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Biomedical subjects

R P Shields

Publications and source records attributed to R P Shields.

30 records · Page 2Linked to original sources
PubMed1977

Fatal generalized feline viral rhinotracheitis in a young adult cat.

A 7-month-old cat died following a 17-day illness. Necropsy findings included sharply demarcated lingual ulcers and multifocal necrotic hepatitis. Intranuclear inclusions were found in the lesions, and a herpesvirus was recovered from specimens of liver and tongue. The virus was identified by neutralization with specific antiserum as feline rhinotracheitis virus.

Animals↗
PubMed1976

Environmental monitoring in a laboratory animal facility.

A study was made of the microbial environmental status of an animal facility. Cultures were made of animal and surgical room floors; the germicidal effectiveness of the phenolic disinfectant-detergent employed in the facility was tested against standard test organisms as well as against other microorganisms isolated from the facility, and killing power of the disinfectant-detergent was evaluated during various steps of the usual cleaning procedures, ie, mops and mop bucket solutions were tested before, during, and after mopping a room. It was found that colony counts for animal rooms cleaned with a chlorhexidine disinfectant were much lower than those cleaned with a phenolic disinfectant. The phenolic disinfectant killed some organisms after 10 min exposure, but no others. Pseudomonads were the most resistant organisms. Contaminated mops and mop bucket solutions appeared responsible for the high counts on floors cleaned with the phenolic disinfectant. Guidelines for achievable levels of cleanliness were suggested.

Animals↗
PubMed1975

Fluroxene toxicity induced by phenobarbital.

Because of reports of fluroxene toxicity in man, the effect of phenobarbital treatment on the toxicity and metabolism of fluroxene was studied in 9 rhesus monkeys. Six monkeys that were exposed to a mean calculated alveolar fluroxene concentration of 5.8% for 4-hr periods up to a total of 16 hr showed no evidence of toxicity. Two animals were sacrificed after a single 4-hr exposure to obtain control measures of fluroxene metabolites in tissues. Four monkeys that had previously survived received exposures to fluroxene and 3 monkeys that had no exposure to fluroxene died during fluroxene anesthesia after treatment with phenobarbital (mean time, 3 hr). Toxicity was manifested by arterial hypotension, pulmonary edema, and arterial hypoxemia. Phenobarbital treatment enhanced production of fluroxene metabolites, including the highly toxic trifluoroethanol. Concentrations of trifluoroethanol in mixed-expired gas, blood, and urine, and of total nonvolatile fluorine in blood, urine, and tissues of animals treated with phenobarbital were 2 to 10 times as in control animals. The results suggest that the rhesus monkey is a valuable model for the study of fluroxene pharmacology and that inclusion of an enzyme-inducing challenge in the evaluation of potential toxicity of other anesthetics seems warranted.

Anesthesia↗
PubMed1975

Skeletal muscle function and structure after depletion of creatine.

Experiments were conducted to determine if normal skeletal muscle function and structure are dependent upon their ability to store large quantities of metabolic energy in the form of N-phosphorylcreatine. Muscle levels of creatine and N-phosphorylcreatine were reduced by feeding young male rats diets containing 1 per cent beta-guanidinopropionic acid (beta-GPA). Muscle function was evaluated by monitoring performance during a 4-week, short duration, high intensity exercise program in a control running wheel. Structural effects were determined by histochemistry, morphometric analysis, and routine histologic procedures using light microscopy. Evidence of abnormal creatine metabolism of rats fed beta-GPA included: excessive creatinuria, reduction in urine creatinine, reduced levels of muscle and brain creatine, and a reduced activity of muscle creatine kinase. In separate experiments, beta-GPA inhibited the reaction of creatine with creatine kinase in vitro. When muscle function was evaluated by running, the percentage of expected revolutions for the group of rats fed beta-GPA was below the expected normal values. The white (type II) fibers from the gastrocnemius of exercised rats fed beta-GPA were smaller than fibers from the same muscle areas of rats fed normal diets. The histochemical characteristics of red (type I) and white fibers of all rats tested were within normal limits. It is concluded that feeding beta-GPA will result in structural and functional changes in skeletal muscles of exercised young male rats. These changes are believed to result from the ability of beta-GPA to block creatine entry into muscle and thereby prevent muscle from accumulating and maintaining its normal complement of creatine and N-phosphorylcreatine.

Animals↗