Hypoxemia, either chronic or acute, in patients with chronic obstructive pulmonary disease is important for diagnosis and prognosis. However, its pathophysiology has not been wholely elucidated. The role of erythrocyte 2, 3-diphosphoglycerate (2, 3-DPG) on oxygen transport has not attracted attention until recently, and the metabolite is a sourse of conflicting results in patients with chronic obstructive pulmonary disease.
This study was designed to clarify the role of 2, 3-DPG on oxygen transport in 30 patients with chronic hypoxemia due to chronic obstructive pulmonary disease. The patients were divided into two groups according to PaO₂ levels; group A consisted of 16 patients with PaO₂≥60mmHg (mean 67.4±5.1mmHg); group B had 14 patients with PaO₂<60mmHg (mean 51.0±7.5mmHg). Arterial and mixed venous blood gases and pH, 2, 3-DPG, Hb, Ht and cardiac output were 23 measured. Controls were normal males.
1) The concentration of 2, 3-DPG in normal males was 12.3±1.9μmol/gHb.
2) The concentration of 2, 3-DPG in patients was 13.8±3.2μmol/gHb in group A and 16.0±2.9μmol/gHb in group B. The value of group B was significantly higher than that in normal males.
3) Correlation coefficients between 2, 3-DPG and PaO₂, PvO₂ and MCHC were -0.483, -0.362 and -0.374, respectively. However correlation between 2, 3-DPG and pH, PaCO₂, Hb, Ht and cardiac output were not significant.
4) Arterio-venous differences of PO₂ (Δa-vPO₂) was inversely correlated with 2, 3-DPG and this may explain the decrease of Δa-vPO₂ in patients with PaO₂ less than 60mmHg, i. e. 2, 3-DPG may be one of the factors compensating for decrease of Δa-vPO₂.
5) P₅₀ calculated from 2, 3-DPG, MCHC, base excess, pH and body temperature were 3 to 4mmHg higher in group B than normal values. This increase coincides with the increase of the concentration of 2, 3-DPG in group B.
These results indicate that hypoxemia due to chronic obstructive pulmonary disease induces the elevation in 2, 3-DPG to decrease oxyhemoglobin affinity and improve oxygen delivery to tissues.

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We studied the content and properties of glucocorticoid receptors in adult rat lung tissue and bronchoalveolar cells using ³H-betamethasone or ³H-prednisolone.
1) Measurement of the glucocorticoid receptor content of lung tissue by the cell free assay system according to the method of Granberg et al. at 4°C showed it to be localised mainly in the cytosol fraction. The glucocorticoid receptor content of cytosol fraction of lung tissue was about 53fmol/mg protein, and was similar to that of the liver. These two organs showed the highest receptor content levels of the organs tested. The glucocorticoid receptor in lung cytosol fraction bound equally to each glucocorticcid tested, i. e. hydrocortisone, betamethasone, dexamethasone and prednisolone.
2) The glucocorticoid receptor content of bronchoalveolar cells obtained by broncho-alveolar lavage was measured at the cell level; the cells were incubated with radioactive glucocorticoid in vitro, and then the cellular radioactive uptake was measured.
The glucocorticoid receptor content of bronchoalveolar cells was 10fmol/10⁶ cells (about 6, 000 binding sites per cell). The content is considered to reflect the glucocorticoid receptor content of alveolar macrophages, becouse they constituted about 90% of the bronchoalveolar cells.

