Platelet aggregability in humans: contrasting in vivo and in vitro findings during sympatho‐adrenal activation and relationship to serum lipids

Abstract

Platelet aggregability was studied in 18 healthy volunteers during mental stress (a colour word test; CWT) and low- and high-dose adrenaline infusions using an ex vivo technique (filtragometry) and conventional in vitro aggregometry. CWT and high-dose adrenaline (3.4 nmol l-1 in plasma) shortened filtragometry readings, suggesting increased platelet aggregability in vivo. Low-dose adrenaline had no effect despite higher adrenaline levels in plasma (0.9 nmol l-1) than during CWT (0.4 nmol l-1). Platelet sensitivity to ADP in vitro was reduced following CWT and further reduced following adrenaline infusions. In vitro, adrenaline (50 nmol l-1) had little effect on platelet aggregation per se, but enhanced aggregability evoked by ADP (at ED50). Adrenaline potentiation of ADP-induced aggregation was enhanced after CWT, but was not related to filtragometry responsiveness to stress in vivo. Serum LDL-cholesterol levels were inversely correlated to filtragometry readings at rest, suggesting an adverse influence on platelet aggregability in vivo. HDL-cholesterol levels were inversely correlated to platelet sensitivity to ADP in vitro, suggesting a positive influence. Thus, sympatho-adrenal activation enhances platelet aggregability in vivo (as assessed by ex vivo filtragometry), but adrenaline alone cannot explain the pro-aggregatory effect of mental stress. Serum lipoprotein alterations associated with increased risk for atherosclerosis seem to enhance platelet aggregability. The conventional in vitro technique may poorly reflect platelet aggregability in vivo.

Hemoconcentration and Hemostasis During Acute Stress: Interacting and Independent Effects

“…Additionally, many studies report increases in the levels of the platelet activation markers circulating platelet factor 4 (PF4) and beta-thromboglobulin (BTG) among healthy individuals [6,[116][117][118][119][120][121] and among individuals with essential hypertension [122] and with angina pectoris [123]. However, not all studies have reported significant changes in platelet aggregability [124][125][126] and platelet activation markers [123,127,128] in response to acute stress. For example, Wallén and colleagues [123] reported that acute stress did not elicit elevations in these platelet activation markers in elderly healthy volunteers.…”

Markers of Thrombosis and Hemostasis in Acute Coronary Syndromes: Relationship to Increased Heart Rate and Reduced Heart‐Rate Variability

“…6 Abnormal plasma markers of endothelial damage (von Willebrand factor (vWF)), 7 platelet activation (soluble P-selectin (s-Psel), 8 CD 40 -ligand (CD 40 L)) 9 and thrombogenesis (D-dimer) 10 are recognized in AMI, but their linkage to autonomic tone is untested. Autonomic tone and platelet-induced thrombosis in vitro is linked by α 2 receptor mediation 11,12 and seen in vivo 13 in studies examining mental stress and dynamic exercise. 14,15 The association of sympathetic stimulation to platelet activation is deduced from β 1 -blockade preventing platelet activation and aggregation.…”

Αξιολόγηση Βιοχημικών Παραμέτρων Μετά Από Αγωνιστική Προσπάθεια Σε Αθλητές Και Αθλήτριες Της Ποδοσφαίρισης

“…Η άσκηση προκαλεί την έκκριση της επινεφρίνης από το μυελό των επινεφριδίων και αυτή με τη σειρά της επάγει την ενεργοποίηση των αιμοπεταλίων610 . Άλλος ένας διαφορετικός μηχανισμός μπορεί να είναι ο μετασχηματισμός των α2 αδρενεργικών υποδοχέων των αιμοπεταλίων μετά από οξεία άσκηση, η παραγόμενη από την άσκηση επινεφρίνη ενεργοποιεί τους γλυκοπρωτεινικούς προσδέτες ΙΙb/ΙΙΙ του Ινωδογόνου στην επιφάνεια των αιμοπεταλίων παρουσία του ADP που υπάρχει άφθονο από τους συστελλόμενους μύες λόγω της οξείδωσης του ΑΤP για την παραγωγή ενέργειας· το Ινωδογόνο τέλος ενεργοποιεί τα αιμοπετάλια προς το σχηματισμό θρόμβου[610][611][612][613][614] . Η προκαλούμενη απώλεια ύδατος κατά την οξεία και παρατεταμένη άσκηση προκαλεί αυξημένη αιμοσυγκέντρωση.…”