capacity of the lungs during continuous breathing of carbon monoxide, and also during a period of breath holding. They realized that the first of these methods was made unreliable by the difficulty of calculating the alveolar ventilation, from which the mean tension of CO in the alveoli was derived. This is a critical measurement in the calculation of diffusing capacity since this mean tension is the denominator of the fraction which constitutes it. Riley's method circumvents this difficulty since the mean alveolar 02 gradient is calculated without direct dependence on the dead space. However, difficulty is encountered when the tidal volume exceeds about 1 1., since in these circumstances a small error in the measured arterial pCO2 leads to a very considerable change in calculated effective dead space. In a recent paper Riley (Riley et al. 1954) notes this difficulty, and as he finds that the dead space so calculated is often obviously erroneous, he prefers to substitute a more likely value during estimations on exercise, thus in effect 'correcting' the arterial pCO2. It should be noted that this difficulty observed by Riley operates reciprocally so that during exercise with increasing ventilation, the assumed value of the respiratory dead space influences the calculated mean alveolar CO tension to a smaller and smaller extent. It will be shown later that very different values for respiratory dead space may be assumed during exercise, without these

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In order to evaluate the effects of the chronic uremic syndrome upon some aspects of carbohydrate metabolism in vivo, determinations of gastric and intestinal glucose absorption, and of hepatic glycogen deposition were made in 39 chronically uremic rats and in 49 litter-mate controls. A surgical method for producing chronic uremia was developed. Rats fasted for 24 hours were given a glucose gavage of standard concentration. Three hours later residual gastric and intestinal glucose content and liver glycogen content were determined. No statistically significant difference between the two groups was found in either glucose absorption from the gastrointestinal tract or in glycogen deposition.

To define areas of carbohydrate metabolism which might be altered in uremia, determinations of gastric and intestinal absorption of glucose and deposition of glycogen in the liver of 9 acutely uremic and 24 control rats were performed. Residual gastric and intestinal glucose contents and hepatic glycogen contents were determined 3 hours after glucose lavage in rats fasted for 24 hours. No statistically significant difference was observed in gastrointestinal absorption of glucose and in hepatic deposition of glycogen of the uremic and control animals.