Glycolipids, mucopolysaccharides and glycoproteins from human lung carcinomas of different histological types were investigated. Adenocarcinoma was found to be characterized by markedly lower total glycolipid and total mucopolysaccharide contents, and by predominant accumulation of sulfatide (galactocerebroside sulfate) and an increment of glycopeptide fraction derived from the tissue glycoproteins, compared to other types of carcinoma.
Lower amounts of total glycolipids in adenocarcinoma were mainly due to profound decreases of ceramide monohexoside, -dihexoside, and hematoside. Squamous cell carcinoma had the highest levels of total glycolipids, which appeared to be predominantly due to enriched concentrations of ceramide dihexoside and hematoside, and of total mucopolysaccharides which resulted principally from increased amounts of hyaluronic acid and chondroitin sulfates. Small cell undifferentiated carcinoma in which only glycolipids were examined demonstrated an overall glycolipid pattern similar to that of squamous cell carcinoma but differed from the latter in having lower levels of hematoside and higher levels of sulfatide. Although the constituent classes of glycoconjugates of normal lung tissue were qualitatively the same as those of tumor tissues examined herein, whole and individual concentrations in three groups of glycoconjugates clearly differed from those of any type of tumor.

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Seven patients with aspirin-induced asthma were challenged with intravenous injection of sulpyrine, inhalation of sulpyrine and of aspirin. FEV_1.0 and clinical symptoms were recorded serially. In all of seven patients, inhalation of sulpyrine solution with concentrations from 3 to 50mg/ml induced bronchoconstriction, but this reaction was weaker and milder than did aspirin.
A close correlation was found among the minimum effective doses of the drugs used in these three challenge tests studied.
We also studied the in vivo inhibitory action of aspirin, sulpyrine and some other aspirin-like drugs on arachidonic acid-induced bronchoconstriction in the guinea pig and found that sulpyrine is weaker and milder in activity than is aspirin and one of the most reversible of the tested drugs which is consistent with the above clinical findings.
Our results are compatible with the hypothesis that aspirin hypersensitivity is related to the inhibition of prostaglandin synthetase in the lung.

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Angiotensin I-converting enzyme (ACE) converts inactive angiotensin I (A I) to angiotensin II (A II), a potent vasopressor peptide, by releasing the C-terminal dipeptide, and also inactivates bradykinin, a potent depressor peptide. This enzyme is thought to be located mainly in the lung and to work physiologically in the lung. To elucidate the physiological role of ACE in the lung, the change of the activity of this enzyme in the lung and in plasma of rabbits with experimental pneumonitis was examined.
Experimental pneumonitis was produced by injection of Complete Freund's Adjuvant (acute pneumonitis) and of N-nitroso-N-methylurethane (chronic pneumonitis). ACE activity was measured both in plasma and in pulmonary tissue by a spectrophotometric method using Hippuryl-Histidyl-Leucine. Aerfusion experiment was also done. The lung was perfused with Tyrode solution from pulmonary artery without taking out the lung from the thorax, after ligation of the aorta perfusate was collected from the left ventricle. AI and AII were measured by radioimmunoassay, and BK was measured by biological assay, using the rat uterus.
In acute experiment, ACE activity in lung tissue was significantly decreased, namely, 2997±311nmol/mg prot/min on 2nd day (<0.001), 4930±729nmol/mg prot/min on 7th day (P<0.001), 4530±867nmol/mg prot/min on 14th day (P<0.001) compared with normal lung 6940±323nmol/mg prot/min. Plasma ACE was also decreased from 57.23±3.21nmol/ml/min to 42.41±4.20nmol/ml/min on 2nd day (P<0.05). In the perfusion experiment, conversion of AI to AII and inactivation of BK were significantly decreased, from 81.65±2.84% to 70.76±2.88% (P<0.05) and from 92.20±2.46% to 85.9±1.12% (P<0.001), respectively, in the acute experimental group.
On the other hand, in the chronic pneumonitis group, the activity of conversion of AI to AII and the inactivation of BK was not changed compared with the normal group in the perfusion experiment. ACE activity in lung tissue and in plasma also showed no deviation from normal controls.
In the case of decreased activity of ACE in the lung, less AII will be released into systemic circulation and BK will pass through the pulmonary circulation into systemic circulation, thus this may result in the decrease of systemic blood pressure.

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Bronchial asthma is a clinical syndrome manifested by reversible and intermittent obstruction of bronchi. The reported incidence of aspirin and indomethacin-induced asthma is the highest among all drug-induced asthmas. Nevertheless the etiology of indomethacin-induced asthma is still unknown.
The present investigation was conducted to explore the effect of indomethacin on the relaxing responses of guinea pig tracheal tissues with various bronchodilators.
Male guinea pigs, weighing 250-300g, were sacrificed. Guinea pig tracheas were removed, cut spirally in strips 1.0-1.5mm in width and 3.0-4.0cm in length, suspended in bioassay glass jackets, superfused with Krebs-Henseleit solution at 37°C, and saturated with oxygen and carbon dioxide (95:5, v/v). Relaxation of tissues was detected by an isotonic transducer and displayed on a polyrecorder.
1) The relaxing responses of guinea pig tracheal tissues with various doses of isoproterenol and prostaglandin E₂ were potentiated slightly with continuous infusion of indomethacin at a dose of 5×10^-8M, afterwards they showed the significant decrease by increasing the dose of indomethacin.
2) The relaxing responses of guinea pig tracheal tissues with 5ng/ml of salbutamol hemisulfate and 500ng/ml of aminophylline were attenuated dose-dependently with continuous infusion of indomethacin.
3) The above results suggest that inhibition of endogenous prostaglandin E₂ synthesis by indomethacin may cause indomethacin-induced asthma.

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The histopathological appearance of the lungs from two fatal cases of paraquat poisoning are reported.
At autopsy, case 2 died 7 days following ingestion and showed hemorrhage, congestion, edema and hyaline membrane formation. Case 1 died 19 days following ingestion and showed typical intra-alveolar fibrosis. The pulmonary lesion of paraquat poisoning can be divided into three phases. The early phase shows hemorrhage, congestion, edema and hyaline membrane formation and the middle phase shows intra-alveolar fibrosis and slight interstitial fibrosis. The late phase shows diffuse parapleural collapse and honeycomb lung.
As the toxic action of paraquat is increased by oxygen, oxygen inhalation must be performed carefully.

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