Protein concentrations have little effect on reabsorption of fluid from isolated rat lungs.

A study was conducted to determine whether differences in the concentrations of large molecules between the air space and perfusate solutions altered the rates at which fluid was reabsorbed from isolated fluid-filled perfused rat lungs. Four groups of experiments were conducted: 1) 5 g/dl albumin in the air spaces and perfusate, 2) 15 g/dl albumin in the air space and 5 g/dl albumin in the perfusate, 3) 5 g/dl albumin in the air space and 15 g/dl albumin in the perfusate, and 4) a mixture of 5 g/dl albumin and 7 g/dl Dextran 70 in the air spaces and 5 g/dl albumin in the perfusate. Fluid reabsorption was determined by following the concentration of albumin labeled with Evans blue (T-1824) in the air space and perfusate compartments.

Polyamines, DNA synthesis, and tolerance to hyperoxia of mice and rats.

Adaptation to hyperoxia has been attributed to increased activities of protective enzymes, but we suggest that an additional factor may be the lung's capacity to repair itself in hyperoxia. Such repair would require increased polyamines, but there are reports that two key enzymes of polyamine metabolism are suppressed by hyperoxia or oxidants. Because rats can adapt to hyperoxia but mice cannot, we compared their changes of polyamine metabolism and judged cell repair by using [3H]thymidine to estimate DNA synthesis.

Effects of food restriction and hyperoxia on rat survival and lung polyamine metabolism.

We fed Sprague-Dawley rats either freely or by restricting them to 20% of their usual diet for 21 days. In one experiment, we refed half of the food-restricted rats for 12 h, then exposed the three groups to air or 85% O2 for 5 days. The mortalities in 85% O2 were 100, 33, and 0% for the food-restricted, restricted-refed, and freely fed groups, respectively.

Effect of dietary vitamin E level on the biochemical response of rat lung to ozone inhalation.

We examined the effects of dietary vitamin E level on rat lung response to ozone (O3) inhalation. In one study, we fed 1-month-old Sprague-Dawley (SD) rats a test diet containing 0 or 50 IU vitamin E/kg for 2 months, and then exposed one-half of the animals from each dietary group to 0.8 ppm (1,568 micrograms/m3) O3 intermittently (8 hours daily) and the other half to room air for 7 days.

Influence of age on the biochemical response of rat lung to ozone exposure.

We have previously examined the influence of animal age on the pulmonary response to ozone (O3) in rats between 7 and 90 days of age (Elsayed et al., 1982a). In the present study, we expanded the age groups of rats, and examined in greater detail the relationship between animal age and pulmonary response to inhaled O3.

Suppression of polyamine biosynthesis prevents monocrotaline-induced pulmonary edema and arterial medial thickening.

Previous work in our laboratory has shown that the continuous administration of alpha-difluoromethylornithine (DFMO), a highly specific irreversible inhibitor of ornithine decarboxylase (ODC), which is the rate-limiting enzyme in polyamine biosynthesis, prevented the development of pulmonary hypertension and right ventricular hypertrophy induced in rats 21 days after a single injection of monocrotaline (MCT). We now report that DFMO treatment did not influence the proposed first step of MCT pneumotoxicity, that is, the hepatic metabolism of MCT to toxic pyrrolic metabolites. In contrast, DFMO treatment blunted the development of lung perivascular edema at Day 7, inhibited the respective four- and twofold increases in lung putrescine and spermidine contents at Day 21 without significantly altering spermine content, and prevented the arterial medial thickening at Day 21.

Hyperoxic lung injury and polyamine biosynthesis. Age-related differences.

To determine if lung cell replication and repair might be different between younger (30-day-old) and older (60-day-old) rats, we studied polyamine and DNA biosynthesis in rats exposed to 1.0 atm oxygen for 24, 48, 56, or 72 h. By 24 h, no statistically significant changes were observed, but by 48 h, ornithine decarboxylase and putrescine increased; S-adenosylmethionine decarboxylase activity increased by 56 h in the younger rats but not in the older rats.

Polyamines in clinical disorders.

