A B S T R A C TFor purposes of quantitation these curves are approximated by a simple hyperbolic function, the parameters of which are evaluated by a least squares fit of the data. The parameter A denotes curve shape such that the higher the value of A, the greater the increase in ventilation for a given decrease in PAO2 and hence the greater the hypoxic drive. Curves are highly reproducible for each subject and curves from different subjects are similar. In 10 normal subjects at resting PAcO2, A = 180.2 +14.5 (SEM). When PACO, is adjusted to levels 5 mm Hg above and below control in six subjects A = 453.4 ±103 and 30.2 ±6.8 respectively. These latter values differed significantly from control (P < 0.05). These changes in curve shape provide a clear graphic description of interaction between hypercapnic and hypoxic ventilatory stimuli. At normal PACo2 the VE-PAO2 curve has an inflection zone located over the same P02 range as the inflection in the oxygenhemoglobin dissociation curve. This indicated that ventilation might be a linear function of arterial oxygen saturation or content. Studies in four subjects have
Although morphine depresses respiration the mechanism of this depression remains unknown. Accordingly, ventilatory responses to hypoxia and to hypercapnia were measured before and after administration of 7.5 mg of morphine sulfate subcutaneously in six normal subjects. This procedure produced resting hypoventilation manifested as a peak rise in alveolar carbon dioxide tension from 42.9 plus or minus 1.7 to 45.4 plus or minus 1.5 mm Hg (plus or minus S.E.M.) at 30 minutes ( greater than 0.01). Hypoxic ventilatory drive, measured by an index of the relation between ventilation and hypoxia (parameter A), decreased from a control of 108 plus or minus 17.6 to 42.8 plus or minus 5.3 at 60 minutes after morphine (p greater than 0.01); Hypercapnic ventilatory drive, measured as the slope of the ventilatory response to hypercapnia, also decreased from 1.69 plus or minus 0.24 to 0;98 plus or minus 0.20 (p greater than 0.01) 75 minutes after morphine. Decreased responsiveness to the chemical stimuli to breathing may contribute to the ventilatory depression frequently seen after administration of morphine.
A B S T R A C T To determine whether chronic exposure to hypoxia during adulthood produces alterations in the control of ventilation, measurements of the resting ventilatory response to hypoxia and hypercapnia, as well as ventilatory response to hypoxia during exercise, were carried out in a group of 10 long-term (3-39 yr) nonnative residents of Leadville, Colo. (elevation 3100 m). A group of 8 subjects native to Leadville was also studied and 10 low altitude subjects of Denver, Colo. (elevation 1600 m) served as controls. Hypoxic ventilatory drive was measured as the shape parameter A of isocapnic VE-PAo2 curves. In the non-native high altitude resident this parameter averaged 43% of the value for low altitude controls (P <0.05) denoting a diminished ventilatory response to hypoxia. The degree of attenuation was related to the length of time spent at high altitude. In the high altitude natives the parameter A averaged 9.6% of control (P < 0.01). Similarly hypercapnic ventilatory drive as measured by the slope of the isoxic VE-PACO, lines was reduced in the non-native residents to 65% of control (P <0.05) and in the natives averaged 54% of control (P <0.01).In contrast with these findings at rest induction of hypoxia during exercise produced an increase in ventilation comparable to that in the controls in both groups of highlanders.Hence chronic exposure to hypoxia during adulthood in man results in marked attenuation of the ventilatory response to hypoxia at rest and this is a function of the length of exposure to hypoxia. This attenuation of the ventilatory response to hypoxia was associated with a decrease in hypercapnic ventilatory drive. The fact that hypoxic ventilatory drive was almost completely absent while hypercapnic drive was only partially reduced parallels closely the more important role of the peripheral chemoreceptors in mediating ventilatory responses
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