A computerized prediction-correction scheme has been devised for the control of alveolar gases. First, a model is run off-line to predict the inspiratory gas tensions at each second that should yield the desired alveolar patterns. Second, during the experiment, there is feedback correction based on the deviation of the actual alveolar values from the desired alveolar values. The actual alveolar values are found by a second computer and passed to the controlling computer using interrupts. The controlling computer has four digital-toi-analog outputs for controlling CO2, O2, N2, and air flows so as to achieve the commanded inspiratory PCO2 and PO2 (CO2 and O2 partial pressures, respectively). The scheme is illustrated for the generation of sinusoidal alveolar PCO2 with alveolar PO2 held constant and for steps of alveolar PCO2 at constant alveolar PO2.

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SUMMARY1. The effects of moderate degrees of hypercapnia in hypoxia and in hyperoxia on the baroreceptor-cardiodepressor reflex have been studied in nine normal men.2. The beat-by-beat relation between pulse interval (I) and systolic pressure (P) during transient elevations of arterial pressure induced by intravenous injections of angiotensin II and phenylephrine was used to assess the sensitivity (XI/AP) and setting (I at a single reference arterial pressure) of the reflex..3. There was no consistent change in reflex sensitivity in any of the conditions studied.4. In hyperoxia (PA, 02 200 torr) hypercapnia was associated with significant re-setting of the reflex in the direction of tachycardia. The extent of the re-setting was correlated with the degree of hypercapnia and with the accompanying increase in breathing.5. When hyperoxia with hypercapnia was replaced by hypoxia (PA 02 55 torr) with hypercapnia (which causes substantial arterial chemoreceptor activity), pulse interval at constant arterial pressure was further decreased.6. The tachycardia of hypoxia could not be accounted for by change of arterial pressure, PA, co. or pulmonary ventilation, since it was most clearly demonstrable at constant values of pressure andeitherPA cOorventilation.

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SUMMARY1. Breathing hypoxic gas through an external dead space (ca. 1200 c.c.) stimulated ventilation disproportionately. A loop (ca. 250 c.c.) in the inspiratory pathway reduced the effect.2. The alveolar time patterns of P C02 and P02 characteristic of tube breathing with or without the loop have been simulated in moderate hypoxia by changing the composition of inspired gas at selected intervals after the beginning of inspiration.3. Supplying C02-free gas in late inspiration usually stimulated ventilation, but less than did real tube breathing. Supplying C02-free gas early in inspiration usually depressed ventilation. The difference between the 'C02-free late' and 'C02-free early' effects was 20 % of the control ventilation (P < 0.001), i.e. was nearly the same as between the effects of real tube breathing without and with the loop.4. Tube-like PA,02 time patterns had no effects.5. A-a P C02 and P02 gradients remained constant throughout. 6. The IXE, f and VT relations were unaltered in tube breathing. 7. The respiratory system can discriminate between small differences in time patterns of PA, CO 2but not of PA,02 ; the signal is amplified by steady hypoxia. The arterial chemoreceptors are probably responsible for these effects.