Heparinization, systemic

Fig. 9 demonstrates the proportionality between the amount of immobilized trypsin and the lytic activity of the trypsin-containing material. The higher lytic efficiency of the binary trypsin-heparin systems seems unexpected (cf. curves 2 and 4, and 5 and 6 of Fig. 9), however. Thus, immobilized trypsin and heparin of the described polymeric materials mutually affected each other. This is manifested by the enhanced anticoagulant action of heparin promoted by trypsin and by greater lytic efficiency of trypsin provoked by heparin. 

Earlier data (3) obtained with tests in cones and chemical determination suggested that the anticoagulant effect of heparin introduced on the wall was greater than that to be expected if all the heparin were dissolved in the plasma. This conclusion requires checking with more uniform heparin layers and improved coagulation test techniques on flat surfaces. It is known that some heparin goes into solution in plasma from GBH or PVPyrH surfaces, as prepared by us, and it seems probable that this is generally true for any adsorbed heparin system in which the... 

The thermodynamic and co-operativity parameters of the Acridine Orange-heparin system have been reported. 

For KS, in common with many other carbohydrate polymers of the GAG family (e.g. the heparan sulphate/heparin systems) and elsewhere, the anticipated molecular structures are not unique. They are present as distributions, both in terms of molecular size and in the nature of substituents and their placements placements. Thus they differ greatly from the ordered world of peptides and proteins and are more akin to synthetic polymers in their nature, their chromatographic and spectroscopic behaviour and in the resultant analytical problems. It is apt to consider substituent placements along the repeat unit backbone as exhibiting microstructural patterns within diad, triad or larger groups of monomer units, for which statistical data can be elicited, e.g. in terms of sulfation and its distribution. The spectroscopic route to KS structure can also be similar to that used for synthetic macromolecules. 

In contrast to heparin, the coumarinic acid anticoagulants are inactive in vitw ]6k.e heparin they are active in vivo. The phenylindanedione-type compounds (7) (36) and warfarin (2) produce their in vivo inhibitory effect on the coagulation system by competitively antagonizing the normal activity of vitamin (8) (37—44). 

Heparin Sulfate Proteoglycans Hepatic Lipase Hepatitis Hepatitis C Heptahelical Domain Heptahelical Receptors HERG-channels Heterologous Desensitization Heterologous Expression System Heterotrimeric G-Proteins Hidden Markov Model High-density Lipoprotein (HDL)... 

The infusion system was similar to that described by Findley et al. (1972). The catheter was attached to a valve system that allowed slow continuous administration (55 to 60 mL in 24 hours) heparinized saline (5 units/mL) via a peristaltic pump to maintain catheter patency. Drug was injected into the valve system by means of a second pump and then flushed into the animal with 5 mL of saline from a third pump. This system necessitated a delay of approximately 20 seconds between the onset of drug delivery and actual injection into the vein. Drugs were delivered within a 2-minute period. 

Johnson Z, Kosco-Vilbois MH, Herren S, et al. Interference with heparin binding and oligomerization creates a novel anti-inflammatory strategy targeting the che-mokine system. J Immunol 2004 173 5776-85. 

Essentially as a result of its ability to bind to basic sites, heparin interacts with many proteins.398 Although most of these interactions (such as that with protamine, a basic protein frequently used to neutralize heparin399) are probably not of biological significance, binding to plasma proteins and to proteins exposed on the surface of endothelial cells has an important influence on the circulation system. 

There are various inhibitors within the coagulation system that counterregulate activation of the coagulation cascade. Among them, antithrombin III (AT-III) and protein C (PC) are the most important (SI). AT-III binds in the presence of heparin the activated factors F-IXa, F-Xa, and F-IIa (thrombin). PC is activated by a complex formed between thrombin and thrombomodulin, a surface protein of endothelial cells. Once activated, PC in the presence of protein S (PS) specifically degrades activated factors F-Va and F-VIIIa. PC decreases in the course of sepsis in relation to the severity of the condition (L15). Experimental studies have... 

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