Arthur B. Otis

VENTILATORY IMPLICATIONS OF PHONATION AND PHONATORY IMPLICATIONS OF VENTILATION

The primary physiological function of breathing is respiratory, i.e., it is concerned with the regulation of the partial pressures of carbon dioxide and oxygen in the body. Physiologists have devoted much thought and effort to an attempt to determine the nature of the control mechanisms involved in this regulation. An important secondary function of breathing is the part it plays in the production of sounds. The most highly developed example of this function is probably human speech, which requires an exceedingly precise control of breathing. especially during the expiratory phase. Physiologists seem to have given relatively little attention to the interaction between these two functions of breathing, but it does seem that the control mechanism regulating airflow for phonation and that regulating the gas tensions of the body may at times be somewhat competitive and that situations may arise in which one may temporarily override the other. We have approached this problem by asking the following questions: What are the ventilatory implications of phonation? Do we, when we talk, breathe optimally for respiratory purposes, or too much, or too little? What are the phonatory implications of ventilation? When we increase Our ventilation in response to an augmented respiratory load, how is our ability to talk affected?

Studies of alveolar-mixed venous CO2 and O2 gradients in the rebreathing dog lung

Abstract Measurements were made of PCO2 and PO2 in alveolar gas of dog lungs rebreathing in situ and in the pulmonary arterial blood. The PCO2 in alveolar gas was almost always found to be higher than that of the blood under a variety of experimental conditions. The Po2 was also usually higher in alveolar gas than in blood, but less consistently than in the case of CO2. The magnitude of the observed gradients showed no consistent relationship to duration of experiment or rate of blood flow through the lung. Respiratory acidosis increased the CO2 gradient, but reduced that for O2. Inhibition of blood carbonic anhydrase enhanced the CO2 gradient. When normalized with respect to plasma bicarbonate concentration, the CO2 gradient is inversely related to plasma pH. No definitive explanation is offered for these observations.

THE PHYSIOLOGY OF CARBON MONOXIDE POISONING AND EVIDENCE FOR ACCLIMATIZATION

The most obvious physiological effects of carbon monoxide, at least in vertebrate animals, seem to be related to its propensity for competing with oxygen as a ligand in various hematin-containing respiratory pigments, thus preventing, or interfering with, the normal carriage, transfer, or reduction of oxygen. Organisms lacking such pigments are not known to be affected by CO, and animals with great anaerobic capacities, such as certain species of turtles can, as demonstrated by Dr. Belkin in my laboratory, tolerate an atmosphere of pure CO for many hours. Except for carboxy-heme formation, CO might be regarded as physiologically inert gas, were it not for the demonstrated facts that it is both produced and consumed by metabolic processes, albeit it at very slow rates, described in this monograph by Professors Sjostrand and Fenn. The affinity of CO for hemoglobin is orders of magnitude greater than that for other respiratory pigments, and it appears that when a mammal is exposed to CO, the only readily observable physiological effects are related to the formation of COHb. This not only decreases the oxygen transport capacity of blood but also makes more difficult the unloading of that amount of oxygen which is carried, as is so clearly shown by the graphic representation of Roughton and Darling1 I should, at this point, pay tribute to Claude Bernard, who first discovered the great affinity of CO for hemoglobin, and to J. S. Haldane and his collaborators,2 who did much of the early work on the quantitative relationships of this combination. The hypoxia caused by CO be-rs some resemblance to that resulting from exposure to an environment low i c i oxygen, such as occurs at altitude, or to that resulting from right-to-left shunts in the circulation of individuals with certain congenital defects. It is well known that either chronic exposure to altitude or the presence of a right-to-left circulatory shunt produces certain physiological changes to which we sometimes refer as acclimatization. Such changes may be interpreted as being of adaptive value.3 What is the evidence that acclimatization to CO actually occurs? If it does occur, what are the basic physiological changes involved? The evidence that it occurs in man is not as well documented as it is in the case of acclimatization to altitude, perhaps because controlled exposures to a constant or well-defined environment are, in the case of CO, more difficult to achieve. Most of the evidence is anecdotal in nature. In referring to experiments that he and Smith4, performed on themselves, Haldanez says the following:

Comparison of blood and alveolar gas composition during rebreathing in the dog lung.

Abstract In each often dogs, one lung was connected to a rubber bag and made to rebreathe while the other lung was allowed to breathe freely. Blood samples were taken from a pulmonary vein of the rebreathing lung and from the pulmonary artery, and gas samples were taken from the rebreathing bag. pco2 and PO2 of the gas phase were higher than the corresponding partial pressures in either blood sample. pCO2 of pulmonary venous blood was higher than that of pulmonary arterial blood, but there was no significant difference between the values for PO2 of the two samples. Pulmonary venous blood had a slightly lower pH than pulmonary arterial blood. Plasma bicarbonate tended to be higher in pulmonary venous blood than in pulmonary arterial blood, but the difference was not statistically significant. Over a period of two hour plasma bicarbonate decreased slightly, and negative base excess increased by a similar magnitude. These experiments confirm but do not explain the results of other investigators in demonstrating the presence of positive gradients for CO2 between gas and blood phases during rebreathing.

CO2 Retention in Anesthetized Dogs after Inhibition of Carbonic Anhydrase.

Summary CO2 elimination of anesthetized dogs was temporarily reduced after injection of carbonic anhydrase inhibitor. Reduction was greater for dogs in which ventilation was held constant than for dogs ventilating spontaneously. Results indicate that increased gradient for Pco2 from tissues to the alveolar gas is essential for reestablishing a steady state of CO2 elimination when carbonic anhydrase is inhibited. The required increase in this gradient can be produced by means of augmented ventilation, by increased tissue Pco2, or by combination of these 2 factors.

Pressure-flow relationships and power output of breathing

The pressure-flow relationship obtained by Agostoni and Fenn (1960) during maximal inspiratory efforts against various external resistances contains information from which inferences regarding the power output, and the internal impedance of the breathing system can be made. Similar inferences can be made from measurements obtained with submaximal but constant inspiratory efforts. An analysis is presented to reconcile the observed linear pressure-flow relationships with the usually observed hyperbolic force-velocity relationship of muscle.

EFFECT OF CHRONIC EXPOSURE TO HYPOXIA ON BLOOD PRESSURE AND THYROID FUNCTION OF HYPERTENSIVE RATS

Abstract : Chronic exposure to an atmosphere containing 13% oxygen protects against development of renal hypertension in rats. The mechanism through which the rats are protected may involve the thyroid gland since certain criteria for assessment of thyroid function, using radioactive iodide, suggest depression of activity. Other physiologic mechanisms, brought into play as a result of hypoxia, may also contribute and need to be studied.