The proportion and absolute numbers of T and B cell population were measured by the sheep red blood cell ro sette formation technique; the activity of β-galactosidase, lysosomal enzymes of peripheral blocd monocytes; the reduction of Nitro Blue tetrazorium of peripheral blood polymorph nuclear cells; the levels of serum immunoglobulins, ESHS-globulins, Hapto-globulins and complement 3 were investigated in 38 patients with primary lung cancer. The results are summarized as follows.
Both tuberculin reaction and DNCB reaction were reduced in these subjects, especially the latter reaction showing a decrease according to the clinical stage. Absolute numbers of T cells in all clinical stages were decreased, as were B cells in the fourth stage only. The activity of β-galatosidase of blood monocytes in all clinical stages was reduced. NBT reaction was reduced in clinical stages I to III but was observed to increase in stage IV. IgG tended to increase with each stage, but on the contrary IgA tended to decrease. The levels of IgM showed no definite tendency.
From the above results it is thought that cellular immunity was more reduced than humoral immunity in patients with primary lung cancer particularly as the clinical stage advanced, therefore the patients were easily infected in later clinical stages.

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Distribution of transthoracic electrical impedance pulse in pulmonary diseases was evaluated by perfusion studies using ^99mTc-macro aggregated albumin (MAA) on 27 subjects.
Impedance was measured at six points in the upper, middle and lower regions of the left and right thorax by a tetrapolar electrode configuration system using a 50kHz current. Pulse height (ΔZ) and the time differential dZ/dt were measured and compared with radioactivity following intravenous administration of ^99mTc-MAA.
In the right and left lung the ratio of radioactivity (Y) to impedance pulse (X) was Y=1.16X, with a correlation coefficient of 0.963.
The shift of pulmonary blood flow before and after bronchography was investigated, and it was found out that after bronchography the amplitude of the impedance pulse decreased and showed the same tendency as the decrease of radioactivity in the lung in which bronchography was performed. Ventilatory volume, calculated from transthoracic electrical impedance variation, decreased in the lung in which bronchography was performed and displayed a strong correlation with changes in the distribution of ^99mTc-MAA. From these results it may be thought that impedance pulses obtained at the thoracic wall may reflect changes in the pulmonary blood flow. Perfusion lung scintigraphy by ^99mTc-MAA is useful in geographically assessing pulmonary blood flow while the impedance method is a useful extra-corporal method for short-term repeated examinations or long term monitoring of pulmonary hemodynamics.

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A comparison of two different analytical approaches for xenon-133 washout curves was made. To estimate regional ventilation from the xenon-133 washout curve, a mathematical approach was made with a model lung which has a common dead space and regional wellventilated (fast) and poorly ventilated (slow) spaces. For the convenience of analysis a backward projection method has generally been used instead of the simulation model. An attempt was made to clarify the difference in values obtained by the two methods from the standpoint of respiratory physiology.
Experimental data showed that regional tidal ventilation values (computed V_Ti) obtained mathematically using the simulation model were always larger than those (manual V_Ti) obtained from the backward projection method in both fast and slow spaces.
Assuming computed V_Ti to be the sum of two valves; regional alveolar ventilation(corrected V_Ti) and regional dead space ventilation(V_Dsi), corrected V_Ti was compared with manual V_Ti. In fast space corrected V_Ti and manual V_Ti were almost equal and in slow space, corrected V_Ti tended to be slightly smaller than manual V_Ti. Manual V_Ti, calculated by analytical methods used heretofore, approximates ventilation values obtained from the simulation model when the volume of common dead space is omitted.

