Changes in the coronary vascular system following prolonged exposure to stress

• Published in: Pharmacology, biochemistry and behavior Vol. 6; no. 3; p. 311
• Main Authors: Bassett, J R, Cairncross, K D
• Format: Journal Article
• Language: English
• Published: United States 01-03-1977
• Subjects: Animals; Blood Cell Count; Blood Platelets - cytology; Coronary Vessels - ultrastructure; Corticosterone - blood; Endothelium - ultrastructure; Intercellular Junctions - ultrastructure; Lipids - analysis; Male; Myocardium - ultrastructure; Rats; Stress, Physiological - blood; Stress, Physiological - pathology
• ISSN: 0091-3057
• DOI: 10.1016/0091-3057(77)90030-2

Hearts of stressed rats showed marked changes in the coronary vasculature. It was suggested that such morphological changes could be explained on the basis of an increased coronary vascular permeability. Endogenous inflammatory substances could induce swelling of the endothelial cells and cause separation of the neighbouring cells from one another, thus allowing the passage of lipid molecules through the endothelial lining. In order to gain supportive evidence for the above hypotheses an electron microscope study was undertaken. The presence of junctional gaps in the endothelial lining of the coronary vascular system was observed following prolonged stress, as well as platelet aggregation. The use of lipid staining of frozen sections indicated the presence of large lipid deposits in the arteriole walls, corresponding to vacuoles seen previously. It would appear therefore, that prolonged exposure to stress may result in pathological changes in the myocardium associated with changes in the vascular endothelial permeability, and platelet aggregation. Pathological changes induced in this way, however, should be inhibitd by high glucocorticoid levels and should not be manifested until adaptation of the steroid response to stress has occurred. Measurement of plasma glucocorticoid levels over the period of prolonged stress shows a good correlation between the adaptation of the steroid response and the onset of a progressive degeneration of the coronary vascular system.