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Results for “Cachexia”

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At least 181 records · Page 10Linked to original sources
PubMed1988

Observations on dopamine receptor antagonists and gastric ulceration associated with experimental anorexia cachexia.

Gastric ulceration is frequently reported to occur in tumour-bearing animals and man, even when such tumours are not associated with organs of digestion. That central and peripheral dopamine (DA) containing neurones may be relevant to this phenomenon, is supported by the fact that the DA receptor antagonists domperidone (0.1 and 0.05 mg/kg) and pimozide (0.1 mg/kg) were observed to prevent gastric ulceration commonly reported in rats bearing the Walker 256 carcinosarcoma. Daily administration of these drugs prevented the formation of ulcers similar to those observed in vehicle-treated animals. These results demonstrate that DA neurone function is important in the formation of gastric ulcers in tumour-bearing animals and suggest that such compounds may be useful in cancer management.

Animals↗
PubMed1985

Cancer cachexia: a manifestation of hypersensitivity?

More than thirty years ago, as a corollary of the experimental analysis of the systemic hypersensitivity reaction, it was postulated that the general symptoms of tuberculous patients may be due to the action of the specific antigen upon the sensitized host. The same hypothesis can be extrapolated in order to interpret some hitherto unexplained findings that are observed in cancer hosts, as well as organ transplant recipients.

Animals↗
PubMed1986

Tumor cachexia and hypercalcemia in nude rats and mice bearing human renal carcinomas.

Human hypercalcemia-inducing renal tumors have been established as xenografts in nude mice and nude rats. Animals bearing these tumors became cachexic and hypercalcemic and these changes could be reversed by excision of xenograft tumors. Metabolic studies carried out in nude rats suggested that the hypercalcemia-inducing factor was effecting renal excretion of calcium but was probably not parathyroid hormone. Although the hypercalcemia-inducing property of the tumor was stable throughout serial transplantation of tumor from animal to animal, it was lost after passage through cells in culture.

Animals↗
PubMed1984

Cancer cachexia.

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Cachexia↗
PubMed1991

Cancer cachexia.

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Body Weight↗
PubMed1990

Prevention of adjuvant-induced cachexia in rats by cyclosporin A.

The changes in food intake and biochemistry following Freund's adjuvant (AJ)-induced inflammation in rats were investigated. Injection of AJ into rats resulted in a transient anorexia but a sustained decrease in body weight. Within 14 days, body weight decreased by 12% (P less than 0.05) and adipose tissue (retroperitoneal fat pads) decreased by more than 50%. Biochemical changes seen in association with the AJ-induced wasting included decreased plasma concentrations of triglyceride and cholesterol. Injection of cyclosporin-A (CS) (20 mg/kg) with the AJ decreased the anorexia, prevented the sustained loss of body weight and adipose tissue and reversed the effects on plasma triglyceride and cholesterol concentrations. Insulin concentrations were not significantly affected by the AJ or AJ/CS treatments. Peritoneal macrophages from AJ-treated rats produced 3-fold more tumour necrosis factor-alpha (cachectin) than control rats. This effect was not observed in rats treated with AJ plus CS. The results are consistent with CS preventing the release of cytokines which have anorectic and catabolic actions (IL-1, TNF), although there is also the possibility that CS has effects involving endocrine mechanisms.

Adipose Tissue↗