Blood interaction with vessel wall

For pH sensors used in in-vivo applications, especially those in continuous pH monitor or implantable applications, hemocompatibility is a key area of importance [150], The interaction of plasma proteins with sensor surface will affect sensor functions. Thrombus formation on the device surface due to accelerated coagulation, promoted by protein adsorption, provided platelet adhesion and activation. In addition, variation in the blood flow rate due to vasoconstriction (constriction of a blood vessel) and sensor attachment to vessel walls, known as wall effect , can cause significant errors during blood pH monitoring [50, 126],... 

Blood-vessel wall relationships (interactions of flowing blood with the... 

BLOOD-VESSEL WALL RELATIONSHIPS (INTERACTIONS OF FLOWING BLOOD WITH THE VESSEL/VASCULAR PROSTHESIS WALL)... 

Interactions of blood, or more precisely of plasma macromolecules and blood cells with the vessel wall, should the latter be natural or artificial, depend upon several parameters the mechanical properties of the vascular conduit, on the one hand, the morphology and the physical and chemical characteristics of the blood-contacting surface on the other. 

Sakariassen, K. S., Aarts, P. A. M. M., de Groot, P. G., Houdijk, W. P. M. and Sixma, J. J. (1983). A perfusion chamber developed to investigate platelet interaction in flowing blood with human vessel wall cells, their ECM, and purified components. J. Lab. Clin. Med. 102, 522-535. 

The nitrates act by releasing nitric oxide, which relaxes vascular smooth muscle. The discovery that endothelium-derived relaxing factor (EDRF) is nitric oxide (1) stimulated new interest in these drugs, as nitric oxide not only controls local vessel wall tension in response to shear stress, but also plays a role in regulating the interaction of platelets with blood vessel walls. The release of nitric oxide from the walls of atheromatous arteries is reduced, because of malfunctioning or absent endothelium. Atheromatous arteries behave differently from healthy arteries, in that these vessels vasoconstrict rather than vasodilate when stimulated by acetylcholine. This impairment of the acetylcholine vasomotor response appears to be related to serum cholesterol concentration (2). 

Relaxation of blood vessels appears to be at least partially under the control of endothelial cells and their secreted products, especially endothelium-derived relaxation factor (EDRF). Oxidized LDL directly inhibits the endothelial cell-associated vessel relaxation. The generation of increased reactive oxygen species in association with elevated levels of blood cholesterol has also been reported. One of these reactive oxygen species, superoxide (O2), may interact with vasoactive EDRF (nitric oxide) locally in the artery wall, preventing endothelial cell-dependent vasodilation. In addition, a product of the reaction of nitric oxide and superoxide, the reactive peroxynitrite, may act to stimulate lipoprotein oxidation, which, as noted above, is regarded as an early step in atherosclerotic plaque generation. 

In order to prevent the acute events in vascular disease death, maintaining a physiologic balance between blood components, blood vessel wall, and circulatory function is important. Many approaches that may help control vascular disease are available. However, the interaction of the blood components with the diseased blood vessel wall, and the interaction of the blood components with each other must be considered as an important area to attack in the treatment of these diseases. In the search for weapons to help regulate the physiologic balance, antithrombotic agents should play an important role. Therefore development of new and potent antithrombotic agents would be an important contribution to the control of vascular disease. 

In conclusion, this section has highlighted the potential pathogenic contribution of blood neutrophils to the CNS injury that accompanies the ischaemia-reperfusion injury of stroke. From experimental models of this disorder, it appears that the second wave of tissue damage is induced either by neutrophil-mediated vasoocclusion or by the infiltration of neutrophils into the ischaemic tissue with concomitant release of lytic factors. Antagonising both neutrophil attachment to endothelium and the transendothelial migration of these cells at the level of the blood-brain barrier is likely to be of clinical benefit to cerebral ischaemia-reperfusion injury. Consequently, it is anticipated that a further unravelling of the mechanisms that promote neutrophil interaction with cerebral vessel walls will lead to the introduction of a more specific therapeutic intervention for the treatment of stroke. 

Problems of leukocyte distribution in the microcirculation and their interaction with the microvascular endothelium have attracted considerable attention in recent years [17]. Leukocyte rolling along the walls of venules, but not arterioles, has been demonstrated. This effect results from differences in the microvascular endothelium, mainly attributed to the differential expression of adhesion molecules on the endothelial surface [24]. Platelet distribution in the lumen is important because of platelets role in blood coagulation. Detailed studies of platelet distribution in arterioles and venules show that the cross-sectional distribution of these disk-shaped blood elements is dependent on the blood flow rate and vessel hematocrit [25] molecular details of platelet-endothelium interactions are available [26]. Considerable progress has been made in computational modeling of leukocytes in microvessels and their interaction with red blood cells [27-29]. 

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