Thrombus, formation

Platelet aggregation increases like an avalanche because, once activated, platelets can activate other platelets. On the injured endothelial cell, a platelet thrombus is formed, which obstructs blood flow. Ultimately, the vascular lumen is occluded by the thrombus as the latter is solidified by a vasoconstriction produced by the release of serotonin and thromboxane A2 from the aggregated platelets. When these events occur in a larger coronary artery, the consequence is a myocardial infarction involvement of a cerebral artery leads to stroke. 

The von Willebrandt s factor plays a key role in thrombogenesis. Lack of this factor causes thrombasthenia, a pathologically decreased platelet aggregation. Relative deficiency of the von Wille-Liillmann, Color Atlas of Pharmacology 

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Oxagrelate (104) is of interest as a platelet antiaggretory agent and is thus of potential value in preventing thrombus formation in blood vessels. It may also be of potential value in preventing arteriosclerotic lesions in coronary arteries - a substantial cause of morbidity and mortality in... 

Due to the pivotal role of platelets in thrombus formation, especially in the arterial system, inhibition of platelet function has become a central pharmacological approach. Antiplatelet drugs are given in order to prevent and treat thromboembolic diseases such as coronary heart disease, peripheral and cerebrovascular disease. They have also revolutionized the procedures of invasive coronary interventions as they reduce the risk of restenosis and thrombosis. 

Prevention of thrombus formation after valve replacement... 

It is also important that the nurse monitor for any indication of hypersensitivity reaction. The nurse reports reactions, such as chills, fever, or hives, to die primary health care provider. When heparin is given to prevent the formation of a thrombus, the nurse observes the patient for signs of thrombus formation every 2 to 4 hours. Because the signs and symptoms of dirombus formation vary and depend on the area or organ involved, die nurse should evaluate and report any complaint die patient may have or any change in die patient s condition to die primary health care provider. 

Stock et al. used P4HB scaffolds and tissue engineered the patch with a porosity of 95% and pore sizes in the range of 180-240 p,m by salt-leaching and solvent evaporation. The sheep autologous cells (endothelial, smooth muscle, and fibroblast cells) were seeded on the scaffold before implantation. Results confirmed that the cell-seeded implants induced progressive tissue regeneration with no thrombus formation, stenosis, or dilatation. 

Dissection of the internal carotid and vertebral arteries is a common cause of stroke, particularly in young patients. Although many occur due to trauma, it is estimated that over half occur spontaneously. The mechanism of stroke following arterial dissection is either by artery-to-artery embolism, by thrombosis in situ, or by dissection-induced lumenal stenosis with secondary cerebral hypoperfusion and low-flow watershed infarction. Occasionally, dissection may lead to the formation of a pseudoaneurysm as a source of thrombus formation. Vertebrobasilar dissections that extend intracranially have a higher risk of rupture leading to subarachnoid hemorrhage (SAH). ° ... 

Venous thromboembolism (VTE) is one of the most common cardiovascular disorders in the United States. VTE is manifested as deep vein thrombosis (DVT) and pulmonary embolism (PE) resulting from thrombus formation in the venous circulation (Fig. 7-1).1 It is often provoked by prolonged immobility and vascular injury and is most frequently seen in patients who have been hospitalized for a serious medical illness, trauma, or major surgery. VTE can also occur with little or no provocation in patients who have an underlying hypercoagulable disorder. 

FIGURE 8-2. Platelet aggregation. This figure shows the process of platelet aggregation. Vessel injury occurs resulting in adhesion of the platelets to the vessel wall. This leads to continued adhesion and aggregation of platelets resulting in thrombus formation. 

Hypercoagulable state A disorder or state of excessive or frequent thrombus formation also known as thrombophilia. 

Pulmonary embolism A disorder of thrombus formation causing obstruction of a pulmonary artery or one of its branches may result in pulmonary infarction. 

Blood that has been stored for 60 min in the presence of heparinized PET films (Sample ho. 4), when put into another glass vessel was clotted within 5 min, which is the clotting time of blood not exposed to heparinized materials (4). Therefore, any reduction in thrombus formation on the heparinized film surface can only be attributed to the activity of bound heparin, i.e. the free heparin was not eluted into the blood. 

