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Factor XII – A Limitation for Divers?

100%
Radziwon P., Olszański R., Korsak J., Siermontowski P.
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2015
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vol. 52
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issue 3
7-12
EN
The lack of evidence for the tissue-factor dependent activation of the coagulation system and the release of thrombin on one hand, and a decreased concentration of factor XII after short term air, saturated air and heliox exposures, as well as an increased concentration of the plasmin-antiplasmin complex (PAP) after short dives indicate that diving and decompression possibly affect fibrinolysis. The aim of our research was to verify the assumption that diving and decompression activate the system of fibrinolysis and the clarification of the pathomechanism of this activation. The study involved 50 healthy volunteers who were subjected to short-term, air hyperbaric exposures at 400 kPa and 700 kPa, which correspond to 30m and 60m dives. Decompression was applied in accordance with Naval tables of decompression. Before hyperbaric exposition and after decompression the following factors were determined: activity of factor XII, concentration and activity of t-PA, concentration and activity of PAI-1, concentration of alpha2- antiplasmin, concentration of PAP, concentration of neutrophil elastase. The following observations have been made: a statistically significant increase in the factor XII activity, increase in the PAP complex concentration and a simultaneous significant decline in the α2-AP activity. No measurable t-PA activity or significant changes in t-PA concentration have been observed. In addition, a statistically significant decline in both the activity and concentration of PAI-1 has been observed, which was more pronounced after the expositions that corresponded to 60 m dives. The concentrations of granulocyte elastase did not differ significantly before and after decompression. Conclusions: People qualified for diving should have the following risk factors examined: risk factors of increased fibrynolytic activity - haemostasis abnormalities that increase the risk of haemorrhage, possibility of parietal blood clots/thrombi.
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The involvement of Na+/K+-ATPase in the development of platelet procoagulant response

88%
Tomasiak M., Stelmach H., Rusak T., Ciborowski M., Radziwon P.
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2007
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vol. 54
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issue 3
625-639
EN
In circulation, platelets may come into contact with both exogenous (cardiac glycoside treatment) and endogenously produced inhibitors of Na+/K+-ATPase. We examined whether blocking of platelet Na+/K+-ATPase by ouabain results in generation of procoagulant activity. It was shown that an in vitro treatment of platelets with ouabain (20-200 µM for 20 to 60 min) is associated with an intracellular accumulation of sodium ([Na+]i), generation of a weak calcium signal, and expression of procoagulant activity. The ouabain-induced procoagulant response was dose- and time-related, less pronounced than that evoked by collagen and similar to that produced by gramicidin, not affected by EDTA or aspirin, and strongly reduced in the absence of extracellular Na+ or by hyperosmolality. Flow cytometry studies revealed that ouabain treatment results in a unimodal left shift in the forward and side scatter of the entire platelet population indicating morphological changes of the plasma membrane. The shift was dose related, weaker than that evoked by collagen and similar to that produced by gramicidin. Ouabain-treated platelets express phosphatidylserine (PS). The ouabain-evoked PS expression was dose- and time-dependent, weaker than that produced by collagen and similar to that evoked by gramicidin. Electronic cell sizing measurements showed a dose-dependent increase in mean platelet volume upon treatment with ouabain. Hypoosmotically-evoked platelet swelling resulted in the appearance of procoagulant activity. Thromboelastography measurements indicate that, in whole blood, nanomolar (50-1000 nM, 15 min) concentrations of ouabain significantly accelerate the rate of clot formation initiated by contact and high extracellular concentration of calcium. We conclude that inefficiently operating platelet Na+/K+-ATPase results in a rise in [Na+]i. An increase in [Na+]i and the swelling associated with it may produce PS exposure and a rise in membrane curvature leading to the generation of a procoagulant activity.
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