The Vmax at a given percentage of the vital capacity obtained from MEFV curves has been widely used, but there is large variation according to the individual. This study was designed to investigate whether the variability was due to individual difference in airway size.
Twenty four healthy subjects with a mean age of 29±5 were studied. Anatomic dead spaces (V_D) were measured by Fowler's technique under three different conditions, namely, with no breath-holding (V_D0), five and ten seconds breath-holding (V_D5, V_D10) at end-inspiratory level.
The results were as follows: Significant correlations were found between V_2.5 and V_D0-V_D5, between V₅₀ and V_D0-V_D10 and between PEF and V_D10. This suggested that V₂₅ and V₅₀ are closely related to the size of the lower airways and PEF to the size of the upper airways, because V_D0-V_D5 and V_D0-V_D10 are considered to reflect the volume of the relatively peripheral airways.
To confirm the above results V_D variables and Vmax were measured in nine of the subjects before and after salbutamol inhalation. The mean values of V_D0, V_D0-V_D5, V_D0-V_D10, V₅₀ and V₂₅ increased significantly, but V_D5, V_D10 and PEF were unchanged. These results imply that relatively peripheral airway dilatation was reflected by the increase of V_D0-V_D5 and V_D0-V_D10, leading to the increase of V₅₀ and V₂₅, and the lack of increase in V_D10 was compatible with no change in PEF.

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Experimental emphysema in guinea pigs was induced by intratracheal instillation of hog pancreatic elastase to investigate the role of proteolytic factors in the pathogenesis of pulmonary emphysema. Ultrastructural and morphometric studies were performed on the elastase-induced emphysema.
The severity of the experimental emphysema induced by elastase instillation was compared in four species of animals and the emphysema-inducing capacity of four proteases was studied using guinea pigs.
The following results were obtained:
1) In the histologic sections in vivo, marked intraalveolar bleeding and interstitial edema were seen 2 hours after intratracheal instillation of hog pancreatic elastase. The bleeding and edema were diminished and focal destruction of alveolar septa found on the 2nd day, and marked emphysematous changes were seen on the 7th day.
2) Ultrastructural studies in vivo showed interstitial edema and degradation of fibrous tissue 2 hours after, fragmentation of elastin and dissociation of elastic tissue and collagen fibers on the 2nd day, and apparent degradation and fragmentation of elastin on the 7th day.
3) In the experimental emphysema by elastase in vitro, emphysematous changes were seen in guinea pigs, rabbits and rats. The most remarkable changes were found in the guinea pigs by the light microscopy. These emphysematous changes correlated well with the dose of elastase by mean linear intercept values.
4) Elastase and papain possess an emphysema-inducing capacity but trypsin and collagenase did not induce emphysematous changes.

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Morphologic studies on elastase-induced emphysema have been reported previously. The purpose of this paper was to report the characteristics of lung protease inhibitor in the guinea pig and to partially purify this substance.
The role of lung antiprotease obtained from the lung lavage of guinea pig, protease inhibitory capacity and inhibition of experimental emphysema were defined. Furthermore, an attempt was made to separate this lung antiprotease and to clarify the nature of it.
The following results were obtained:
1) SLAPN is more sensitive and more specific than previous synthetic substrates as NBA. Activity against elastin-agar plates was only detectable in elastase, whereas the elastolytic activity of papain was not detectable on elastin-agar plates and SLAPN.
2) Lung inhibitor in the lung lavage of guinea pig showed elastase inhibitory activity and also inhibited the induction of experimental emphysema by elastase. On the other hand, trypsin inhibitory activity was not detectable in this material.
3) The molecular weight of the lung inhibitor was determined to be about 60000 by gel filtration. Activities of the lung inhibitor were unstable against heating and acid. Partial purification increased the elastase inhibitory activity about twenty-two-fold following affinity chromatography using Sepharose 4B-elastase column.

