What is reported in the following pages is an example of work achieved in a relatively short time by the co-operation of a sufficient number of institutions and individuals. The venue of this research was in the Andes, and the work was carried out in the winter 1921-1922, yet its organisation only commenced definitely in the early summer of 1921, when a group of British and American physiologists secured the support of the various universities or other institutions to which they were attached. This support was given in the most ungrudging way. It included the liberation from immediate duty of the members of the party, often at considerable inconvenience to those who remained at home, the loan of apparatus, the contribution of substantial funds, and a great body of goodwill, which was perpetually translating itself into increased efficiency of the work actually accomplished. The following collaborated in one or more of the ways indicated above:— The Department of Physical Chemistry of Harvard University. The Proctor Fund of Harvard University. The Elizabeth Thompson Fund. The Rockefeller Institute of Medical Research, New York City. Columbia University.—From a fund, to which contributions were made by Dr. Walter B. James, Mr. Cleveland H. Dodge, and a contributor who wishes to withhold his name, but to whom thanks are none the less due. The Royal Society of London. The Research Grant to the Physiological Department of the University of Toronto. The Moray Fund, Edinburgh. The Carnegie Fund, Edinburgh. Sir Robert Hadfield, Bart., F. R. S. Sir Peter Mackie, Bart.
The liability to fatigue of the respiratory center is a subject which needs to be studied. Davies, Haldane, and Priestley (1) were the first to investigate the manner in which breathing adapts itself to increased resistance, and the point at which the adaptation begins to fail. They showed that the normal response in man to respiratory resistance in both phases of respiration is slow and deep breathing. When the resistance is excessive respirations become progressively shallower and more frequent and the subjects then become cyanotic. Haldane and his coworkers believe that this is due to fatigue of the respiratory center. They believe anoxemia hastens greatly the onset of fatigue and the ease with which it is produced. They conclude that the mechanism involved in the immediate response is the HeringBreuer reflex, pointing out that as a result of resistance, the time required for inflation or deflation of the lungs to reach the point at which the Hering-Breuer stimulus becomes effective is prolonged, that CO~ accumulates in the meantime, and that the next respiration is deep and vigorous. The more or less sudden onset of rapid, shallow breathing Haldane interprets as evidence of fatigue of the respiratory center, with a resulting predominance of the peripheral stimuli over the central impulses normally governing breathing.A study of these effects in animals was undertaken by us with several points in mind. We hoped for additional information as to the nature and origin of rapid and shallow breathing, which we have previously considered in both clinical and experimental studies (2-5). It seemed highly desirable to learn something about the liability to fatigue of so vital a structure as the respiratory center. Transferring the problem
1. Oxygen in concentrations of over 70 per cent of an atmosphere is poisonous to dogs, rabbits, guinea pigs and mice. 2. The poisonous effects manifest themselves in drowsiness, anorexia, loss of weight, increasing dyspnea, cyanosis and death from oxygen want. 3. The cause of oxygen want is a destructive lesion of the lungs. 4. The lesion may be characterized grossly as an hemorrhagic edema. Microscopically there is to be seen in varying degrees of intensity (a) capillary engorgement with hemorrhage, (b) the presence of interstitial and intraalveolar serum, (c) hypertrophy and desquamation of alveolar cells, (d) interstitial and alveolar infiltration of mononuclear cells. 5. The type of tissue reaction is not characteristic of an infectious process and no organisms have been recovered at autopsy from the heart's blood or from lung puncture. 6. The poisonous effects of inhalations of oxygen-rich mixtures do not appear to be related to impurities in the oxygen, nor are they related to faulty ventilation, excessive moisture or increased carbon dioxide in the atmosphere of the chambers in which the experimental animals were confined.
Peabody in 1912 (1) published a paper on the metabolism in pneumonia, in which he reviewed the previous literature and studied among other factors the blood gases and acid-base balance. Since Peabody, a number of other investigators have studied the blood gases and the question of the existence and importance of acidosis in pneumonia. The present paper is a report of observations on these subjects, in which recently developed methods have made possible the attainment of more complete results and apparently have justified the drawing of deductions more definite in some respects than those attainable from previous data.
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