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Biomedical subjects

R C Piper

Publications and source records attributed to R C Piper.

48 records · Page 3Linked to original sources
PubMed1986

7-(Trifluoromethyl)-4-aminoquinoline hypotensives: novel peripheral sympatholytics.

A family of 7-(trifluoromethyl)-4-aminoquinolines that are hypotensive agents and that act by a novel sympatholytic mechanism is described. Structure-activity relationships in this series have been elucidated. Some of the more potent hypotensives were evaluated for safety in the mouse. A candidate, 1-[(4-fluorophenyl)sulfonyl]-4-[4-[[7-(trifluoromethyl)-4- quinolinyl]amino]benzoyl]piperazine hydrochloride (losulazine hydrochloride) has been selected for clinical development. Losulazine hydrochloride is a hypotensive agent in the rat, cat, and dog. At acute effective hypotensive doses, it does not block the response of the sympathetic nervous system to stimuli. Both animal pharmacology and clinical experience suggest that losulazine hydrochloride may be free of the clinically limiting side effects that often plague compounds that decrease blood pressure by interfering with autonomic neurogenic function.

Aminoquinolines↗
PubMed1981

Protective effects of 16,16-dimethyl PGE2 on the liver and kidney.

The ability of subcutaneous 16,16-dimethyl PGE2 to protect the liver and the kidney against damage induced by carbon tetrachloride and ANIT (alpha-napthylisothiocyanate) was examined. Rats were given 5-75 micrograms/kg of 16,16-dimethyl PGE2 24 and 0.5 hrs before challenge with 1 ml of oral carbon tetrachloride with an additional prostaglandin dose 6 hrs later. Twenty-four hrs after carbon tetrachloride animals was sacrificed by decapitation. 16,16-Dimethyl PGE2 partially prevented fat accumulation and necrosis in the liver with complete or partial reduction in the SGPT caused by the hepatotoxin. Higher doses of carbon tetrachloride (1.5 ml) caused elevation in BUN and uric acid also; these changes were prevented by 16,16-dimethyl PGE2 even when doses of the prostaglandin were too low to protect against liver necrosis. Elevated serum bilirubin observed 48 hrs after oral ANIT (30 mg/kg) was prevented by 100 micrograms/kg of 16,16-dimethyl PGE2 given 24 and 0.5 hrs prior to the challenge with additional doses 6 and 24 hrs after ANIT. Higher doses of oral ANIT (200 mg/kg) when combined with small doses of carbon tetrachloride (0.25 ml per rat) resulted in elevated BUN and uric acid levels in the serum although neither compound produced these changes when given alone. 16,16-Dimethyl PGE2 (75 micrograms/kg) administered by the same schedule as used for protection against ANIT resulted in normalization of these parameters in the absence of significant liver protection. Thus, it appears that 16,16-dimethyl PGE2 can protect the liver against necrosis induced by moderate amounts of carbon tetrachloride and ANIT. At higher doses of these hepatotoxins, the liver is not protected by prostaglandins. Elevation of BUN and uric acid is observed under these conditions, however, and can be prevented by 16,16-dimethyl PGE2.

1-Naphthylisothiocyanate↗
PubMed1976

Lesions associated with Orthohalarachne attenuata (Halarachnidae) in the northern fur seal (Callorhinus ursinus).

In northern fur seals (Callorhinus ursinus) up to at least 4 years of age there is virtually 100% prevalence of infestation with the nasal mite Orthohalarachne attenuata. Although clinical observations and gross examination indicate that the condition is not serious, some erosion and inflammation of the nasal turbinates and nasopharynx were seen associated with mites in histological sections.

Animals↗
PubMed1975

Selenium-vitamin E deficiency in swine fed peas (Pisum sativum).

An experiment was conducted to study the effects of feeding a 96.8% cull pea basal ration, low in selenium (0.061 ppm) and vitamin E (7.0 IU alpha-tocopherol/kg of ration), to growing pigs with and without supplementation of selenium, vitamin E, or both. The basal ration was high in crude protein (25.2%) and contained no supplemented fat. Nine of 10 pigs fed the unsupplemented basal ration had lesions attributed to selenium-vitamin E deficiency, and 8 of these pigs died during the 160-day experiment. The deficiency was usually characterized by sudden death (with no prior signs of illness), massive hepatic necrosis, hemoglobinuric and to a lesser extent cholemic nephrosis, degenerative myopathy of cardiac and skeletal muscles, edema, icterus, and acute terminal congestion and hemorrhage. Clinical signs, deaths, or lesions attributed to selenium-vitamin E deficiency were not observed in any of the pigs fed the basal ration supplemented with as little as 0.01 ppm selenium as sodium selenite or 100 ppm alpha-tocopherol. Pigs fed the unsupplemented basal ration gained more slowly (P less than 0.01) and less efficiently and had higher serum glutamic oxalacetic transaminase (SGOT) levels (P less than 0.01) than pigs fed the basal ration supplemented with selenium, vitamin E, or both. There was no difference (P greater than 0.05) in albumin-to-globulin (A/G) ratios among dietary treatment groups. Using the criteria of this study, the minimum selenium requirement of growing pigs fed a low tocopherol cull pea diet was determined to be between 0.06 and 0.07 ppm.

Anemia↗