We determined whether vasodilator doses of inhaled nitric oxide (NO) prevented the progression of pulmonary hypertension (PH) and vascular changes in monocrotaline-induced PH. Short-term NO inhalation in rats 3 wk after the injection of monocrotaline reduced mean pulmonary artery pressure (PAP) from 30.7 +/- 2.2 (SE) to 26.4 +/- 1.4 mmHg at 10 parts per million (ppm) and from 30.2 +/- 1.3 to 25.8 +/- 1.4 mmHg at 40 ppm. There were no differences among rats exposed to air only and rats exposed to 10 ppm of NO for 19 days after a single subcutaneous injection of monocrotaline, in mean PAP (34.3 +/- 1.9 mmHg air vs. 32.8 +/- 1.4 mmHg NO), right ventricular hypertrophy (RVH), medial wall thickness (MWT) of muscular arteries, and the percentage of muscularized arteries at alveolar wall (%AW) and duct (%AD) level. Additional groups exposed to air only and 40 ppm of NO for 19 days again showed no difference in mean PAP, RVH, MWT, and %AD, except that this dose slightly reduced %AW (60.6 +/- 3.4% air vs. 46.9 +/- 5.2% NO, P = 0.04). Urine nitrate (NO3) level was higher in rats that had inhaled NO. In contrast to chronic hypoxic PH, vasodilator doses of NO inhalation did not prevent the development of PH in this malignant form of experimental PH.

Depressive symptoms estimated by the Beck Depression Inventory (BDI) were examined in winter and summer in a total of 242 Japanese adults staying less than 2 years or longer than 10 years in Stockholm, where the length of daylight changes dramatically throughout the winter and summer seasons. In spite of the difference in the period of residency, both groups of subjects showed more mental and somatic depressive symptoms in the winter than in the summer. Moreover, the winter BDI score of long stayers was significantly higher than that of short stayers. Accordingly, our results suggest that, although seasonal mood variation is essentially produced by a chronobiological factor, Swedish lifestyle to which long stayers have been accustomed also influences the seasonal mood variation.

No abstract

Death certificates issued in Yokkaichi, Japan, during the 21 yr from 1963 until 1983 were surveyed to determine the relationship between changes in air pollution and mortality due to bronchial asthma and chronic bronchitis. The following results were obtained. In response to worsening air pollution, mortality for bronchial asthma and chronic bronchitis began to increase. Mortality due to bronchial asthma decreased immediately in response to improvement of pollution, whereas mortality due to chronic bronchitis decreased to the level in the control area 4 to 5 yr after the concentration of sulfur dioxide (SO2) began to satisfy the ambient air quality standard. In the polluted area, mortality due to bronchial asthma in subjects who were 20 yr of age was higher during the period in which higher concentrations of sulfur oxides were prevalent.

Biotransformation of NO, nitrite and nitrate was investigated in rats and mice in a 15NO inhalation experiment and intraperitoneal injection experiments of 15N-nitrite and 15N-nitrate, and the following results were obtained: (1) Rats were forced to inhale 15NO (145 ppm, 123 minutes) or were given an intraperitoneal injection of 15N-nitrite (2 mg animal-1 as 15N) or 15N-nitrate (2mg animal-1 as 15N), and determination of 15N recovery in urine was made up to 48 h later. The results were 55, 53 and 78% of the inhaled or injected 15N, respectively. (2) 15N-nitrate in the urine was converted into a 6-nitro derivative of 3,4-xylenol and its identification and quantitative determination were made by the GC-MS method. As to 15N-urea in the urine, identification and quantitative determination were made by the urease method. 15N was present in the urine of rats after 15NO inhalation in the form of NO3- and urea. 75 and 24% respectively. In the urine of rats injected with 15N-nitrite, about 20% of unidentified 15N-compounds not discovered in the inhalation experiment was found. The content of 15N-urea in the urine after injection with 15N-nitrate was lower than that after injection with 15N-nitrite. (3) When 15N-nitrite (0.617 mg animal-1 as 15N) was injected intraperitoneally in mice, 60.7, 7.8 and 0.3% of the injected 15N were found in the urine, feces and exhaled gas (NO, NO2 and NH3 in the gas were caught) up to 48 h after injection respectively, and 1.6% was found in the body 48 h after injection, but the remaining 30% of 15N could not be recovered.