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In order to clarify the phagocytic and bactericidal activities of human pulmonary alveolar macrophages (PAMs) under various pulmonary pathophysiological conditions, we examined the phagocytosis of yeast particles and NBT reduction by PAMs. PAMs were obtained by segmental bronchoalveolar lavage (BAL) from 10 normal volunteers aged 22.6±1.1 years and the lesion-free regions of 45 patients with respiratory ailments, aged 59.4±11.7 years. The average pack-years of smokers in the former group was 4.6, and 20 to 50 in the latter group.
1. NBT reduction:
1) When human PAMs were cultured for 30 minutes, 4 or 20 hours in vitro, NBT reduction by the PAMs from both the smokers and nonsmokers was the highest after culture for 4 hours.
2) In the normal volunteer group, value of NBT reduction by human PAMs was similar to that in smokers and nonsmokers when the PAMs were cultured for 30 minutes or 4 hours. In the patient group, however, it was significantly higher in the smokers than in the nonsmokers. Probably increase of NBT reduction by PAMs from the smokers depends on the extent of smoking. The values of NBT reduction by human PAMs were not significantly influenced by the underlying diseases.
3) Human IgA or SIgA did not enhance NBT reduction by human PAMs but the 250G supernatant from BAL-fluid or human IgG showed significant enhancement.
4) The patterns and values of NBT reduction by PAMs obtained from the rats to which complete Freund's adjuvant had been injected were different a week after the injection.
These results indicate that NBT reduction by PAMs is influenced by the pathophysiological conditions of lung.
2. Phagocytosis:
1) The yeast-phagocytic activity of human PAMs was lower in smokers than in nonsmokers in both normal volunteer and patient groups, when the assay was performed at 30 minutes, but it was similar in the smokers and nonsmokers on assay at 60 minutes. These results suggest that phagocytic rate of PAMs is lower in smokers than in nonsmokers.
2) The phagocytic activity of PAMs of the cases that had abstained from smoking for 1 to 5 months, was almost the same as that of nonsmokers.
3) There was a reverse correlationship between the yeast-phagocytic activity and NBT reduction by human PAMs.

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The purpose of this paper is to demonstrate the pathophysiological changes in re-expansion pulmonary edema (REPE) in spontaneous pneumothorax. The clinical findings of a case of REPE were presented. Experimental REPEs were induced by experimental pneumothorax in rabbits to clarify unsolved problems observed in clinical cases.
1) A case of left spontaneous pneumothorax was complicated by REPE two hours after commencing aspiration therapy for the collapsed lung. Edematous shadow on the ipsilateral side was found on his chest roentgenogram. Moist rales on auscultation were heard in both lung fields.
2) In the experimental REPE there were no significant difference in the incidence of edema between the group aspirated at -10cmH₂O and the group at -30cmH₂O. The regional blood flow in the collapsed side decreased to the level of one-sixth of its control. During aspiration of intrathoracic air, it reached to the one-third of its control. When pontamine skyblue was injected in the aural vein, exudation of the dye was found in bilateral lung tissues of rabbits with re-expanded lungs. This phenomenon was observed in neither collapsed lung nor normal lung.
3) The effects of several drugs upon REPE were studied. One-shot dose of chlorpheniramini maleas (4mg/animal) and continuous infusion of hydrocortisone (50mg/animal/24h) were the most effective methods for the prevention and therapy of REPE.
However, the dosage of chlorpheniramini maleas used in this study was much higher than usual clinical doses. Therefore clinical applications require further clarification. Continuous infusion of hydrocortisone, however, appears usefull for prevention and treatment of REPE. Some significant prophylactic and therupeutic effects were also observed in the atropini sulfas and phenoxybenzamin groups.
Based on the above results the following were discussed: (a) the possibility of the occurence of subclinical edema in contralateral lungs in clinical cases, (b) the value of the hypothesis that occurence of REPE depends on acute over filling of pulmonary artery, capillaries, and veins resulting from aspiration of extreme negative pressure”, (c) the increase in permeability of pulmonary vessels a factor in the occurence of REPE, (d) neurohumoral factor as a cause of REPE.

