pancreas. New Engl. J. Med. 260: 951, 1959. CrossrefMedlineGoogle Scholar26. Hurst A: Familial emphysema. Amer. Rev. Resp. Dis. 80 (no. 1, part 2): 179, 1959. MedlineGoogle Scholar27. LeopoldGough JGJ: The centrilobular form of hypertrophic emphysema and its relation to chronic bronchitis. Thorax 12: 219, 1957. CrossrefMedlineGoogle Scholar28. McLean KH: Pathogenesis of pulmonary emphysema. Amer. J. Med. 25: 62, 1958. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Seattle, Washington*Received for publication December 27, 1960.Presented in part before the Medical Session of the American Trudeau Society, May, 1960.†Supported in part by a grant from the National Tuberculosis Association and in part by Grant H-1892 from the U. S. Public Health Service.‡Present address: City of Hope Medical Center, Duarte, Calif.Requests for reprints should be addressed to C. J. Martin, M.D., Firland Sanatorium, 1704 E. 150th St., Seattle, Wash. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byIs pulmonary tuberculosis a true risk-factor for chronic obstructive pulmonary disease?Rehabilitation, optimized nutritional care, and boosting host internal milieu to improve long-term treatment outcomes in tuberculosis patientsProfil spirométrique et radiographique des patients anciens tuberculeux pulmonaires traités et guéris au service de pneumologie du CHU de BrazzavilleTuberculosis associated chronic obstructive pulmonary diseaseIs there a rationale for pulmonary rehabilitation following successful chemotherapy for tuberculosis?Pulmonary Impairment in Tuberculosis Survivors: The Korean National Health and Nutrition Examination Survey 2008-2012A Systematic Review of the Association between Pulmonary Tuberculosis and the Development of Chronic Airflow Obstruction in AdultsThe Risk of Obstructive Lung Disease by Previous Pulmonary Tuberculosis in a Country with Intermediate Burden of TuberculosisPulmonary Function Test and TuberculosisLong term non-invasive domiciliary assisted ventilation for respiratory failure following thoracoplasty.LungentuberkuloseDyspnea: Psychologic and physiologic observationsThe Prognostic Value of a Reduced Maximum Breathing Capacity in TuberculosisSmoking and the Health of Older MenTHE DIFFUSE OBSTRUCTIVE PULMONARY SYNDROME IN A TUBERCULOSIS SANATORIUM. II. INCIDENCE AND SYMPTOMS*†C. J. MARTIN, M.D., F.A.C.P., W. Y. HALLETT, M.D. 1 June 1961Volume 54, Issue 6Page: 1146-1155KeywordsAsthmaChronic obstructive pulmonary diseaseEmphysemaMedical servicesPeptic ulcersPneumoniaPulmonary diseasesSilicosisSurgeryTuberculosis ePublished: 1 December 2008 Issue Published: 1 June 1961 PDF downloadLoading ...

SINCE blood has a pH of about 7.4, media used for organ and tissue culture are usually adjusted to this hydrogen ion concentration. However, when the chemically defined medium BGJb1 was first formulated, sodium bicarbonate was added in excess (3.5 g/l.), with the result that the medium had a pH of 7.68 when equilibrated with 5 per cent carbon dioxide in air. Mouse fallopian tubes continued to function2 and embryonic long bones developed1 under these alkaline conditions. Paff3 studied the effect of hydrogen ion concentration on embryonic chick femora cultivated on plasma clots in the presence of both air and 5 per cent carbon dioxide in air. The pH of the media under these conditions was 7.8–8.0 and 7.0–7.3 respectively. After cultivation for 14 days, the femora grown at the lower pH contained more bone and had a higher calcium content. However, the conditions required for mineralization may be quite different from those needed for cell division and cellular hypertrophy in the cartilaginous rudiment. We have, therefore, investigated the influence of hydrogen ion concentration on the growth of cartilaginous tibiotarsi of the embryonic chick. This was done by varying the bicarbonate concentration of the medium while maintaining a constant atmosphere of 5 per cent carbon dioxide in air.

The times to the loss of somatosensory evoked potentials (SEPs) and the onset of suppressed and isoelectric electroencephalogram (EEG) were investigated in turkeys as they were stunned with gas mixtures consisting of one of three mixtures: (A) 30 per cent carbon dioxide and 60 per cent argon in air (2 per cent residual oxygen and 8 per cent residual nitrogen); (B) 90 per cent argon in air (2 per cent residual oxygen and 8 per cent residual nitrogen); (C) 65 per cent carbon dioxide in air (7 per cent residual oxygen and 28 per cent residual nitrogen). The time to the loss of SEPs, EEG suppression and the onset of an isoelectric EEG, respectively, were 22, 16 and 35 seconds in mixture A, 44, 41 and 101 seconds in mixture B, and 15, 15 and 67 seconds in mixture C. Stunning turkeys with mixture A or B would be suitable under commercial conditions. Mixture C, containing 65 per cent carbon dioxide in air, is considered on humanitarian grounds to be unacceptable for stunning turkeys owing to the pungency of the carbon dioxide at this concentration.

