Effect of Body Temperature on Pulmonary Gas Exchange

1957 ◽  
Vol 188 (2) ◽  
pp. 355-359 ◽  
Author(s):  
A. B. Otis ◽  
James Jude
Keyword(s):  
Carbon Dioxide ◽  
Carbon Monoxide ◽  
Steady State ◽  
Body Temperature ◽  
Gas Exchange ◽  
Diffusing Capacity ◽  
Body Temperatures ◽  
Pulmonary Diffusing Capacity ◽  
Normal Body ◽  
Anesthetized Dogs

Measurements were made of the arterial-alveolar carbon dioxide gradient in anesthetized dogs at body temperatures ranging from normal down to 16°C. Pulmonary diffusing capacity was determined by a steady-state carbon monoxide method in anesthetized dogs at normal body temperatures and at 25°C. From the results it is concluded that although diffusing capacity is reduced at low body temperatures, it is still adequate for transfer of both CO2 and O2 because the metabolic requirements for gas exchange are also reduced.

Effect of exercise on pulmonary diffusing capacity

1963 ◽  
Vol 18 (3) ◽  
pp. 447-456 ◽  
Author(s):  
G. M. Turino ◽  
E. H. Bergofsky ◽  
R. M. Goldring ◽  
A. P. Fishman
Keyword(s):  
Carbon Monoxide ◽  
Young Adults ◽  
Steady State ◽  
Body Position ◽  
Diffusing Capacity ◽  
Pulmonary Diffusing Capacity ◽  
Graded Exercise ◽  
Normal Man ◽  
The Difference

The effect of graded exercise on the pulmonary diffusing capacity for both oxygen and carbon monoxide measured simultaneously was studied in healthy young adults by steady-state methods. Pulmonary diffusing capacity for oxygen increases progressively with increasing severity of exercise; it exceeds the DlCO at high levels of exercise by amounts greater than can be accounted for by the difference in diffusivity of the test gases. Diffusing capacity for carbon monoxide increases less than DlOO2 for comparable grades of exercise but no definite plateau value could be established. The supine or upright body position does not influence the values of either DlOO2 or DlCO during exercise. Diffusing capacity of the lung for oxygen does not limit the maximum levels of exercise which may be achieved by normal man. Submitted on August 6, 1962

Ventilatory Responses of Rats to Electrical Stimulation in CO2 Containing Atmospheres

1957 ◽  
Vol 191 (3) ◽  
pp. 423-427 ◽  
Author(s):  
William S. Yamamoto
Keyword(s):  
Carbon Dioxide ◽  
Electrical Stimulation ◽  
Steady State ◽  
Body Temperature ◽  
Gas Exchange ◽  
Wistar Rats ◽  
Ventilatory Responses ◽  
Constant State ◽  
Made In ◽  
Stimulation Of

Steady state measurements of metabolic gas exchange, ventilation and body temperature were made in anesthetized (urethane) Wistar rats breathing gas mixtures in compositions ranging from 20 to 30% oxygen, 0 to 10% carbon dioxide, and nitrogen. Metabolic rate was caused to vary by interrupted electrical stimulation of limb muscles. From 218 such determinations a regression was calculated, Vcoco2 = 0.00843 V (0.999Fe – Fi) – 0.091. It is concluded that the coco2 exchange of rats is similar to those reported in man and dog. Particular care was taken to assure a steady (constant) state at the time of measurement. Homeostatic defense against internally produced CO2 is good, whereas that against environmental CO2 changes is poor.

scholarly journals An Assessment of the Steady-state Carbon Monoxide Method of Estimating Pulmonary Diffusing Capacity

Thorax ◽  
1959 ◽  
Vol 14 (2) ◽  
pp. 166-175 ◽  
Author(s):  
J. MacNamara ◽  
F. J. Prime ◽  
J. D. Sinclair
Keyword(s):  
Carbon Monoxide ◽  
Steady State ◽  
Diffusing Capacity ◽  
Pulmonary Diffusing Capacity

