Experimental alteration of pulmonary functions.

Knowledge of the effects of experimental pulmonary disease on pulmonary function has bearing on the effects of various human diseases on pulmonary function I n addition, information about reserves of pulmonary function present in normal animals and the types of functional limitation that occur under various conditions may be related to human disease. For the purpose of this review, pulmonary function will be subdivided into ventilation, diffusion and distribution of blood and gas in the lung. Ventilatory function, of which the end result is alveolar ventilation, includes the phenomena responsible for the nervous and chemical control of respiration, the thoracic and diaphragmatic innervation and musculature, the compliance of the lung and chest, the resistance to airflow through the airways and the size of the lung dead space. Dif fus ion refers to the diffusion of oxygen from the alveoli into the blood circulating through the alveoli. The measurement of this function, the diffusing capacity of the lung, is defined as the volume of oxygen consumed by the lung per minute per mm. mercury pressure difference between the alveolar tension and the mean oxygen tension in the blood flowing through the lung capillaries. Distribution refers to the areas to which blood and gas flow in the lung, particularly in reference to one another. The pulmonary circulation will be considered as a component of the distribution function. A number of methods are available for producing impairment of one o r more of these functions, and the effects of various experimental diseases and procedures on these functions will be reviewed. Limitation of each of the three functions results in distinctly different physiological abnormalities.' Reduction o f alveolar ventilation results in elevation of alveolar and arterial carbon dioxide tensions with comparable reductions of alveolar and arterial oxygen tensions. Because of the flat shape of the oxygen dissociation curve above an oxygen tension of 70 mm. Hg., the arterial oxygen tension has to be greatly reduced before arterial unsaturation results. However, slight elevation of the carbon dioxide tension results in acidosis until i t is compensated by renal retention of bicarbonate. Impaired diflusion results, eventually, in anoxemia which is greatly aggravated by inspiration of a low oxygen mixture, ascent to high altitude, o r by increased oxygen consumption such as occurs during muscular exercise. Because of the relatively great diffusibility of carbon dioxide, Con retention would only be expected t o be significant when anoxemia were present to an extent incompatible with life. Impaired distribution may take the form of an effective right-to-left shunt which results in anoxemia from the mixture of venous blood with blood arterialized in the lung. Carbon dioxide retention need not occur when reduction of the arterial oxygen saturation