TRANSIENT LOSS OF SERUM PROTECTIVE ACTIVITY FOLLOWING SHORT-TERM STRESS - A POSSIBLE BIOCHEMICAL LINK BETWEEN STRESS AND ATHEROSCLEROSIS

Very low density lipoproteins (VLDL) are toxic to aortic endothelial cells in vitro, and toxicity preventing activity (TxPA) inhibits this toxic effect of VLDL. Stress, an established arteriosclerosis risk factor, was examined for its effect on TxPA and on the ability of serum to protect endothelial cells from in vitro injury by VLDL. A standardized mirror tracing task with noise was administered to four healthy subjects. Blood samples were obtained at 0, 30, (stressor) 35, 50 and 80 min. Cortisol and non-esterified fatty acids increased during the stress period. TxPA significantly decreased following the stressor and had recovered by 80 min. When the ratio of non-TxPA/TxPA rose above 2, serum was no longer able to protect the cells from VLDL injury. If endothelial cells in vivo respond similarly to the endothelial cells in culture, the effect of stress on atherosclerosis may be mediated through these transient decreases in TxPA.