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The mechanism of hypoxic pulmonary hypertension remains incompletely understood. There is suggestive evidence that the response is mediated by chemical substances but these substances have not been fully identified.
We studied the effect of cytochrome oxidase inhibitors (sodium azide, sodium cyanide) on the pulmonary vascular reactions to hypoxia in isolated cat lungs and in anesthetized cats.
1) The hypoxic pulmonary hypertension was completely blocked in isolated cat lungs, which were perfused with perfusate containing large doses of sodium azide or cyanide. However, isolated cat lungs with sodium azide-or cyanide-induced blockade of hypoxic pulmonary hypertension retained pulmonary pressor responses to prostaglandin F_2α, histamine and serotonin.
2) The pulmonary hypoxic vasoconstriction was also blocked in anesthetized cats with small doses of sodium azide or cyanide, but the blockade was weaker than that in isolated cat lungs.
Sodium azide and sodium cyanide are inhibitors of cytochrome oxidase in the electron transport chain. These, in turn, inhibit oxidative ATP production which consequrntly inhibits metabolism in cells. This action of sodium azide and cyanide may inhibit in the metabolism of a pressor substance, either its production, its activation or its liberation of chemical mediators from lung tissue during hypoxia.

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A case of acute chlorine poisoning was reported. A 60 year-old engineer was exposed to chlorine gas when working with hydrochloric acid. On admission, his chest film revealed marked pulmonary edema and arterial gas examination showed hypoxemia. Immediately, he received oxygen inhalation and intravenous injection of a large dosage of hydrocortisone (Sorcortef 5g). On the seventh day of hospitalization, his condition improved as did radiologic findings. On the thirteenth day of hospitalization, transbronchial lung biopsy of the right lower bronchus showed peribronchial thickening and alveolar capillary dilatation. One month after exposure, symptoms of diffuse panbronchiolitis were recognized but they regressed by steroid treatment. Thereafter, chest film and pulmonary function returned to normal.
It was suggested that large dose steroid treatment at an early stage would be effective to manage diffuse panbronchiolitis and pulmonary edema due to acute chlorine poisoning.

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We experienced a thirty year-old male with a chief complaint of severe cough and sputum which started four months prior. On physical examination the supraclavicular, right cubital and inguinal lymphnodes which were movable and nontender were palpable. Slight macular degenerative change was observed, but the uveitis was not detectable. His plain chest film showed atelectasis of right lower lobe, but the cause was not indicated, even by tomography. Bronchography disclosed stenosis close to the orifice of the right lower lobe bronchus.
On admission in March 1978 because of pneumonia after bronchography the leucocyte count was 11200/mm³, the blood sedimentation rate was 35mm per hour and the C-reactive protein was positive. The serum Ca concentration was normal.
Bronchoscopy showed irregular tracheal bifurcation, unclear bronchial cartilagenous grooves and longitudinal mucosal corrugation of the right main bronchus and the intermediate portion, remarkably reddened and erosive mucosal membrane, suggestive of severe inflammation. The orifice of the right lower lobe bronchus was almost completely obstructed.
Biopsy near the orifice of the right lower lobe bronchus showed chronic bronchitis but a second biopsy near the same region revealed a small tubercle suggestive of sarcoid. The right supraclavicular lymphnode was removed. This microscopically showed tubercles composed of epithelioid cells, with an occasional Langhans giant cell and asteroid body but without any caseation. An inguinal lymphnode was removed. This also showed a non-caseating epithelioid cell granuloma. All stains for tubercle bacilli were negative. Mantoux's reaction was negative and sputum culture revealed no tubercle bacilli.
We thought that the atelectasis was primarily due to the endobronchial sarcoid granuloma and treated it as a case of bronchial sarcoidosis with atelectasis with predonisolone. After two weeks the superficial lymphnodes became nonpalpable, but there was no improvement of atelectasis. Even after four months the atelectasis remains completely unchanged. We think that some irreversible change other than sarcoid granuloma, perhaps inflammatory scar formation of the bronchus may be involved with the atelectasis.

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39才主婦2児の母, 昭和52年1月以来6回右自然気胸発生, 何れも月経開始前後数日間に発生す. 開胸すると横隔膜に経1～2mmの円形楕円形の小さな凹みが30コあり, 内7コが穿孔している. 凹みは非常に薄い膜であり, 切除施行後組織所見で子宮内膜腺腔構造及び子宮内膜間質組織を認めた.

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