Mathematical simulation of pulmonary O 2 and CO 2 exchange.

Rate of gas absorption during atelectasis.

Nomograms for correction of blood Po2, Pco2, pH, and base excess for time and temperature.

We have used low temperature pressure broadening data from a collisional cooling experiment to make improvements on an existing HCl-He potential $surface.^{1}$ As evidenced in earlier work on the CO-He $system^{2}$, theoretically calculated pressure broadening cross sections at 77 K and above are quite insensitive to details of the intermolecular potential surface. However, at very low temperature ($<10$ K) where resonance phenomena dominate, small changes in the potential surface can have dramatic effects on predicted cross sections. These cross sections are especially sensitive to changes in the short range, attractive part of the potential. Using pressure broadening data on the $J=0-1$ transition of DCl taken at temperatures between 1.8 and 4.2 K and at 300 K, incremental modifications were made to an existing potential surface to more faithfully reproduce both the low temperature and room temperature data. The resulting $potential^{3}$ surface predicts both low temperature and 300 K cross sections to within $\\sim$10\\% and is in good agreement with other determinations of the isotropic part of the HCl - He potential.

Carbonic anhydrase: chemistry, physiology, and inhibition.

Mean Circulatory Filling Pressure Measured Immediately After Cessation of Heart Pumping

Effect of temperature and hemoglobin concentration on solubility of O2 in blood.

Telemetered cardiac response to selected running events.

obtained from such studies is often difficult to interpret because the precise work intensity is not known and/or the duration of the exercise is too short for cardiorespiratory function to stabilize and a “Steady state” of exercise to be achieved. WASSERMAN, KARLMAN, ANTONIUS L. VAN KESSEL, AND GEORGE G. BURTON. Interaction of physiological mechanisms during exercise. J. Appl. Physiol. 22(1): 71-85. rg67.-The effects of work intensity and duration on the metabolic circulatory and ventilatory response to exercise are quantitated in healthy male subjects during cycle ergometer exercise. There is a wellordered relationship between work rate and oxidatve energy sources. Steady-state time for 02 consumption (Vo,) is dependent on work intensity (the time arterial blood lactate concentration stops increasing). At moderate work, anaerobic metabolism is a very small part of credit oxidation, while at very heavy work, the pyruvate-lactate mechanism is the major creditor. The increase in gas exchange ratio (R) reflecting the production of CO2 from bicarbonate (buffering of lactic aid) is transient. After the steady state is reached, R decreases. The heart rate increase during constant-load exercise parallels the increase in vo,. Physiological dead space/tidal volume ratio decreases from .33 to .17 during exercise. The reduction is independent of work duration and only slightly reduced as work intensity increases. Arterial 02 tension does not decrease during exercise at sea level even at maximal rates of 02 transport. Arterial-end tidal CO2 tension differences suggest a fluctuation in pulmonary capillary CO2 tension of approximately 8 mm Hg during the respiratory cycle of the exercising subject. Changes in minute ventilation are best predicted from the rate of CO2 production and the extent of respiratory compensation for metabolic acidosis.

Alveolar CO2 during the respiratory cycle.

The interrelationships between the changes in plasma volume, hematocrit, and plasma proteins during muscular exercise and bed rest were investigated. Proportionally, the changes in hematocrit are always smaller than the changes in plasma volume. For this reason changes in the concentration of blood constituents can only be quantitated on the basis of plasma volume changes. During short periods of intensive exercise, there was a small loss of plasma proteins. With prolonged submaximal exercise there was a net gain in plasma protein, which contributes to stabilization of the vascular volume. Prolonged bed rest induced hypoproteinemia; this loss of plasma protein probably plays an important role in recumbency hypovolemia.

<i>‘Ideal’ Alveolar Air and the Analysis of Ventilation-Perfusion Relationships in the Lungs</i>

Effects of exercise on adrenocortical function.

Effect of adrenergic agents on toad bladder response to ADH, 3',5'-AMP, and theophylline.

since the 1970s, over 200 studies with acetazolamide have shown it safe and 60–80% effective in acute mountain sickness (AMS). Despite much investigation, our understanding of its action in AMS remains incomplete and more complicated than generally taught. This should come as no surprise

To determine to what extent the increases in concentration of plasma proteins and electrolytes with short maximal work were a result of hemoconcentration, the changes in plasma volume and total content of the plasma constituents were simultaneously evaluated. The results obtained from six human subjects indicated that in comparison to preexercise values there was a net decrease in total content of plasma protein, sodium, and chloride in the first 2 min of the postexercise period, due primarily to a significant loss (13-15%) of plasma fluid. The total plasma potassium content was increased immediately after exercise but was significantly below the preexercise plasma content after 2 min of recovery.