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The effects of the β-stimulant clorprenaline and the phosphodiesterase inhibitor aminophyllin on acute inflammatory edema were studied in rats and compared with those of adrenergic drugs, papaverine and phenylbutazone. In paw edema induced by carrageenin, noradrenaline and adrenaline of 0.1mg/kg s. c. inhibited edema formation markedly during the first 1 hour and moderately inhibited second phase edema after 1 hour. The inhibitory effects of adrenaline on the first phase edema were not influenced by combination with propranolol, but the effect on the second phase was decreased significantly by propranolol. On the other hand, 1mg/kg s. c. isoproterenol inhibited the first phase slightly and the second phase moderately. Clorprenaline showed a similar mode of action to isoproterenol on carrageenin edema in s. c. and p. o. administration, but the activity was significantly more potent than that of isoproterenol and was not influenced by combination with propranolol. Aminophyllin and papaverine also inhibited second phase edema. Clorprenaline and aminophyllin showed markedly inhibitory effects on paw edema induced by dextran in which histamine and serotonin contributed to edema formation and the inhibitory activity was more potent than that of phenylbutazone. Both test drugs increased pain thresholds in the inflamed foot which decreased by injection of brewers yeast by Randall and Selitto's method.
From the above results, it was found that clorprenaline and aminophyllin significantly inhibited acute inflammatory edema. It may be considered that the anti-edematous effect of both test drugs is produced partially due to an increase of the concentration of cyclic AMP in the inflamed tissue, but a great deal of the effect depends on the inhibition of release and antagonistic action on such chemical mediators as histamine and serotonin. Moreover, the cardiac and diuretic action of aminophyllin may indirectly produce the anti-edematous effect. Therefore, clorprenaline and aminophyllin appear to be effective drugs in the therapy of brochial asthma because of reduction of edema in mucosa of the respiratory tract in addition to bronchodilation by relaxation of smooth muscle.

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We previously reported that clorprenaline and aminophyllin were found to have potent inhibitory effects on acute inflammatory edema. In this paper, the effects of clorprenaline and aminophyllin on each stage in the process of inflammatory reaction, that is anti-inflammatory activity, were assessed by main standard tests with oral administration. Both drugs inhibited the increased vascular permeability induced by histamine in rats and by acetic acid in mice. The activity was almost the same as the anti-edemateous one and was more potent on histamine than on acetic acid. Neither clorprenaline nor aminophyllin inhibited ultraviolet erythema in guinea pigs or proliferation of granulation tissue with the cotton pellet method and adjuvant arthritis in rats. Furthermore, both drugs did not display analgesic effects in acetic acid stretching tests. From the above results, clorprenaline and aminophyllin have no effect on the proliferation of granulation and chronic inflammatory disease, but were found to have inhibitory effects on such acute inflammatory reactions as increased vascular permeability and edema.

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Metabolism of prostaglandins results in its biological inactivation and since this inactivation is extremely efficient it has generally been assumed that the pulmonary metabolites of prostaglandins have little biological activity. However, recently 15-keto metabolites were found to be more potent than the parent prostaglandins on several isolated smooth muscle preparations. Others have reported that 13, 14-dihydro metabolites showed appreciable biological activities. We have, therefore, examined the effects of both of these metabolites of prostaglandin E₂ and F_2α on airways and circulation in vivo and also investigated the inactivation of these metabolites by the pulmonary circulation, using a superfusion technique.
The results of the present study clearly demonstrated that, of all those metabolites of prostaglandins studied, 13, 14-dihydro metabolites had marked effects on airways, pulmonary vascular bed and systemic blood pressure of guinea pigs. Moreover, the the potency of these metabolites was roughly the same as that of parent prostaglandins, however other metabolites, 15-keto prostaglandins, were less potent than the parent prostaglandins.
The inactivation of prostaglandins (PGs) is an important characteristics of the pulmonary vascular bed. Although the metabolism of the parent PGs in the pulmonary circulation have been extensively studied, no studies have been made on the inactivation of their metabolites. In the isolated perfused guinea pig lungs, the biological activity of 15-keto PG E₂ was least affected by passage through the lungs, while 82% of infused 15-keto F_2α was inactivated in one passage. Up to 88% of 13, 14-dihydro-PG E₂ suffered inactivation, while only 63% of 13, 14-dihydro PG F_2α was inactivated. 13, 14-dihydro-15-keto PG F_2α was inactivated only 49%. Thus, within this very closely related group of substances, the degree of inactivation in one passage through the lung differs for each metabolite, and it was also found that a discrepancy existed between E and F groups
Based on these results, it would be conceivable that several of the biological effects of prostaglandins released in anaphylactic shock or in bronchial asthma may be due to a high level of prostaglandin metabolites. The PGs metabolites, such as 15-keto PG E₂, 13, 14-dihydro PG F_2α and 13'14-dihydro-15-keto PG F_2α, the initial activity of which was preserved after the passage through the lung, might function as actual circulating hormones.

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Routine chest roentgenogram and tomograms of a housewife with typical symptoms and findings such as clubbed fingers, cyanosis, dyspnea during exercise and polycythemia, showed only a slightly abnormal shadow.
Pulmonary angiography revealed the reason to be that almost all the arteriovenous fistulae shadows were relatively small and mainly overlapped the heart and diaphragm shadows.

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