The purpose of the present study is to investigate the characteristics of alterations occurring in the right ventricle of the heart and their influence on the left ventricle by morphologic and morphometric studies on 7 human autopsy cases with chronic cor pulmonale, and on 60 rats with experimentally induced cor pulmonale, in comparison with 6 human control hearts and 20 control rats
The results are as follows.
I. Human autopsy study.
1. The free walls of the right ventricles showed a significant increase in myocardial thickness, weight and diameter of the myocardial fibers, and prominent hypertrophy.
2. The ventricular septa were increased in weight and hypertrophied. Morphometric studies showed that the myocardial fibers in the right side of the septum (RS) were hypertrophied, while those on the left side (LS) were unchanged.
3. Concerning the free walls of the left ventricles, the average weight was not significantly different from that of control hearts. However, there were varying results in the morphometry of myocardial thickness and the diameter of myocardial fibers in each cases and no definite tendencies could be shown.
4. The ventircular septum tended to bulge toward the left ventricular chamber in some cases, resulting in so-called “reverse Bernheim phenomenon”, which might greatly influence hemodynamics in the left ventricle.
II. Experimental study. Four week-old male Sprague-Dowley rats were given a single injection (30mg/kg) of monocrotaline, a pyrrolizidine alkaloid, which has been known to produce a pulmonary hypertension associated with cor pulmonale in experimental animals.
1. 14 days after a monocrotaline injection, development of cor pulmonale was evident by the results of dilatation, the increase of relative weight and myocardial fiber diameters of the right ventricle.
2. Although there was a significant correlation (r=+0.89, p<0.001) between the diameters of the right ventricular myocardial fibers and relative weight of right ventricle, the correlation between fiber counts in a given area and relative weight of the right ventricle showed a reversely significant result (r=-0.87, p<0.001).
3. The increase of relative weight and myocardial fiber diameter in the ventricular septum as well as in the right ventricle in the 14 and 21 day groups were observed, while those in the free walls of the left ventricle were not significantly different in the experimental and control groups.
4. The cross section of the heart taken from the experimental group sacrificed 29 days after a monocrotaline injection showed displacement of the ventricular septum toward the left ventricular chamber with flattening or invagination into the left ventricle and reduced volume of cavity of the lfet ventricle. Morphometrically, myocardial fibers in the right side of the ventricular septum showed marked hypertrophy, but no noticeable changes on the left side of the septum were observed.
III. Based on these results, it was concluded that the alterations observed in the ventricular septum of the heart in chronic cor pulmonale may play an important role in the function of right ventricle, but on the other hand these may have some influence on the malfunction of the left ventricle.

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Pulmonary edema was induced in isolated, perfused cat lung by raising outflow pressure. Samples of perfusate and foam during pulmonary edema were collected for measuring the levels of protaglandins (PGF_2α, PG E) and vasoactive lung peptides (VLP) by a radioimmunoassay. In additon, the effects of PG F_2α, PG E₂ and VLP on the pulmonary and systemic circulation and airway were studied in anesthetized cats and dogs.
1) PG F_2α and PG E increased significantly in edema foam but in perfusate during pulmonary edema, did not significantly change. The increase of PG F_2α in foam was remarkably.
In intact cats, PG F_2α increased significantly pulmonary arterial pressure and airway pressure whereas cardiac output and systemic arterial pressure were significantly decreased. PG E₂ resulted in a significant increase in pulmonary arterial pressue but in a significant decrease in systemic arterial pressure whereas cardiac output was not altered. These results indicated that both of PG F_2α and PG E₂ caused pulmonary vasoconstriction.
2) VLP increased in foam during pulmonary edema. This VLP has not been extracted and purified completely yet but has been found to contain at least two active principles, one of which relaxed and the other contracted isolated smooth-muscle organs.
Both pulmonary peptide fructions induced systemic vasodilation, evidenced by an increase in femoral blood flow with a fall of systemic blood pressure. But in pulmonary circulation, the isolated pulmonary vascular smooth-muscle actions of these two peptides suggested that one peptide (spasmogenic) induced pulmonary vasoconstriciton and other (relaxant) caused pulmonary vasodilation. Particularly, the smooth-muscle action of spasmogenic VLP mimiced these of the prostaglandins and prostaglandin-related compounents.
The above biological activities of PGs and VLP, which were demonstrated in foam during pulmonary edema, suggest that pulmonary edema may be caused by these vasoactive substances and moreover, these vasoactive substances may contribute to the production of bronchoconstriction, systemic hypotension and pulmonary hypertension during pulmonary edema.