The efficacy for the euthanasia of day-old chicks of mixtures of carbon dioxide and air, or carbon dioxide and argon containing 1, 2 or 5 per cent residual oxygen, or argon containing 1 or 2 per cent residual oxygen was tested in three experiments. The time to the onset of unconsciousness of individual chicks, determined from the time to loss of posture, was similar during their exposure to 2 per cent oxygen in argon, 20, 30 or 40 per cent carbon dioxide in argon with 2 per cent residual oxygen, or 90 per cent carbon dioxide in air. The exposure of chicks in batches of 20 to a mixture of 20, 30 or 40 per cent carbon dioxide in argon resulted in the death of all the chicks within two minutes. However, a residual oxygen level of 5 per cent in these mixtures resulted in the survival of some chicks for longer than two minutes. With argon alone the level of residual oxygen was critical; less than 2 per cent was essential to achieve 100 per cent mortality within three minutes, and a rise from 2 to about 3 per cent resulted in up to 20 per cent of the chicks surviving for seven minutes.

Pigs were exposed individually to either 90 per cent argon in air (anoxia), a mixture of 30 per cent carbon dioxide and 60 per cent argon in air (hypercapnic anoxia)...

The effects of inhaling 5 per cent carbon dioxide in air on the pulmonary arterial blood pressure and flow were studied in 5 subjects with normal pulmonary circulations and in 10 patients with chronic pulmonary emphysema. In the 5 control subjects, with an average increase in arterial P CO CO2 of 6 mm. Hg (37 to 43) and a 3-fold increase in minute ventilation, both pulmonary arterial blood pressure and flow remained unchanged. In the 10 patients with chronic pulmonary emphysema with a similar increase in arterial P CO CO2 (45 to 52) and a 2-fold increase in minute ventilation, there was a 14 per cent increase in cardiac output and a rise in pulmonary arterial mean pressure of 4 mm. Hg. In these patients an increment in pulmonary arterial pressure was invariably associated with an appreciable increment in blood flow. The present study affords no support for the view that the breathing of air enriched with carbon dioxide elicits pulmonary vasoconstriction in either normal subjects or in patients with chronic pulmonary disease.

Gastric Acid Secretion in Chronic Obstructive Pulmonary Emphysema

The effect of breathing 2.5 to 10 per cent carbon dioxide in air on specific airway conductance was determined by plethysmography in 9 normal subjects and in 8 subjects with mild asthma. In 9 normal subjects, during breathing of 5, 7.5, and 10 per cent carbon dioxide, mean (± SE) values of specific airway conductance decreased by 15.8 ± 6.1, 24.4 ± 6.0, and 28.4 ± 7.9 per cent with increases in end-tidal carbon dioxide tension of 5.0 ± 1.6, 12.3 ± 2.3, and 20.2 ± 2.5 mm Hg, respectively. These changes were not significantly affected by prior administration of atropine or propranolol except that atropine prevented the decrease in specific airway conductance during 5 per cent carbon dioxide breathing. Isocapnic hyperventilation decreased specific airway conductance (15 ± 6 per cent) but to a lesser extent than during similar increases in ventilation due to breathing of 10 per cent carbon dioxide. In contrast, in 8 subjects with asthma, specific airway conductance did not change during carbon dioxide breathi...

Extracellular glycollate is liberated by Chlorella pyrenoidosa during growth in medium bubbled with air or 3 per cent carbon dioxide in air. With air the rate of release of glycollate per cell decreases, with 3 per cent carbon dioxide it increases, with increase in cell number. Glycollate is released during short-term experiments when C. pyrenoidosa, grown under low light and high carbon dioxide, is transferred suddenly to high light and low carbon dioxide. No other combina tion of these factors produces a comparable release of glycollate. The quantity of glycollate released in short-term experiments increases exponentially with the relative growth-rate of the culture from which the cells are derived. A crucial condition for maximum glycollate release is that growth of the culture prior to the experiment should not be limited by carbon-dioxide concentration. The effect of pH is related to its effect on growth-rate; i.e. C. pyrenoidosa has a lower relative growth-rate at pH 8 3 and produces correspondingly less glycollate than faster growing cultures at pH 6-4. During short-term experiments under high light and low carbon dioxide the rate of glycollate release drops after 50-100 minutes suggesting exhaustion of the glycollate precursor.

Spontaneous electroencephalograms (EEG) and somatosensory evoked potentials (SEPS) were recorded in turkeys while they were kept in an atmosphere of either 49 or 86 per cent carbon dioxide in air. The time to the loss of SEPS was not related to the concentration of carbon dioxide, but the time to the onset of an isoelectric EEG was shorter at the higher concentration of carbon dioxide. In comparison with other gas stunning methods it was considered that stunning with these high concentrations of carbon dioxide would not have any welfare advantages over stunning in argon with 2 per cent residual oxygen or in a mixture of 30 per cent carbon dioxide and 60 per cent argon in air.

Bullous disease of the lung

Autoagglutination and the specificity of the indirect fluorescent antibody test applied to the identification of Taylorella equigenitalis