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The ability to detect added resistance at rest was compared to the magnitude of breathlessness (evaluated by a modified Borg scale) during bronchoconstriction in 27 stable asthmatics. Threshold for resistive load detection was analyzed in terms of the Weber fraction (delta R/R0) and mouth pressure (P) at the threshold. Bronchoconstriction was induced by inhalation of aerosolized acetylcholine. Both delta R/R0 and P correlated inversely with the Borg score during bronchoconstriction (r = -0.537 and r = -0.689, respectively; p less than 0.01). On the other hand, during bronchoconstriction the Borg score did not correlate with increased lung volume, acute changes in arterial blood gas composition and drive and timing component of ventilation during bronchoconstriction, although bronchoconstriction caused significant changes in these variables. These results indicate that central processing of afferent stimuli rather than peripheral sensor contribute both to the ability to detect added resistance at rest and to the magnitude of breathlessness during bronchoconstriction in asthmatics.

In 58 patients with chronic obstructive pulmonary disease, pulmonary gas exchange efficiency was assessed by the ratio: arterial to mixed venous PO2 difference (efficient part) versus alveolar to mixed venous PO2 difference (driving pressure for O2 transport). Patients with PaO2 below 75 mm Hg had a ratio lower than 50%. Patients with PaO2 below 60 mm Hg had lower values for arterial to mixed venous O2 content difference and higher blood lactic acid concentration than patients with PaO2 over 60 mm Hg. Arterial to mixed venous PO2 difference decreased linearly against PaO2 till PaO2 reached 60 mm Hg from which the difference began to attenuate. These figures in PaO2 are in close agreement with the criteria for pulmonary failure presented by the Ciba guest symposium (PaO2 below 75 mm Hg) and for respiratory failure by the National Heart, Lung and Blood Institute (PaO2 below 60 mm Hg).

To assess the effect of brain blood flow on hypoxic ventilatory response, we measured arterial and internal jugular venous blood gases and ventilation simultaneously and repeatedly in eight healthy male humans in two settings: 1) progressive and subsequent sustained hypoxia, and 2) stepwise and progressive hypercapnia. Ventilatory response to progressive isocapnic hypoxia [arterial O2 partial pressure 155.9 +/- 4.0 (SE) to 46.7 +/- 1.5 Torr] was expressed as change in minute ventilation per change in arterial O2 saturation and varied from -0.16 to -1.88 [0.67 +/- 0.19 (SE)] l/min per % among subjects. In the meanwhile, jugular venous PCO2 (PjCO2) decreased significantly from 51.0 +/- 1.1 to 47.3 +/- 1.0 Torr (P less than 0.01), probably due to the increase in brain blood flow, and stayed at the same level during 15 min of sustained hypoxia. Based on the assumption that PjCO2 reflects the brain tissue PCO2, we evaluated the depressant effect of fall in PjCO2 on hypoxic ventilatory response, using a slope for ventilation-PjCO2 line which was determined in the second set of experiments. Hypoxic ventilatory response corrected with this factor was -1.31 +/- 0.33 l/min per %, indicating that this factor modulated hypoxic ventilatory response in humans. The ventilatory response to progressive isocapnic hypoxia did not correlate with this factor but significantly correlated with the withdrawal test (modified transient O2 test), which was performed on a separate day. Accordingly we conclude that an increase in brain blood flow during exposure to moderate hypoxia may substantially attenuate the ventilatory response but that it is unlikely to be the major factor of the interindividual variation of progressive isocapnic hypoxic ventilatory response in humans.

Minute ventilation (VE) during sustained hypoxia is not constant but begins to decline within 10–25 min in adult humans. The decrease in brain tissue PCO2 may be related to this decline in VE, because hypoxia causes an increase in brain blood flow, thus resulting in enhanced clearance of CO2 from the brain tissue. To examine the validity of this hypothesis, we measured VE and arterial and internal jugular venous blood gases simultaneously and repeatedly in 15 healthy male volunteers during progressive and subsequent sustained isocapnic hypoxia (arterial PO2 = 45 Torr) for 20 min. It was assumed that jugular venous PCO2 was an index of brain tissue PCO2. Mean VE declined significantly from the initial (16.5 l/min) to the final phase (14.1 l/min) of sustained hypoxia (P less than 0.05). Compared with the control (50.9 Torr), jugular venous PCO2 significantly decreased to 47.4 Torr at the initial phase of hypoxia but did not differ among the phases of hypoxia (47.2 Torr for the intermediate phase and 47.7 Torr for the final phase). We classified the subjects into two groups by hypoxic ventilatory response during progressive hypoxia at the mean value. The decrease in VE during sustained hypoxia was significant in the low responders (n = 9) [13.2 (initial phase) to 9.3 l/min (final phase of hypoxia), P less than 0.01], but not in the high responders (n = 6) (20.9–21.3 l/min, NS). This finding could not be explained by the change of arterial or jugular venous gases, which did not significantly change during sustained hypoxia in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Factors affecting erythrocyte K+ content and plasma electrolytes during light exercise were examined in 8 normal subjects and 27 patients with chronic obstructive lung disease. The patients were classified into bronchitis, emphysema and intermediate groups. Arterial blood was obtained during rest, after 2, 5, and 7 min. of exercise on a bicycle ergometer (30 km/h without mechanical brake), and at 10 and 20 min. during recovery for analysis of PO2, PCO2, plasma H+, Na+, K+, and Cl(-), erythrocyte K+ content and whole blood lactate. Plasma H+ increased significantly in all subjects after 2 min. of exercise and PCO2 rose in normal, bronchitis, and emphysema groups during exercise, whereas PO2 did not change significantly. Plasma K+ rose promptly after the beginning of exercise and remained at high values during exercise. The rapid rise in PCO2 was associated with a significant decrease of calculated erythrocyte K+ in patients with chronic bronchitis. Although changes in plasma H+ were dependent on both PCO2 and lactate, erythrocyte K+ changes were significantly related only to changes in PCO2. These results indicate that the decrease in erythrocyte K+ is mainly controlled by changes in arterial PCO2 during light exercise in patients with chronic bronchitis.

Summary We describe herein a newly defined pulmonary tumor presenting as an irregular shaped nodule in the peripheral lung, arising in a 62-year-old man. Histologically, the tumor showed papillary configuration, bronchioloalveolar spread, and a mucus lake, consisting of ciliated columnar cells and goblet cells with basaloid cell proliferation. The tumor was diagnosed as ciliated muconodular papillary tumor of the peripheral lung.