The first aspect of biocompatibility is a natural immune response. When a foreign object enters the blood stream, it can be attacked by the body s defense system. The first step is protein adsorption on an object surface. It is believed that the amount and type of protein adsorption is one of the most important steps determining whether the object is tolerated or rejected by the body. The next step is cell adhesion, which may cause aggregation and activation of platelets and triggering of the blood coagulation system with resulting thrombus formation. It may not only lead to sensor failure via surface blocking but directly threatens the patient s health. 

Another major challenge for implantable pH sensors is the biological response of living systems toward sensors when making contact with blood or tissue [134], The experiments often showed a progressive loss of function and lack of reliability of the implanted sensors. This lack of reliability and progressive loss of function, common to all implantable sensors, is believed to be caused by tissue or blood reactions such as inflammatory response, fibrosis, and loss of vasculature and thrombus formation [135, 136], The delivery of anti-inflammatory drugs to the sensor site can minimize tissue reactions and extend the lifetime of the device [50, 137],... 

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],... 

In practice, some anticoagulation agents such as heparin or antiplatelet agents, e.g. nitric oxide (NO) are delivered to sensor sites in order to reduce the risk of thrombus formation. Nitric oxide (NO), which is a potent inhibitor of platelet adhesion and activation as well as a promoter of wound healing in tissue, has been incorporated in various polymer metrics including PVC (poly(vinyl-chloride)), PDMS (poly-dimethyl-siloxane) and PU (poly-urethanes). Those NO release polymers have been tested in animals as outer protection coatings and have shown promising effects for the analytical response characteristics of the sensor devices [137],... 

Ischemic strokes account for 88% of all strokes and are due either to local thrombus formation or to emboli that occlude a cerebral artery. Cerebral atherosclerosis is a causative factor in most cases of ischemic stroke, although 30% are of unknown etiology. Emboli can arise either from intra- or extracranial arteries. Twenty percent of embolic strokes arise from the heart. 

In carotid atherosclerosis, plaques may rupture, resulting in collagen exposure, platelet aggregation, and thrombus formation. The clot may cause local occlusion or may dislodge and travel distally, eventually occluding a cerebral vessel. 

The final result of both thrombus formation and embolism is arterial occlusion, decreasing cerebral blood flow and causing ischemia and ultimately infarction distal to the occlusion. 

CVD is a generic denomination mainly integrated by coronary heart disease (CHD) and stroke. Although not considered as a form of CVD in some instances, venous thromboembolic disease (VTED) shares with the other forms of CVD the territorial assignment, the vascular tree, although clear differences exist in the main pathophysiological mechanisms. In most CVD forms, however, thrombus formation plays a crucial role. 

The vascular tree is divided into two main, well-demarcated areas composed of the arterial and the venous trees. They both define different microenvironments that create the conditions for the development of focal episodes determining the occurrence of obstructive phenomena that are at the base of CVD. Arterial episodes (CHD and stroke) occur at sites of inflamed arteries, while VTED or venous stroke episodes develop as a result of thrombus formation at discrete locations in the venous tree. 

A very innovative area of research has focused on the determinants of plaque stability. An important role seems to be played by enzymes involved in the degradation of the extracellular matrix. The rupture of unstable plaques induces platelet activation, too. Acute thrombus formation under these conditions seems fundamental to the onset of acute ischemic events. 

N-Nitrosamines have been shown to be inhibitors of cysteine-containing enzymes. For example, dephostatin and other N-methyl-N-nitrosoanilines (1) were found to be inhibitors of the protein tyrosin phosphatases, papain and caspase [90,91]. Inhibition results from the S-nitrosation of the critical cysteine residues in the active sites of the enzymes by the nitrosamines. Compounds 6 and 7 have been found to inhibit thrombus formation in arterioles and venules of rats [92], while N-nitrosamide 9 exhibited vasodilation and mutagenicity as a result of NO release [93]. 

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