Rheological study on coagulation of blood with special reference to the triggering mechanism of venous thrombus formation

Abstract

A markedly reduced blood flow, an elevation of hematocrit and an increased aggregability of erythrocytes [red blood cells (RBCs)] are risk factors for venous thrombus formation (intravascular blood coagulation). However, these risk factors alone seem to be insufficient to stimulate the coagulation cascade in the absence of a primary triggering mechanism. In this paper, our rheological and biochemical studies on blood coagulation, especially focusing on procoagulant activity of RBCs, are summarized. It is shown that the intrinsic coagulation pathway is triggered by the activation of factor IX (F-IX) by RBCs. The F-IX-activating enzyme in normal human erythrocyte (RBC) membranes was purified, identified and characterized. The activation of F-IX by RBCs was enhanced by a decrease in flow shear rate and an elevation in hematocrit. The procoagulant ability of RBCs and coagulation of blood obtained from individuals with a relatively high level of hypercoagulability were enhanced compared with those for normals. The studies demonstrated a new triggering mechanism for coagulation or thrombus formation that may occur under stagnant flow conditions.

Simultaneous measurement of blood coagulation and erythrocyte sedimentation by means of a rheological technique

“…In Table 1, the Ti values for aged donors were smaller than those for normal young adults aged 64 years or less (Ti 31.2 ± 5.5 min [13]). The Ti value for the type II group was somewhat smaller than that for the type I group.…”

Hydrodynamical evaluation of microporous covered stent for the treatment of intracranial aneurysms: Comparison of flow reduction property with flow diverter stent by using particle imaging velocimetry and in vitro flow simulator

“…In this scenario, a high-shielding stent is advantageous for IA embolization but is disadvantageous for side-branch vessel flow patency. The influence of blood flow shear rate on thrombosis promotion has been reported in previous papers [10,11]; therefore, we only studied the relationship between the pore design of the shielding stent and the shear rate of IA flow [17]. Both reliable IA embolization and patency of the perforating arteries were achieved by placing MCS (NCVC-CS1) in a previous study [9].…”

“…By shielding the IA neck using a stent, blood flow entering the IA from the parent vessel is significantly reduced. Various studies have demonstrated that thrombus formation is promoted by reducing hydrodynamic parameters, especially shear rate [10,11]. Stagnation of the blood flow in the IA causes thrombosis of the entire IA area, which enables IA treatment to be accomplished via endothelialization of the stent lumen.…”

Influence of age and hematocrit on the coagulation of blood

“…Our previous studies demonstrated that the activation of factor IX by RBCs and subsequent propagation reaction on RBC and platelet membranes are important for initiating and controlling blood coagulation reactions [20]. The ability of F-IX activated by F-IX-activating enzyme in RBC membranes to cause coagulation is low as compared with that activated by factor XI, and RBCs from different individuals differ in their capacity to activate F-IX and to promote the propagation reaction on RBC membranes [14,16,20]. In addition, it is reported that levels of fibrinogen, coagulation factors VII, VIII and IX, high molecular weight kininogen, prekallikrein and vWF are known to increase with age [21,22].…”

“…It was also shown that the F-IX activation by RBCs was enhanced by a decrease in the flow shear rate [15]. Therefore, we considered that this pathway suggests one route to coagulation or thrombus formation that occurs in stagnant flow regions (venous thrombus) [16].…”