Platelet activation in mental stress

Abstract

Platelets are known to become activated in vivo by different stressful stimuli such as surgery and dynamic exercise. Mental stress has been shown to increase platelet aggregability. Platelet activation is thought to be of major importance in atherogenesis and cardiac fatalities. In order to clarify further stress-induced platelet activation with special reference to the period after the stress, we studied eight young, healthy volunteers during and for 1 h after a mental stress test (Stroops Colour Word Conflict Test). Using highly standardized techniques, we have measured platelet aggregability ex vivo and the platelet release products beta-thromboglobulin, platelet factor 4 and serotonin in plasma. As markers of the stress response we measured cyclic-AMP in plasma, heart rate, cardiac output and blood pressure. The stress test induced a significant cardiovascular response with increases in heart rate, blood pressure, and cardiac output and as a measure of adrenergic activity an increase in cyclic AMP in plasma during the test. Platelet aggregability was unaffected during the test but decreased following the stress. During the first hour following the test and release products beta-thromboglobulin and serotonin increased significantly in plasma. We conclude that platelets are activated during mental stress and that this activation involves a post-stress release of vasoactive compounds from platelets.

Hemostatic Changes Following Surgery

“…In this study, the postsurgical alterations in the plasmatic hemostatic variables in patients of Arab origin conform to a greater extent with earlier studies in Caucasians [1][2][3][4][5][6][7][8][9][10]. The increases in fibrinogen and factors VIII and V levels and the decrease in platelet count, especially during the first three postoperative days, are well documented [2,6,7,19].…”

“…In our patients, platelet responses to a wide range of aggregating agents was unaffected by surgery . More recently, however, Naesh et al [8] found increases in serum cortisol (an index of stress response), platelet BTG and thromboxane B2 (TXB2) during surgery and normalization of levels during the postoperative period in the absence of complications. However, platelet hyperaggregability was recorded throughout the postoperative period.…”

“…On the other hand, the fibrinolytic inhibitor alpha 2-antiplasmin did not show any significant fluctuations following surgery and this differs from the findings of others [2] who demonstrated a significant increase. Despite the decrease in the number of platelets in the immediate postoperative period, their adhesiveness and aggregation may be enhanced [3,8] thereby contributing further to the hypercoagulability [5] during the postoperative period. In our patients, platelet responses to a wide range of aggregating agents was unaffected by surgery .…”

Restoration of blood rheological properties with the help of THz-band electromagnetic waves of nitrogen oxide molecular spectrum occurrence

“…It has been argued that the erythrocytes deformability increase in plasma with a high fibrinogen (and its degradation products) level is the protecting mechanism of an organism, which prevents an acute blood flow failure. The findings about an increase of erythrocyte aggregation and their flexibility growth under the immobilization stress do not contradict with the findings (experiments with different pathological states) of other authors [31][32][33]. This also may be connected with fibrinogen increase in blood and its degradation products caused by fibrinolytic blood potential [34,35].…”

Rofecoxib does not compromise platelet aggregation during anesthesia and surgery

“…Specifically, the declines in sympathoadrenal activity and stress hormone levels associated with anesthesia can affect platelet aggregation. 8,24,25 Furthermore, it has been noted that inhalational agents such as halothane and sevoflurane suppress platelet aggregation and increase bleeding times by a variety of interacting mechanisms; and, by seemingly different mechanisms, midazolam and propofol also inhibit platelet aggregation. 7,[16][17][18][19] Our data are consistent with these findings in that the PLAC and ROF groups both had declines in aggregation intraoperatively.…”