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Relationships between patients' and their sons' arterial blood gases, pH, HCO₃^- concentration and respiratory chemosensitivity to hypoxia (A) and hypercapnia (S) were examined in 19 patients with chronic obstructive pulmonary disease (COPD), their sons (n=25, mean age=32.3 years), 9 patients with silicosis, and their sons (n=13, mean age=32.0 years).
Arterial blood gases and pH obtained during clinically stable stages were averaged in patients to compare with data of their sons. Observation periods ranged from 2 months to 6 years in COPD cases and 2 years in silicosis cases. Respiratory chemosensitivities were analyzed by controlling arterial blood gases at predetermined levels and the results were standardized by body surface area (BSA).
Serum HCO₃^- concentration obtained from a Siggaard-Andersen nomogram correlated positively between patients and sons both in COPD (r=0.451) and silicosis (r=0.455). Patient's PaCO₂ correlated inversely with son's A/BSA in COPD (r=-0.538) and silicosis (r=-0.552). Patient's PaCO₂ showed a positive correlation with son's PaCO₂ (r=0.413) and patient's PaO₂ correlated positively with son's A/BSA (r=0.467) in COPD. Correlation between son's A/BSA and patient's PaO₂ remained significant (r=-0.448) after patient's PaO₂ was corrected for their ages in COPD. In silicosis, son's S/BSA and patient's PaCO₂ correlated positively (r=0.494). PaCO₂ obtained during exacerbation periods correlated with son's A/BSA in COPD (r=-0.487).
These results indicate that 1) there are familial components in arterial blood gases, HCO₃^- concentration, and respiratory chemosensitivity, and 2) blunted chemosensitivity antedates respiratory diseases.

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We analyzed the pleural surface pressure by use of a lung-thorax model under static conditions.
The lung-thorax model consists of a balloon covered by a net, hung inside a box. The balloon connects to the outside atmosphere. When pressure in the box is lowered by suction of air, the balloon expands inside it. When the pressure difference between inside the box and inside the balloon exceeds the elastic recoil pressure of the balloon, the balloon surface contacts the net and the mechanical forces, i. e., the contact pressure act on the balloon surface. Therefore the intra-balloon pressure is equal to the sum of the elastic recoil pressure of the balloon, the intra-box pressure and the contact pressure between the balloon and the net. It was shown that pleural contact pressure which varies inversely with pulmonary elastic recoil pressure, i. e., pleural surface pressure, is an important force in the interaction between lung and chest wall.
In the chest cavity in cases of lobar atelectasis, the pleural surface pressure of the chest wall and adjacent expanded lobes increase. Consequently the pleural contact pressure surrounding the atelectatic lobe decreases. Then the mechanical relationship works to increase pleural contact pressure, thereby working against atelectasis. The more extensive the lobar atelectasis the more the contact pressure decreases, therefore mechanical forces against atelectasis work more strongly.

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We reported a case that died suddenly of myocardial sarcoidosis 5 years after pacemaker implantion. A 54 year-old female was hospitalized with a diagnosis of congestive heart failure on December 1979. In 1974, she had uveitis and eruption on the left forehead. Biopsy of the skin showed a sarcoid lesion, and chest x-ray revealed bilateral hilar lymphadenopathy. The electrocardiogram showed complete right bundle branch block. After receiving steroid therapy, the eruption and bilateral hilar lymphadenopathy disappeared. In 1975, she had an attack of Adams-Stokes syndrome and underwent implantation of epicardial pacemaker. Kveim reaction and tuberculin tests were negative. For 6 months before her admission on December 1979, she had experienced symptoms of congestive heart failure. On admission, she had a moon face, mild exophthalmus, moist rales in both lungs, early systolic murmur in 3-4 LSB (2/6 Leveine), accentuation of the second heart sound and tibial edema. Positive laboratory date which led us to suspect hypothyroidism were 73.0μU/ml for TSH, 60ng/dl for T₃, 4.0μg/dl for T₄. By treatment with thyroxin, digitalis and diuretics, her symptoms and signs improved temporarily, but she died suddenly of ventricular tachycardia and fibrillation 3 months after hospitalization. At autopsy the sarcoid lesions were found in right and left ventricles, atrio-ventricular septum, in both lungs, hilar lymph nodes, liver and spleen.

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45才, 男性で呼吸困難を主訴として来院, 胸部レ線にて大量の胸水と両側肺門リンパ節腫脹を認め, 左鎖骨窩リンパ節生検にて典型的サルコイド結節がみられた. 副腎皮質ホルモン投与後1カ月にて胸水を始めとする全ての異常所見は消失した.

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