Abstract
Summary and Conclusions
1) A/Jax and C57BL/6 (both seizure resistant) and DBA/1 (seizure susceptible) strain mice were exposed to subeonvulsive audiogenic stress for 7 days before. and in some instances up to 14 days after intracutaneous injection with 0.025 cc of turpentine. 2) The effect of pretreatment audiogenic stress resulted in moderate repression of ordinary inflammatory response observed in control animals. This was characterized by a sharp localization of the lesion with only a very narrow limiting zone of inflammatory cells. 3) In addition to relative repression of inflammatory response, delayed repair of injury was observed, with a minimal amount of fibroblastic proliferation during first 10 days or more in the majority of animals. 4) No differences were observed in these reactions in mice subjected to posttreatment stress supplementing the initial pretreatment application of stress. This suggests that the mechanism initiated by such audiogenic stress persists for a considerable time. 5) The data were inadequate to establish the way in which the reaction operates, but a certain parallel may be drawn between inhibition of inflammatory response clinically by use of adrenal cortical steroids to suggest that adrenal cortical stimulation may be involved.
Get full access to this article
View all access options for this article.