Chronic Stress Group Research Articles

Corticotropin-releasing factor stimulation of adrenocorticotropin and beta-endorphin release: effects of acute and chronic stress.

The effects of acute and chronic stress on the release of ACTH and beta-endorphin in response to stimulation by ovine corticotropin-releasing factor (CRF) and arginine vasopressin were examined. Pituitaries were removed from rats who had received either acute stress, chronic stress daily for 14 days with the last stress occurring 24 h before decapitation, or chronic stress followed by an acute stress immediately before decapitation (chronic stress-acute stress). Pituitaries from naive unstressed animals were used as the control group. After processing into single cell suspensions, the pituitaries were incubated with various doses of CRF (10(-11) M to 10(-9) M) and AVP (10(-10) M to 10(-8) M). Release of ACTH and beta-endorphin into the medium was measured by RIA. A clear dose-dependent response to both releasers was seen in control pituitaries. In acute stress, a decreased responsiveness to arginine vasopressin and CRF was seen. This same blunted response was not seen in chronic stress even if the animals are stressed immediately before decapitation. At higher doses of CRF (10(-9) M) a substantially increased release of ACTH and beta-endorphin was seen in the chronically stressed rats. When the content of the anterior pituitary lobe was assayed in these animals, both chronic stress groups show increased content of ACTH and beta-endorphin, which may indicate an increase amount of ACTH and beta-endorphin in the releasable pools in chronic stress. In addition, the failure of further stress to alter the response to CRF in the chronic stress-acute stress group may indicate a down-regulation of the steroid feedback on the pituitary. However, it is clear that no down-regulation of the CRF receptor occurs in this chronic stress paradigm.

Systemic stress in the production of cardiac thrombosis in hypercholesterolaemic rats

An experimental study to elucidate the effects of feeding a high fat diet, hypercholesterolaemia and superadded acute and chronic stress on the production of cardiac thrombosis was carried out in rats. The high fat diet contained 25 percent butter rat providing 45 percent calories from fat which produced significant increase of serum cholesterol and other lipids. Acute stress was induced by two injections of adrenaline on a single day which caused a marked transient alteration of haemodynamics. Chronic stress was of two types, physical and metabolic. The physical stress was induced by repeated exposure of the rats to electric shock or roller drum exercise, while metabolic stress was caused by repeated injection of ACTH. Rats of both acute and chronic stress groups showed variable degree of medial degeneration, hyaline and fibrinoid intimal deposits and calcification in coronary arteries. Cardiac thrombi were seen in 30 percent animals subjected to adrenaline shock. Among the chronic stress procedure 17 percent rats exposed to electric shock and only one rat of the ACTH group developed cardiac thrombosis but no thrombus was detected in those exposed to roller drum exercise. The myocardium showed patchy necrosis with or without calcification, Spontaneous mortality was maximum following acute adrenaline shock (25 %) while electric shock caused mortality in 17 percent animals. The other procedures did not lead to spontaneous mortality. This study highlights the significant role of high fat intake, hypercholesterolaemia and systemic stress in the pathogenesis of acute cardiac thrombosis and myocardial necrosis/infarction.