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SUMMARY1. We examined the quantitative and qualitative differences between the steadystate and rebreathing methods of determining C02-response curves before and after each of two doses of intravenous morphine (0 07 and 0-14 mg kg-') in four healthy male humans.2. During each study session steady-state and rebreathing C02-response curves were determined as an ordered pair (separated by 15 min). Carbon dioxide-response curves were determined for control, after 0 07 mg kg-' morphine, and after a total of 0-21 mg kg-1 morphine. Each subject was studied on a second occasion when the order of the C02-response pairing was reversed.3. The results are discussed and related to a model that may account for the differences based on the step increase in CO2 at the onset of rebreathing, the rate of rise of CO2 during rebreathing and the time constant for the central chemoreflex.4. Our empirical conclusion is that morphine causes a parallel right shift of the steady-state CO2-response curve and causes a non-specific decrease in the slope of the rebreathing C02-response curve. We suggest that the parallel shift of the steadystate C02-response curve is specific to drugs acting on opioid receptors.

Arterial oxygen saturation values (Sao2) from 60% to 98% were measured by the Ohmeda 3700 pulse oximeter with the three types of probe available and compared with values of oxygen saturation estimated from direct arterial sampling (arterial oxygen and carbon dioxide tensions and pH) on 65 occasions. The response time of the oximeter was measured after a sudden rise in inspired oxygen concentration. Artefact rejection was assessed by arterial compression proximal to the probe site, and by simultaneous recordings of overnight Sao2 on opposite hands. The ability to recreate patterns of oscillating Sao2 from the data stored in the oximeter was also investigated. With the best probe system the oximeter measured Sao2, relative to arterial values estimated from Pao2, with a mean (SD) difference of -0 4% (1 8%). The response time was comparable with those of previous oximeters. It was not possible to generate artefactual dips in excess of 2% Sao2, and the dual overnight recordings rarely showed even small dips on one tracing alone.

Hypothermia produces a decrease in metabolic rate that may be beneficial under conditions of reduced O2 delivery (Do2). Another effect of hypothermia is to increase the affinity of hemoglobin for O2, which can adversely affect the release of O2 to the tissues. To determine the overall effect of hypothermia on the ability of the peripheral tissues to extract O2 from blood, we compared the response to hypoxemia of hypothermic dogs (n = 8) and of normothermic controls (n = 8). The animals were anesthetized, mechanically ventilated, and paralyzed to prevent shivering. The inspired concentration of O2 was progressively reduced until the dogs died. The core temperatures of the control and hypothermic dogs were 37.7 +/- 0.3 and 30.5 +/- 0.1 degree C, respectively (P less than 0.01). The O2 consumption (VO2) of the control dogs was significantly greater than that of the hypothermic dogs (P less than 0.05), being 4.7 +/- 0.4 and 3.2 +/- 0.3 ml X min-1 X kg-1, respectively. Hypothermia produced a left shift of the oxyhemoglobin dissociation curve (ODC) to a PO2 at which hemoglobin is half-saturated with O2 of 19.8 +/- 0.7 Torr (control = 32.4 +/- 0.7 Torr, P less than 0.01). The O2 delivery at which the VO2 becomes supply dependent (DO2crit) was 8.5 ml X min-1 X kg-1 for control and 6.2 ml X min-1 X kg-1 for hypothermia. The hypothermic dogs maintained their base-line VO2's at lower arterial PO2's than control.(ABSTRACT TRUNCATED AT 250 WORDS)

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