To determine whether hypoxic ventilatory response results, in part, from concomitant systemic sympathoadrenal stimulation, we studied ventilation in 20 healthy subjects before and after administration of a beta-blocking agent. A single oral dose of 100 mg bupranolol (vs placebo) significantly lowered minute ventilation from 9.4 +/- 0.7 to 8.3 +/- 0.2 l/min (mean +/- SEM) during normoxia, and from 10.8 +/- 0.8 to 8.9 +/- 0.2 l/min, when 11% O2 was inhaled. In our study, there were marked oscillations of ventilation on changing from room air to hypoxic breathing and back. They were ascribed to the preceding sampling of specimens for blood gas analysis. However, bupranolol had no influence on these transients. Bupranolol also had only slight cardiocirculatory effects during normoxia and did not prevent significant T-wave flattening, increase in heart rate, and fall in diastolic blood pressure during hypoxia. However, it did block the hypoxic increase in systolic blood pressure. From our results we suggest that (1) in spontaneously breathing conscious subjects, hypoxia-induced hyperventilation is also due to hypoxic sympathoadrenal activity and individual mental state, and (2) these influences do not affect all aspects of the cardiocirculatory response.
27 subjects with healthy lungs received during conscious mouth breathing of room air simultaneously also nasally applied O2. The mean O2 concentration of the expiratory air at the mouth was a measure for the effective inspiratory oxygen concentration. Application through a nasal mask at 4 l/min O2 flow proved only slightly superior to the airtight nose frame (25.2 vs 23.6 per cent by volume O2), whereas the highest concentration was achieved by mask and reservoir (35.3 vol.%; 2P less than 0.001). The five habitual mouth breathers of the subject group did not show any O2 uptake through the nose in any of the experiments, the mean nasal share of the inspiration being calculated at 2.5% against 25% for the other subjects (2P less than 0.001). The interindividual differences proved independent of nose resistance and are ascribed to changing active positioning of the soft palate. This mechanism must be taken into consideration when assessing the arterial blood gases in oronasal respiration.
Chest examinations were carried out in 60 individuals using film-screen and digital storage phosphor techniques and identical radiation doses. 29 of these individuals were patients with interstitial pulmonary disease; 31 were normals. Postprocessing of the digital images was carried out with filtering using an unsharp mask and identical parameters for all patients. An ROC analysis using 10 observers showed no significant difference in the evaluation of the interstitial lung disease. Correlation analysis showed a significant positive correlation (p less than 0.001) for the findings in both techniques. Under the present circumstances, film-screen and digital storage phosphor technique are of equal value in the diagnosis of interstitial pulmonary disease.
To quantitatively examine and compare the effects of β-adrenergic blockade on ventilation, we studied 20 healthy volunteers during inhalation of room air and at steady state CO2 (2.0, 4.4, 6.0%) following a single oral dose of bupranolol (vs. placebo). During room air breathing, minute ventilation (VE) and mean inspiratory flow (Vτ/Tι) were significantly reduced after β-blockade with a concomitant increase in blood PaCO2 (p < 0.01). The timing factor Tι/Ttot and mouth occlusion pressure P0.1 remained unchanged. These differences were, as shown from calculated effective alveolar ventilation, mainly attributed to a decrease in physiological dead space ventilation following β-blockade. With a stepwise increase in FICO2, the difference in PaCO2 between placebo and bupranolol tended to approach zero, whereas VE and Vτ/Tι remained significantly lower during β-blockade (P < 0.05). In contrast, no difference existed in P0.1 between bupranolol and placebo. We suggest that (1) respiratory drive assessed by P0.1 is unaffected by β-blockade and (2) mean inspiratory flow depends also on CO2 elimination characteristics, which are influenced by β-blockade
We examined oronasal flow partitioning in 27 volunteers with normal or slightly increased nasal resistance (mean +/- SD, 0.24 +/- 0.19 kPa/l/s). Mean percentage of inspiratory nasal flow contribution was measured during spontaneous oronasal breathing. The averaged nasal admixture of airflow differed considerably within and between all subjects (mean +/- SD, 20.9% +/- 16.5%; range 1%-70%), showing no correlation to nasal resistance. Five of 27 subjects with a history of habitual mouth breathing had a significantly lower nasal admixture as compared with controls (2.5% +/- 1.7% vs 25.1% +/- 15.4%; P less than 0.005), but with no statistical difference in nasal resistance. To evaluate the hypothesis that velopharyngeal narrowing is due to an increased tone of the soft palate, measurements were also performed under positive nasal pressure, inspiratory resistive loading at the mouth, and during breath-holding. There was no significant difference of airflow distribution between these modifications and unloaded breathing in either group. These data suggest, therefore, that oronasal flow distribution is due to active positioning of the soft palate, and that habitual mouth breathing without any nasal obstruction may be associated with closure of the velopharyngeal isthmus as a consequence of disturbed neural control mechanisms.
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