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Biomedical subjects

C L Vassallo

Publications and source records attributed to C L Vassallo.

At least 19 recordsLinked to original sources
PubMed1979

Static volume-pressure relationship in normal rats at various stages of growth.

Static deflation air volume-pressure (V-P) curves were studied in 136 open-chested normal male rats ranging from 103 to 604 g in weight. The lungs accepted a greater volume of air as rats grew in size, but beyond 8 weeks of age, the volume expressed per g of lung weight progressively decreased. In older rats, V-P curves in precent maximum lung air volume (%MLV) were shifted upward and to the left compared to younger rats. We believe that these differences reflect various phases in the postnatal growth of rat lungs and loss of tiss elasticity due to the aging process, respectively. Lung air volume at 30 cm H2O Ptp (MLV30) showed a significantly higher linear relationship with body weight (r = 0.93) than with lung-heart weight (r = 0.80) as the independent variable. We present V-P nomograms and discuss two techniques of measuring V-P relationships with their specific applications.

Aging↗
PubMed1979

Effects of starvation and refeeding on lung mechanics and morphometry.

Rats receiving one fifth of their usual daily food consumption for 10 days showed a significant increase in static recoil pressure of the lung (Pst[L]) due to surface forces at low lung volumes during inflation; their tissue Pst (L) decreased significantly over the entire volume-pressure loop compared to that of control rats. After 1 week of refeeding, the surface Pst (L) returned almost completely to normal, but tissue Pst (L) remained abnormally low. In starved rats, air-space enlargement with minimal loss of interalveolar septa was associated with a significant increase in mean linear intercept and volume fraction of air spaces, and with a significant decrease in corrected internal surface area and surface fraction of air space. These alterations returned partially toward normal in the refed group. We conclude that starvation increases surface elastic forces, decreases tissue elasticity of lung, and leads to air-space enlargement; redeeding leads to restoration of surface forces without the return of tissue elasticity to normal and to less severe air-space enlargement.

Animals↗
PubMed1977

Pancreatic pleuropericardial effusions presenting as tumor of the lung.

A 45-year-old man presented with what was thought to be a mass in the left upper lung and a pericardial friction rub. He was subsequently discovered to have a loculated pleural effusion and pericardial effusion associated with chronic pancreatitis. This is the first instance we were able to find of pancreatitis mimicking bronchogenic carcinoma with pericardial metastasis.

Adult↗
PubMed1976

Exercise stress and enzyme-induced emphysema.

Rats were exposed to an aerosol of 10% papain for 8 h found in pilot studies to produce marked emphysema. One week after exposure some animals were forced to exercise in a motor-driven activity wheel 2 h daily for 4 wk, while others remained at rest. Another group of rats which served as the control were exposed to saline under the same conditions and divided into exercise and rest groups. Elastic recoil pressure (Pst) of lung was measured from static deflation pressure-volume curves with air and saline. Pst measured in air-filled lungs was not significantly different between the emphysema-rest and emphysema-exercise groups. When inflated with saline the Pst was significantly reduced in the emphysema-exercise compared to the emphysema-rest group at high and mid (100, 80, 60%) lung volumes. Pst in air- and saline-filled lungs was not significantly different between the control-rest and control-exercise groups. We therefore conclude that mechanical stress resulting from physical exercise decreased Pst of lung tissue in emphysematous rats.

Animals↗
PubMed1971

Glutathione-dependent peroxidative metabolism in the alveolar macrophage.

Phagocytosis by rabbit alveolar macrophages (AM) is accompanied by increases in O(2) consumption, glucose oxidation, and H(2)O(2) formation. Two aspects of the interrelations between these metabolic features of phagocytosis have been studied.First, the following evidence indicates that glutathione, glutathione reductase, and peroxidase serve as a cytoplasmic shuttle between H(2)O(2) and NADPH-dependent glucose oxidation: (a) AM contain 5.9 mmumoles of reduced glutathione per 10(6) cells and exhibit glutathione peroxidase and NADPH-specific glutathione reductase activity; (b) oxidized glutathione potentiates NADP stimulation of glucose oxidation; (c) an artificial H(2)O(2)-generating system stimulates glucose oxidation; (d) the cell penetrating thiol inhibitor, N-ethylmaleimide diminishes glucose oxidation. This effect largely depends on inhibition of the glutathione system rather than on inhibition of either H(2)O(2) formation or enzymes directly subserving glucose oxidation.Second, three potential H(2)O(2)-generating oxidases have been sought. No cyanide-insensitive NADH or NADPH oxidase activity could be detected. D-amino acid oxidase activity was 0.48 +/-0.07 U/10(6) cells with D-alanine as substrate.

Animals↗