Basic mechanisms of blood clotting relevant to herbal supplement use
Many herbal products are reported to possess antiplatelet and/or anticoagulant properties, having the potential to impair hemostasis and cause/promote bleeding. Capsella is a fine example. Other herbals are also known to affect hemostasis by other mechanisms. Such as Hamamelis.
The intensity of the effects of the different herbal medicines on hemostasis may vary depending on a number of factors, including the type and dose of the herbs used, the susceptibility of the patient, the severity of blood vessel damage, and the presence of interacting substances. The following is a discussion of the commonly used herbal supplements in USA, with potential consequences on blood clotting.
Under normal physiological conditions, moderate levels of small blood vessel injuries and bleeding, accompanied by reparative responses, occur routinely [21]. However, in certain severe situations, abnormalities in hemostasis can occur, resulting in excessive bleeding (hemorrhage) or blood clot (thrombus formation). The basic mechanisms of blood clot formation following injury/bleeding, and the attendant repair processes are illustrated in Figs. 1 and and22 [21, 22].
Sequences leading to ( a ) formation of platelet plug and vasoconstriction, and ( b ) synthesis of TXA2 (TXA2, thromboxane A2; COX-1, cyclooxygenase-1; PGH2, prostaglandin H2; TX, thromboxane; ADP, adenosine diphosphate; PAF, platelet activating factor; 5-HT, 5-hydroxytryptamine)
Blood clotting (coagulation) cascade and clot resolution (fibrinolysis) (t-PA, tissue plasminogen activator)
Vascular injury and bleeding initiate a series of reactions that stop bleeding and maintain a normal balance within the system. These reactions include vasoconstriction, platelet aggregation, blood coagulation (clot formation), and clot resolution [21, 22]. Although the initial vasoconstriction that follows blood vessel injury contributes to a reduction of bleeding, the cessation of bleeding ultimately depends on the formation of platelet plug and blood coagulation. The creation of platelet plug involves initial adhesion and activation of platelets at the site of injury, followed by further activation and aggregation of platelet by released chemical mediators, such as adenosine diphosphate (ADP), platelet activating factor (PAF), serotonin, and thromboxane A2 (TXA2) (Fig. [1](Checking your browser - reCAPTCHA)a) [21–23]. The platelet plug thus formed serves as a temporary/primary hemostatic plug [21–23]. As shown in Fig. Fig.1b,1b, TXA2 is formed from membrane phospholipids via arachidonic acid pathways involving various enzymes including cyclooxygenase-1 (COX-1) [21–23]. This component of the initial hemostatic process is a major target for the actions of many blood-thinning substances, including herbal supplements.
The process of blood coagulation (clotting) begins with two different and independent pathways, intrinsic and extrinsic pathways, which converge to the same point (a common pathway) after some steps (Fig. 2) [22]. This process takes place at the site of vascular injury with the involvement of intravascular (within blood) and extravascular (from tissue) elements, platelets, and active proteases (active factors). After convergence, both pathways end up with the conversion of prothrombin to thrombin. Thrombin, as an active protease, converts fibrinogen to fibrins, which polymerize to insoluble strands of meshwork. In combination with blood cells, the fibrin meshwork finally forms a more stable clot (thrombus) [21, 22], which provides secondary hemostasis.
Coagulation is regulated by different mechanisms to maintain homeostasis. While the process of fibrinolysis removes excessive clots, other regulatory mechanisms prevent coagulation in uninjured blood vessels, by producing prostacyclin (PGI2), nitric oxide (NO), thrombomodulin, protein C, tissue factor, antithrombin III, and heparin, among others [21, 22]. Vitamin K, on the other hand, counteracts the tendency for bleeding. Overall, coagulation, anticoagulation, and fibrinolysis together provide the means to maintain a delicate balance in the blood, and the regulation of this complex process indicates multiple potential molecular targets of [interference [21–23].
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