The rise in clotting factor VIII induced in man by adrenaline: effect of α‐ and β‐blockers

Abstract

SUMMARY1. Human subjects received intravenous infusions of adrenaline preceded by saline, phentolamine (an a-blocker) or either pronethalol or propranalol (fl-blockers), in different experiments.2. Clinical measurements of blood pressure and pulse rate confirmed that oc-or ,-blockade had been achieved.3. The rise in clotting factor VIII induced by adrenaline was blocked by pronethalol and propranalol but not by phentolamine. This indicated that the effect of adrenaline on factor VIII was mediated by f-receptors.

The Effect of β-Adrenergic Blockade (Propranolol) on the Coagulability of the Blood Across the Human Heart

“…These observations apparently indicate that epinephrine accelerates the mechanisms underlying primary and secondary hemostasis. Some of these changes induced by epinephrine e.g., increased platelet adhesiveness and aggregation, and increased activity of antihemophilic factor were found to be blocked by /5-adrenergic blockade [17,21,22]. These observations further tend to support the role of /5-receptors in mediating at least some of the hemostatic effects of the sympatlio-adrenal system.…”

Activation of human endothelial cells from specific vascular beds induces the release of a FVIII storage pool

“…15,27,28 Interestingly, ␤2-receptor blockade also lowers sustained elevated FVIII:C in patients with deep vein thrombosis. 29 The amounts of FVIII released during acute physical stress are important by comparison to the steady state production of FVIII.…”

Addition of serum from patients with collagen diseases increases to cultured human endothelial cells production and release of von willebrand factor

“…Although it cannot be concluded which factor in serum affects the release of vWF from EC, our results suggest that CRP might be one of the causative serum factors involved in elevated vWF:Ag release. The release of vWF from EC resulting from various types of stimulation has been reported; its release is accelerated by cytokines such as interleukin 1 (IL-1), endotoxin [20], thrombin [21], calcium ionophore A 23187 [22], and adrenaline [23]. In any case, the mechanisms concerned with vWF release have not yet been clarified.…”