EFFECTS OF PROSTAGLANDIN E(2) INHALATION ON HYPERCAPNIC RESPONSE IN NORMAL SUBJECTS

It is known that the ventilatory response to carbon dioxide (CO2) is i ncreased in asthmatics with airway obstruction. Increased vagal affere nt activity as well as increased airway resistance have been postulate d as the causative mech an is ms. However, whether increased vagal aff erent activity without bronchoconstriction increases the ventilatory r esponse to CO2 has not been investigated in humans. We examined the ef fects of prostaglandin E(2) (PGE(2)) inhalation, which is known to sti mulate vagal afferent receptors in the lung without an increase in air way resistance, on the respiratory response to CO2 in seven healthy ma le subjects. Either physiologic saline or PGE(2) (100 mu g/ml) was inh aled through a Bird nebulizer for 3 min. Twenty minutes after each inh alation, the responses of minute ventilation (VE) and occlusion pressu re (P-0.1) to hyperoxic hypercapnia were measured. Both the relationsh ips between VE and P-0.1 to an increase in tension of end-tidal CO2 (P ET(CO2)) were analyzed by linear regression. Although the mean value o f respiratory resistance after PG2E(2) (3.0 cm H2O/L/s +/- 0.4) did no t differ significantly from that after saline (3.1 cm H2O/L/s +/- 0.4) , inhaled PGE(2) significantly increased the hypercapnic response. Thi s result suggests that the increased vagal afferent activity per se pl ays an important role in increasing the hypercapnic ventilatory respon se in humans.