There are several mechanisms involved in the pulmonary arterial pressure response to acute alveolar hypoxia.
The purpose of this investigation is to assess the role of the released histamine as one of the vasoactive substances in systemic and localized hypoxia.
Systemic hypoxia: In 13 dogs, both lungs were ventilated with 10% O₂ in N₂ mixture for ten minutes.
Localized hypoxia: In 7 dogs, the left lung was ventilated with 100% N₂ and the right lung with 100% O₂ for ten minutes without inducing systemic hypoxia.
In the systemic hypoxia group, arterial plasma histamine levels changed markedly in a short period and maximum values elevated more than 100mcg/l in 10 out of 13 dogs. Mixed venous plasma histamine levels elevated more than 100mcg/l in 5 out of 7 dogs.
The pulmonary arterial mean pressure gradually rose in all dogs during the experiment, but there was no relationship between the percentile increases in pulmonary arterial mean pressure and the percentile increases in the amount of histamine release in the arterial blood.
In cases of intense release of histamine, arteriovenous oxygen tension differences indicated below 5mmHg.
In the group of the localized hypoxia, arterial and mixed venous plasma histamine levels elevated more than 100mcg/l in the maximum values in 3 out of 7 dogs. The pulmonary arterial mean pressure did not show the upward trend seen in all localized hypoxia cases.
Although vasoconstriction of the pulmonary vessels was not proved in this investigation, it was clear enough that under acute systemic as well as acute localized hypoxia, histamine was released.
From these results, it is suggested that histamine released during acute hypoxia may not play the major role in the pulmonary arterial pressure response, but it may act as a vasoactive intermediary in the local vasoconstriction that occurs as a response to correct the ventilation and perfusion ratio.

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In order to investigate the metabolism of fatty acids in lung cancer patients, fatty acid composition was studied in the serum of 71 cases of lung cancer and 43 normal subjects or cases of other lung diseases, and in the autopsied lung tissue of 18 cases of lung cancer and 17 cases of cancer of other organs or other non-pulmonary diseases. The results obtained were as follows:
1. In fatty asids composition of serum, increase of C₁₆ and C₁₈₌₁, and decrease of C₁₈₌₂ and C₂₀₌₄ were observed in lung cancer compared with normal controls. However, no changes were seen according to age.
2. In lipid fractions of serum in lung cancer, increase of C₁₆ and decrease of C₁₈₌₂ in ChE, increase of C₁₈₌₁ and decrease of C₁₈ in FFA, and increase of C₁₆ and decrease of C₁₈₌₂ and C₂₀₌₄ in PL were observed compared with normal controls.
3. In lung tissue, fatty acid composition in cancer tissue showed a decrease of C₁₆ and an increase of C₁₈₌₁ and C₂₀₌₄ compared with normal tissues. The changes of C₁₆ and C₂₀₌₄ in cancer tissue were inversely proportional to those in serum.
4. In lipid fractions of lung tissue, decrease of C₁₆ and increase of C₁₈₌₁ and C₂₀₌₄ in ChE, and decrease of C₁₆ and increase of C₁₈₌₁ in PL were observed in cancer tissue compared with normal tissues. The changes of C₁₆ in ChE and PL in lung tissue were inversely proportional to those in serum.
5. Changes in C₁₆ and C₂₀₌₄ in serum were observed in subjects who had liver dysfunction, however, no changes were observed in lung tissue.
6. The effect of treatment on total lipids was observed in lung cancer, i. e., C₁₆ and C₁₈₌₂, and C₁₈₌₁ tended to normlize with FEM, FT-207, ⁶⁰Co and BLM+⁶⁰Co, and ⁶⁰Co and BLM+⁶⁰Co, respectively.

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Hemodynamic studies of 94 patients with autopsy proven and/or clinically diagnosed cases of primary pulmonary hypertension were made. 30 were male and 64 were female and their average age were 31 years (11-66 yrs). These cases were divided into living (44 cases) and dead (50 cases) groups.
Since pulmonary arterial pressure was markedly elevated (PPA=63.5±17.0mmHg) and the cardiac index was slightly lower (2.88±1.00L/min/m²), calculated total pulmonary vascular resistance was increased significantly (1319±611 dynes sec cm^-5). However, pulmonary capillary wedge pressure stayed within normal limits (7.4±4.5mmHg).
When compared living with dead groups, there was no significant difference in cardiopulmonary pressures. However, statistically significant difference were elicited in the CI (3.21±1.17 to 2.50±0.62L/min/m², P<0.02), and RVWI (2.36±1.2 to 1.83±0.73kgm/min/m², P<0.01).
Although there were no correlations between these hemodynamic parameters, the patients' prognosis was poor whoes PPA exceeds 50mmHg and CI was lower than 2.8L/min/m² and/or PRA exceeds 6mmHg and RVWI was under 2kgm/min/m².

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Electrocardiograms of 77 patients with autopsy proven and/or clinically diagnosed (right heart catheterization was performed in all cases) primary pulmonary hypertension were studied. 23 were male and 54 were female and their average age was 31 years. These cases were divided into two groups; survival and terminal, according to prognosis.
The most common electrocardiographic abnormalities as a whole were right axis deviation of ÂQRS (107.6±29.7°) and ÂP (62.1±15.7°), increased amplitude of R in V₁ (11.1±6.9mm), increased R/S ratio in V₁ (6.2±6.5), dylayed ventricular activation time in V₁ (0.04±0.02sec) and deep S in V₅ (9.4±5.1mm).
Comparing the data of the two groups, there was a reasonably good separation in ÂQRS (100.5±30.2° to 118.5±16.8° P<0.01), amplitude of R in V₅ (15.5±6.2mm to 10.6±4.3mm, P<0.001), amplitude of R in V₆ (10.1±4.3mm to 6.8±3.1mm, P<0.001), R/S ratio of V₅ (2.3±2.1 to 1.2±0.8, P<0.005) and R/S ratio of V₆ (3.9±4.4. to 1.4±1.3, P<0.005). SIQIII, SIQIIITIII and inverted T in II. III. aVF were found more often in terminal than survival cases, and this was statiscally signifiant.

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A 18-year-old female case began with fever and cough. Chest roentgenogram showed diffuse ground glass shadows throughout both lung fields, indicative of viral or mycoplasma pneumonia. A peak cytomegalovirus CF antibody titer of 258×was reached on the 25th day of hospitalisation, becoming <4×on the 53rd hospital day. Although cytomegalovirus was not isolated from the throat, on the basis of these findings pneumonia was considered to be caused by a cytomegalovirus infection. The liver function tests were also abnormal and it seemed likely that cytomegalovirus infection gave rise to hepatic injury. It is thought that her marked over work had influence on the clinical manifestation of cytomegalovirus infection.

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