An edited summary of an Interdepartmental Conference arranged by the Department of Medicine of the UCLA School of Medicine, Los Angeles. The Director of Conferences is William M. Pardridge, MD, Associate Professor of Medicine.

Polyamines and the development of monocrotaline-induced pulmonary hypertension.

Previous work in our laboratory has shown that the development of monocrotaline-induced pulmonary vascular disease in rats is preceded by a prolonged activation of lung ornithine decarboxylase (ODC). We now report that significant increases in rat lung adenosylmethionine decarboxylase activity and levels of the diamine putrescine and the polyamines, spermidine and spermine, are produced by a single dose of monocrotaline (MCT). Lung putrescine levels were increased from days 7 through 21, and both spermidine and spermine were first elevated at day 10 following MCT administration.

Dietary antioxidants and the biochemical response to oxidant inhalation : III. Selenium influence on mouse lung response and tolerance to ozone.

We fed female strain A/St mice selenium (Se) test diets containing either no Se (-Se) or 1 ppm Se (+Se) for 11 wk. Both diets contained 55 ppm vitamin E. We then exposed three groups of mice from each dietary regimen to either 0.

Dietary antioxidants and the biochemical response to oxidant inhalation. II. Influence of dietary selenium on the biochemical effects of ozone exposure in mouse lung.

We examined the influence of dietary selenium (Se) on the pulmonary biochemical response to ozone (O3) exposure. For 11 weeks, weanling female strain A/St mice were fed a test diet containing Se either at 0 ppm (-Se) or 1 ppm (+Se). Each diet contained 55 ppm vitamin E (vit E).

Polyamine metabolism in rat lungs with oxygen toxicity.

Ornithine decarboxylase activity increases 2-fold above control after 1 day and 25-fold after 3 days of exposure to 0.85 atm oxygen. Putrescine content nearly doubled by 72 hours which may reflect increased activity or ornithine decarboxylase.

Effects of vitamin E deficiency and nitrogen dioxide exposure on lung lipid peroxidation: use of lipid epoxides and malonaldehyde as measures of peroxidation.

The effect of vitamin E deficiency in male Sprague-Dawley rats upon lipid peroxidation in lung tissue was examined by measuring malonaldehyde and lipid epoxide production. In addition to controls, some animals were also exposed to 3 +/- 0.1 ppm NO2 continuously for 7 d in order to study the effects of oxidant stress on lung lipid peroxidation and vitamin E content.

Influence of vitamin E and nitrogen dioxide on lipid peroxidation in rat lung and liver microsomes.

Rat lung and liver microsomes were used to examine the effects of dietary vitamin E deficiency on membrane lipid peroxidation. Microsomes from vitamin-E-deficient rats displayed increased lipid peroxidation in comparison to microsomes from vitamin-E-supplemented controls. The extent of lipid peroxidation, as determined by measurement of thiobarbituric acid reacting materials, was enhanced by addition of reduced iron and ascorbate (or NADPH).

Biochemical changes in rat lungs after exposure to nitrogen dioxide.

Sixty-day-old male, specific pathogen-free rats were exposed continuously to 5 or 15 ppm NO2 for 1-7 d. Lung tissue from exposed and control rats was then analyzed for biochemical and enzymatic parameters. The exposure resulted in increased lung enzymatic activities, including elevated protein and DNA contents and nonprotein sulfhydryl levels.

Responses of natural wildlife populations to air pollution.

Deer mice (Peromyscus californicus) trapped in areas of Los Angeles with high ambient air pollution are significantly more resistant to ozone (6.6 ppm for 12 h) than are mice trapped from areas with low ambient pollution (56 versus 0% survival, respectively). Laboratory-born progeny of these mice show similar response patterns, indicating a genetic basis to this resistance.

[Improvement in nitrogen sparing by branched amino acids during parenteral nutrition].

Two groups of ten patients each, staying in a Intensive Care Unit, received exclusive parenteral alimentation with different concentrations of branched chain amino acids (BCAA). Group A received studied solution containing 12 g N (852 mmol) with 41,1 p. 100 BCAA.