Biomedical subjects

J A Hayes

Publications and source records attributed to J A Hayes.

At least 73 records · Page 4Linked to original sources

PubMed1976

Streptozotocin and renal amyloidosis in the Syrian hamster.

In the Syrian hamster, administration of the drug streptozotocin was associated with an increased incidence and severity of renal amyloidosis. Some of the more severely affected animals showed a frankly nephrotic picture. Although some of the diseased animals showed decreased levels of serum albumin, no other definite changes in serum proteins were noted, nor was there any evidence of glomerular immunoglobulin or immune complex deposition. None of the lesions previously found after administration of streptozotocin in the Chinese hamster were encountered.

Amyloidosis↗

PubMed1976

Acute lung injury induced by cadmium aerosol. I. Evolution of alveolar cell damage.

Following exposure to an aerosol of 0.1% (.005 M) cadmium chloride, rat lungs were examined at 6 hours and 1, 2, 3, 4, 7, and 10 days. By light microscopy, damage was multifocal and centered about respiratory bronchioles. Ultrastructurally, there was Type 1 cell edema with frequent loss of surface plasma membranes during the first 24 hours. After 2 days, the number of Type 2 cells had markedly increased, and by 3 days the damaged alveoli were lined by plump cuboidal cells closely resembling Type 2 cells. By 4 days, these cells were flatter, the change being more marked by 7 days; by 10 days, the cells had regained the appearance of Type 1 cells through loss of osmiophilic bodies and superficial microvilli. We conclude that CdCl2 damages Type 1 cells, which are then replaced by proliferation of Type 2 cells. These cells lose their osmiophilic bodies and flatten out to replace the lost Type 1 cells, the process being almost complete by 10 days after the injury. This pattern resembles the injury caused by NO2, O3, and O2.

Aerosols↗

PubMed1975

The pathology of elastase-induced panacinar emphysema in hamsters.

A single dose of crystalline, porcine pancreatic elastase injected intratracheally into hamsters induces widespread alveolar enlargement with subpleural bullae. A uniformly severe lesion is consistently induced by 0-2 mg elastase per 100 g body weight and with negligible mortality. Compared with controls, which showed no lesion, elastase-damaged lungs show a highly significant (P less than or equal to 0-001) increase in alveolar size and a decrease in internal surface area. Taken with the associated physiological abnormalities, these findings closely simulate human emphysema of the panlobular (panacinar) type. Histologically it appears that elastase converts the fine elastic fibres in alveolar walls and pleura into thickened, nodular fibres which may also be broken along their length. With higher doses of elastase, i.e., 0-5 mg/100 g body weight, many pulmonary arteries showed segmental loss of inner and outer elastic laminae, usually with thrombosis on the overlying endothelium. The mechanism of this thrombosis is unclear. These experiments suggest that damage to elastic fibres may be an important element in the development of human panacinar emphysema, and that the damage could be one pathogenetic mechanism which produces damage of elastic fibres.

Animals↗

PubMed1975

Cellular proliferation induced in the lung by cadmium aerosol.

Rats were exposed to a polydispersed aerosol of 0.1 per cent cadmium chloride in physiologic saline for a single period of 2 hours, and the evolution of damage was followed for a 10-day period. Control animals were unexposed rats and rats exposed to an aerosol of physiologic saline. Wet lung weight doubled by the fourth day in animals exposed to cadmium chloride, but not in the control groups. Apart from a transient increase in fluid content at 1 day, there was no evidence that the lung weight gain was due to inflammatory edema. Uptake of [3H]thymidine markedly increased during the first four days after exposure to cadmium chloride. Light autoradiography showed that [3H]thymidine labeling occurred almost exclusively in Type II alveolar cells at 1 day: later, the label appeared in interstitial cells and cells lying free within alveoli. These changes correlated well (r=0.70) with the increase in deoxyribonucleic acid on the fourth day after exposure. Uptake of [3H]thymidine and deoxyribonucleic acid content in rats exposed to cadmium chloride showed a significant difference from the control groups (P less than 0.001). These experiments demonstrate that exposure to cadmium chloride aerosol evokes a wave of cellular proliferation in rat lung. This finding is of interest, because heavy industrial exposure to cadmium in humans is known to be associated with severe physiologic impairment and anatomic damage.

Aerosols↗

PubMed1975

Pulmonary insufficiency induced by oleic acid in the sheep: a model for investigation of extracorporeal oxygenation.

Most previous studies of the efficiency of bypass techniques for respiratory support have been conducted in hypoxic but otherwise normal animals. However, mechanisms of improved oxygenation by partial venoarterial bypass in the presence of acute respiratory insufficiency can be better studied with an appropriate pathophysiologic model; for this purpose, acute hemorrhagic pulmonary edema was induced in sheep by injection of oleic acid into the right atrium. The model presented a 3 hour period of elevated pulmonary shunting with stable hemodynamics. This preparation is being employed to the study of the mechanisms of extracorporeal oxygenation.

Animals↗

PubMed1974