Primary Hemostasis and Vessel Participation
المؤلف:
Marcello Ciaccio
المصدر:
Clinical and Laboratory Medicine Textbook 2021
الجزء والصفحة:
p222-223
2025-08-05
225
The participation of the vessels in the hemostatic process is often underestimated, but it is far from secondary. The wall of the blood vessels is composed of a concentric series of layers, including the tunica intima (composed of endothelium and subendothelial layers), the tunica media (with a prevalence of elastic and muscular fibers in the arteries and fibrous tissue in the veins), and the tunica adventitia (com posed mainly of dense connective tissue). Injury to the vessel reflexively causes contraction of the elastic and muscular fibers of the middle layer, a process aimed at reducing the caliber of the vessel and its output. This phenomenon, also known as vasospasm, is mediated by thromboxane A2 (TXA2) and can also be activated secondary to neurogenic stimuli such as pain. The reduced blood flow within the contracting vessel is therefore reflected in a reduction in the amount of blood leaving the vessel following its rupture.
Simplifying the concept, the less blood circulates within the vessel, the less chance it has of escaping from the point where the damage occurred.
It is easy to understand that vascular contraction is very efficient in the arterial district (since in the arteries the middle layer is much thicker), while its efficiency is obviously much lower in the venous district, in which the middle layer consists mostly of fibrous tissue. Nevertheless, this difference has a valid pathophysiological explanation: since the pressure in the arteries is much higher than in the veins, a much more effective vascular contraction is required in the arteries in order to prevent a considerable leakage of blood from the vessel. The functions of vasoconstriction can be summarized in three decisive aspects:
• Reduction of the flow rate of the vessel, thus limiting the amount of blood that can flow out of it
• Promotion of platelet margination at the site of endothelial damage and near the injured area
• Promotion of the accumulation, at the site of endothelial damage, of coagulation factors to enhance the activation and propagation of secondary hemostasis
The vascular endothelium takes part in the hemostatic processes with two prevalent activities: the liberation of tissue factor (Tissue Factor, TF), following the rupture of the cytoplasmic membrane, and the active production of Von Willebrand factor (VWF), contained in the so-called Weibel–Palade organelles, which will be discussed later in relation to secondary hemostasis. Accessory roles played by the endothelium are those related to the inhibition of hemostasis, especially when it is not necessary (intact vessel). In this context, the anti-hemostatic effect of the endothelium is mediated by a series of activities, including:
• Formation of an anatomical barrier to the subendothelium
• Coating with heparinoid substances, which help inhibit the coagulation cascade.
• Coating with thrombomodulin, which modulates the activation of the coagulation protein C and S complex
• Production of antiplatelet substances, such as prostacyclin (PGI-2) and nitric oxide (NO)
• Production of tissue plasminogen activator (t-PA), whose role is to activate fibrinolysis
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