EFFECT OF MEPERIDINE ON OCCLUSION PRESSURE RESPONSES TO HYPERCAPNIA AND HYPOXIA WITH AND WITHOUT EXTERNAL INSPIRATORY RESISTANCE

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Abstract
In 5 normal subjects ventilation and P0.1, the pressure generated by the first 0.1 s of inspiratory effort against a closed airway was measured in response to hypercapnia and hypoxia with and without added inspiratory resistance before and after oral meperidine (1.1-1.3 mg/kg). CO2 responses were studied in the steady state, whereas progressive hypoxia was used to elicit hypoxic responses. In general, resistance decreased ventilatory responses to hypercapnia but increased P0.1 responses to both hypoxia and hypercapnia. Meperidine depressed both ventilatory and P0.1 responses, more so in hypoxia than in hypercapnia. The combination of resistance and meperidine was additive in depressing responses to hypercapnia but in hypoxia produced little more depression than did meperidine alone. In both hypercapnia and hypoxia, meperidine decreased the augmentation of P0.1 that was associated with increased resistance. Normal subjects responded to acute increases of inspiratory resistance by increasing inspiratory motor output; this increase was distinctly blunted by meperidine.

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