Cross tolerance to environmental stress and endotoxin.
Mild DIC-like phenomena develop in rodents exposed to environmental stress, induced by prolonged fluctuation in ambient temperature, known as SART (specific alternation of rhythm in temperature) stress, the symptoms being essentially similar to those produced by endotoxin. The aim of the present study was to investigate whether common mechanisms are involved in the stress-induced DIC-like phenomena and endotoxaemia. The mortality in mice after intraperitoneal injection with endotoxin at 8.3, 16.7 and 33.3 mg/kg increased in a dose-dependent manner. In the mice exposed to stress for 7 days, the death rate following endotoxin at 8.3 mg/kg was markedly lower than that in unstressed mice, although no difference was detected between the two groups following endotoxin at 16.7 and 33.3 mg/kg. Conversely, repeated administration of endotoxin at a low dose, 0.5 mg/kg, during exposure to stress for 7 days inhibited the stress-induced thrombocytopenia and hypofibrinogenemia. These findings indicate the development of cross tolerance to prolonged environmental stress and endotoxin, implying involvement of a common mechanism.[1]References
- Cross tolerance to environmental stress and endotoxin. Kawabata, A., Hata, T., Kuroda, R. Life Sci. (1998) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
