“…These results are similar to those reported by other authors (Mikulaj, Mitro, Murgas and Dobrakova 1973). This suggests this phenomenon is due to an inhibition of ACTH secretion {Nemeth, Vigas and Jurcovicova 1975) or to an increased corticosterone catabolism (Kraus and Erdosova 1973).…”
Male Wistar rats weighing 200-300 g were used. The rats were housed in a temperature and light controlled environment and received water and food "ad libitum". Chronic stress was provoked with an alarm bell and intermittent light applied 1 hour/day during 20 days and a dog was used to provoke acute stress. A modification of Stahl, Hertling and Knappe's (1963) fluorimetric method was used to analyze corticosterone; in order to confirm the specificity of the results some samples were analyzed either by direct radioimmunoassay or after having been previously purified by paper chromatography.
Results and DiscussionAs can be seen in Fig. 1 the dynamic of seric corticosterone response to the presence of a dog differed in the rats submitted to chronic (sound and light) stress (group II) compared with the nonpreviously stressed rats (group I). The initial response to a new stress was slower in group II (p < 0.05 respect to the control) than in group I (p < 0.05 respect to the control), but there was no significant statistical difference at 20-60 min after the stimulus.
“…These results are similar to those reported by other authors (Mikulaj, Mitro, Murgas and Dobrakova 1973). This suggests this phenomenon is due to an inhibition of ACTH secretion {Nemeth, Vigas and Jurcovicova 1975) or to an increased corticosterone catabolism (Kraus and Erdosova 1973).…”
Male Wistar rats weighing 200-300 g were used. The rats were housed in a temperature and light controlled environment and received water and food "ad libitum". Chronic stress was provoked with an alarm bell and intermittent light applied 1 hour/day during 20 days and a dog was used to provoke acute stress. A modification of Stahl, Hertling and Knappe's (1963) fluorimetric method was used to analyze corticosterone; in order to confirm the specificity of the results some samples were analyzed either by direct radioimmunoassay or after having been previously purified by paper chromatography.
Results and DiscussionAs can be seen in Fig. 1 the dynamic of seric corticosterone response to the presence of a dog differed in the rats submitted to chronic (sound and light) stress (group II) compared with the nonpreviously stressed rats (group I). The initial response to a new stress was slower in group II (p < 0.05 respect to the control) than in group I (p < 0.05 respect to the control), but there was no significant statistical difference at 20-60 min after the stimulus.
“…The gradual inhibition of the stress response, despite the unchanged daily stress schedule, represents the stage of resistance of the general adaptation syndrome [Selye, 1976]. Our study indicates that adapta tion is not limited to the pituitary-adrenal system [Mikulaj and Mitro, 1972;Sakellaris and Vernikos-D anellis, 1975], but apparently also en compasses GH, LH and Prl responses, with the rate of adaptation varying according to the stress regimen.…”
To delineate the pattern of adenohypophyseal hormone secretion following chronic stress, adult male rats were exposed daily to 6 h of cold, forced exercise or immobilization for 3, 6, 10, 15, 28 or 42 consecutive days. Groups of these animals were sacrificed at the end of the last stress sessions, and plasma growth hormone (GH), luteinizing hormone (LH), prolactin (Prl) and follicle-stimulating hormone (FSH) levels were measured by radioimmunoassay (RIA). Irrespective of the different stimuli used, long-term stress induced a morphologic and hormonal response characterized by decreased ponderal growth, adrenal enlargement, thymus involution and significant diminutions in GH, Prl and LH levels with no modifications in FSH titers. The magnitude and duration of these changes varied with the severity of the stressors.
“…After repeated exposure to a stressor, the time course of the arousal response is altered such that the maximal response occurs prior to stressor exposure instead of during it. This pattern of results is evident across all species with adrenocortical systems (42). Given the above pattern of results it is possible to postulate a mechanism for achieving adaptation in cases of chronic intermittent stress.…”
A theory of the response to chronic intermittent stress, intergating many diverse studies, is presented. Chronic intermittent stress is presumed to be the type of stress most frequently encountered and most likely to cause physiological changes which predispose an organism to tissue damage. The theory states that all organisms are genetically predisposed to adapt to stress and that the physiological pattern of adaptation is similar across species. This pattern consists of a conditioned endocrine response before the stressor is presented accompanied by a decrease in arousal during the stress. These changes occur because the organism is predisposed to learn cues predictive of stress and to assess the threat potential of the stressor. This pattern is adaptive because it conserves resources and promotes homeostasis. Maladaptation is discussed in terms of failure to learn situational expectancies and appropriate responses. Implications of this theoretical perspective are examined.
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