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Hypo-osmolar aerosol induces hyperventilation in chronic non-asthmatic rhinitics.

The effect of a hypo-osmolar aerosol on transcutaneous O2 and CO2 time course (PtcO2, PtcCO2) was investigated in subjects affected by chronic non-atopic rhinitis, without any history of asthmatic symptoms and no airways hyper-responsiveness. Twelve normal subjects and 12 subjects affected by chronic idiopathic rhinitis, who had normal responsiveness to both hypo-osmolar aerosol and methacholine challenge as measured by the decrease in FEV1 (mean FEV1 decrease = 5% and PC20 > 16 mg, respectively) were studied. By means of a transcutaneous mono-electrode, it was possible to study the time course of PtcO2 and PtcCO2 during and after a 5-min inhalation of ultrasonically nebulized distilled water (output 2 ml/min-1). A significant decrease in PtcCO2 and increase in PtcO2 were observed during the challenge in rhinitics as compared with normal subjects [maximum decrease and maximum increase expressed as mean value (+/- SD) were -22% (+/- 6.9) and +12.6% (+/- 7.2), respectively]. No significant changes in either PtcCO2 and PtcO2 were observed after the test. The results of this study suggest that patients affected by idiopathic chronic rhinitis with absence of bronchial hyper-responsiveness may present a hyperventilatory response to the inhalation of hypo-osmolar aerosol; the mechanism of such a response might be due to an upregulation of the irritant receptors of the upper airways.

Adolescent↗

Hyperventilation with He-O2 breathing is not decreased by superimposed external resistance.

The purpose of this study was to determine the effect of imposed external resistance on the ventilatory response to He-O(2) breathing during peak exercise. To accomplish this purpose, separate inspiratory and expiratory external resistances were applied to offset for the decrease in intrapulmonary airway resistance with He-O(2) breathing. Seven men and three women (69+/-3 years, mean+/-S.D.) with normal pulmonary function performed graded cycle ergometry to exhaustion breathing room air, He-O(2) (79% He, 21% O(2)), He-O(2) with imposed expiratory resistance, and He-O(2) with imposed inspiratory resistance. Ventilation (VE), lung mechanics, and PET(CO(2)) were measured during each 1 min increment in work rate and were analyzed by one-way ANOVA for repeated measures at rest, ventilatory threshold (VTh), and peak exercise. In response, VE was increased and PET(CO(2)) was decreased at VTh (P<0.01) and peak exercise (P<0.01) whenever breathing He-O(2). Thus, VE was increased during exercise above VTh with He-O(2) breathing regardless of increases in inspiratory or expiratory external resistance. In conclusion, these data suggest that inspiratory resistive unloading is no more important than expiratory resistive unloading to the increase in VE with He-O(2) breathing during heavy and peak exercise.

Aged↗

Role of glutamate in the nucleus isthmi on the hypoxia- and hypercarbia-induced hyperventilation of toads.

The nucleus isthmi (NI) is a mesencephalic structure of the amphibian brain that has been reported to participate in CO(2) chemoreception and in the ventilatory response to hypoxia. In the present study, we assessed the role of glutamatergic transmission inside the NI on the hypoxic and hypercarbic drive to breathing. We compared the respiratory responses to 7 and 5% inspired O(2) and 3% inspired CO(2) after microinjecting 10 nmol/100 nl of kynurenic acid (an antagonist of L-glutamate receptors) into the NI of toads (Bufo paracnemis). Kynurenic acid had no effect under resting conditions. Both hypoxia and hypercarbia elicited an increase in ventilation in all groups, with hypoxia acting on tidal volume (V(T)) and hypercarbia on frequency (f). The microinjection of kynurenic acid into the NI caused an increased ventilatory response to hypoxia and hypercarbia due to a higher V(T). We conclude that glutamatergic transmission in the NI has an inhibitory effect when the respiratory drive is high, acting on V(T).

Animals↗