Respiration in man during metabolic alkalosis

1962 ◽  
Vol 17 (1) ◽  
pp. 33-37 ◽  
Author(s):  
Daniel J. Stone
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Lung Function ◽  
Gas Exchange ◽  
Metabolic Alkalosis ◽  
Time Lag ◽  
Respiratory Compensation ◽  
Arterial Ph ◽  
Oral Sodium ◽  
Ventilation Response

A steady state metabolic alkalosis was induced in two subjects over a period of several days utilizing oral sodium bicarbonate in dosages of 50 g/day. The purpose of inducing steady state metabolic alkalosis was to study the effects of such a state on the respiratory center responses to inspired gas mixtures, containing carbon dioxide, and to contrast these results with the control studies. The experiment was so designed that the arterial pH in both subjects tended to return toward normal in the presence of significant increases in blood bicarbonate. Repeated study of ventilation responses with room air and 4% and 6% carbon dioxide in inspired air revealed a definite and significant decrease in ventilation response to carbon dioxide during the periods of steady state alkalosis as compared to the control periods. Normal responses returned after some time lag. A consistent rise in paCOCO2 occurred with alkalosis, thus demonstrating respiratory compensation. In neither subject was total lung function or gas exchange affected by the alkalosis. The experiment was confirmed on several occasions with reproducible results. Note: (With the Research Assistance of Mary Di Lieto) Submitted on May 22, 1961

Effects of successive carbon monoxide exposures on delayed neuronal death in mice under the maintenance of normal body temperature

1991 ◽  
Vol 179 (2) ◽  
pp. 836-840 ◽  
Author(s):  
Hirohisa Ishimaru ◽  
Toshitaka Nabeshima ◽  
Akira Katoh ◽  
Hirotaka Suzuki ◽  
Taneo Fukuta ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Body Temperature ◽  
Neuronal Death ◽  
Delayed Neuronal Death ◽  
Normal Body Temperature ◽  
Normal Body

Effects of altering ventilation on steady-state diffusing capacity for carbon monoxide

1963 ◽  
Vol 18 (1) ◽  
pp. 89-96 ◽  
Author(s):  
Kaye H. Kilburn ◽  
Harry A. Miller ◽  
John E. Burton ◽  
Ronald Rhodes
Keyword(s):  
Carbon Monoxide ◽  
Steady State ◽  
Tidal Volume ◽  
Lung Volume ◽  
Dead Space ◽  
Control Level ◽  
Alveolar Ventilation ◽  
Positive Pressure ◽  
Diffusing Capacity ◽  
Fixed Rate

Alterations in the steady-state diffusing capacity for carbon monoxide (Dco) by the method of Filley, MacIntosh, and Wright, produced by sequential changes in the pattern of breathing were studied in anesthetized, paralyzed, artificially ventilated dogs. The Dco of paralyzed, artificially ventilated control dogs did not differ significantly during 3 hr from values found in conscious and anesthetized controls. A fivefold increase in tidal volume without changing frequency of breathing raised alveolar ventilation and CO uptake 500% and Dco 186%. A high correlation between tidal volume and Dco was noted during reciprocal alterations of tidal volume and rate which maintained minute volume. The Dco appeared to fall when alveolar ventilation was tripled by increments of rate with a fixed-tidal volume, despite a 63% increase in CO uptake. Doubling end-expiratory lung volume by positive pressure breathing without altering tidal volume or rate did not affect Dco. The addition of 100 ml of external dead space with rate and tidal volume constant decreased Dco to 42% of control level, however, stepwise reduction of dead space from 100 ml to 0 in two dogs failed to change Dco. Added dead space equal to frac12 tidal volume (170 ml) reduced Dco to 25% of control in two dogs with a return to control with removal of dead space. Thus, in paralyzed artificially ventilated dogs, tidal volume appears to be the principal ventilatory determinant of steady-state Dco. Dco is minimally affected by increases in alveolar ventilation with a constant tidal volume effected by increasing the frequency of breathing. Prolonged ventilation, at fixed rate and volume, and increased dead space either did not effect, or they reduced Dco, perhaps by rendering less uniform the distribution of gas, and blood in the lungs. Although lung volume was doubled by positive-pressure breathing, pulmonary capillary blood volume was probably reduced to produce opposing effects on diffusing capacity and no net change. Submitted on March 14, 1962

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