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Primary pulmonary hypertension is a disease of unknown cause with progressive course resulting in death and characterized by exertional dyspnea, dizziness and syncope.
Recently, we demonstrated that the ordinary contractile responses or rabbit aortic and pulmonary arterial strips induced by vasoconstrictors were markedly increased with continuous infusion of low doses of various vasoactive substances.
The present investigation was conducted to demonstrate the effect of phenoxybenzamine on the contractile responses of rabbit aortic and pulmonary arterial strips induced by various vasoconstrictors.
Male rabbit, weighing 2.7-3.0Kg were killed, the pulmonary artery and the descending aorta were removed and suspended in a bioassay glass jackets superfused with krebs-Henseleit solution saturated with oxygen and carbon dioxide (95:5, v/v). Contraction of tissue was detected by an isotonic transducer and recorded using a polyrecorder.
1) The contractile responses of rabbit aortic and pulmonary arterial strips by prostaglandin F_2α and angiotensin II were not affected with continuous infusion of phenoxybenzamine.
2) The contractile responses of rabbit aortic and pulmonary arterial strips by adrenaline, noradrenaline and serotonin (5HT) were completely abolished with continuous infusion of phenoxybenzamine.
3) The dose-response curve of serotonin in rabbit pulmonary arterial strips was shifted downward with continuous infusion of phenoxybenzamine (100ng/ml).
4) These results suggest that serotonin may play an important role in pathogenesis of primary pulmonary hypertension.

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Rats fed on a vitamin E-deficient diet (E-depleted group) and a vitamin E-supplemented diet (E-supplemented group) were exposed to 0.3ppm of ozone three hours a day, five days a week for seven months. Then animals from each group were sacrificed and electron microscopic studies on the lung and biochemical examinations on the lung and liver were performed. 1) Vitamin E concentration in serum decreased following ozone exposure in the E-supplemented group, whereas it remained unaffected in the E-depleted group. 2) TBA and % release of lysosomal enzyme (acid phosphatase) of the liver were already increased in vitamin E-depleted air-exposed rats, and showed higher values following ozone exposure. Both showed the highest value in vitamin E-depleted ozone-exposed rats, thus demonstrating that there is a marked increase in lipid peroxide and a fall in the labilization of lysosomes in this instance. 3) Arachidonic acid (20:4) of total lipid, phospholipid and lecithin in the lung tissue showed a tendency to decrease in vitamin E-depleted air-exposed rats. Those in the ozone-exposed animals showed in both groups a tendency to increase in total lipid and lecithin, and to decrease in phospholipid. However, a change in the fatty acid composition following ozone exposure was generally mild. 4) The fatty acid composition of phospholipid in lung washings did not show a remarkable change following ozone exposure in both groups, thus suggesting that it has the resistivity to oxidation. 5) Morphological observations on the lung with the scanning and transmission electron microscope did not reveal any clear differences between both groups.
The defensive effect of vitamin E on ozone toxicity induced by long-term exposure to ozone was not made clear by the morphological examination, however, biochemical findings suggested the possibility that this vitamin will play the role of antioxidant effect in vivo.

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A 63 year old man was admitted to our institute with a chief complaint of “Dyspnea”. The cardiopulmonary function tests revealed restrictive ventilatory disturbance and prominent alveolar hypoventilation with pulmonary hypertension.
The main causes of “dyspnea” were considered to be due to the intercostal muscle atrophy and weakness associated with fasciculations as a result of diaphragmatic kymography and biopsy of intercostal muscle findings.
He had no characteristic symptoms of amyotrophic lateral sclerosis, except slight atrophy of the small muscles of the hands in the early stage.
A rare case of amyotrophic lateral sclerosis was later diagnosed, by electromyogram and exaggeration of jaw reflex.

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The paper reports a case of bronchial asthma induced by alclofenac and indomethacin.
The patient, a 59-year-old housewife, had frequent episodes of dyspnea since 1973 and was treated with oral bronchodilaters and intermittent corticosteroids. She had no nasal polyp and skin tests were negative. In 1977 she was admitted to Isesaki Public Hospital for treatment of acute bronchial asthma. In February of 1977, because of an acute asthmatic attack after administration of indomethacin suppository for lumbago, alclofenac was prescribed for pain relief. About half an hour after ingestion of alclofenac, a severe asthmatic attack occurred. To confirm the suspected relationship between the drugs and asthmatic attacks, provocative challenge tests with the drugs were performed. She developed typical signs and symptoms of asthma with marked decrease of PEFR and FEV₁ about 20 minute and 50 minute after administration of an indomethacin suppository (40mg) and ingestion of alclofenac (250mg) respectively. Challenge with benzydamine hydrochloride (50mg) was also positive but tiaramide hydrochloride was negative.

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A 52 year old female of multiple myeloma with alveolar calcification in the lung was reported.
Bence Jones λ type myeloma was diagnosed by serum immuno-electrophoresis, and treated with cyclophosphamide and large doses of corticosteroid.
Chest X-ray film showed diffuse disseminated miliary lesions or spotty shadows in both lung fields in the late stage.
Postmortem soft X-ray examination and histopathology revealed that these shadows were deposits of calcium salts in the interalveolar septa.

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