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EN
Haemostatic materials such as: gelatine sponges, oxygenated cellulose meshes, tissue sealants, collagen matrices with human thrombin and fibrinogen are gaining on popularity in gastrointestinal surgery, especially in colorectal surgery. We searched for available scientific publications in the Pubmed and Cochrane database on the use of individual hemostatic materials in the field of gastrointestinal surgery. The analysis focused on the assessment of the safety of the use of individual materials in terms of the rate of bleeding complications and the rate of anastomotic leakage cases. The use of haemostatic materials has for years been a recognized method of reducing the rate of intra- and postoperative complications, both in gastrointestinal surgery and in other surgical specialties. Based on the available studies, it can be concluded that the use of hemostatic materials such as matrices, sponges and adhesives in gastrointestinal surgery, even in patients at high risk of anastomotic leakage and bleeding complications, reduces the incidence of complications. The growing popularity of haemostatics and sealants in surgery means that they are currently used in a wide range of indications, and surgeons are more and more willing to use them even in case of standard surgical procedures, which is reflected in the available studies. Choosing a haemostat should be a conscious decision, taking into account the site and type of bleeding, mechanism of action, ease of use, efficacy, safety, and price, among others.
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Content available Wpływ hiperbarii na wybrane parametry hemostazy
75%
PL
Przeprowadzanie nurkowań i dekompresji według opracowanych tabel dekompresyjnych nawet skorygowanych dopplerowską oceną przebiegu desaturacji nie zabezpiecza w pełni nurków przed wystąpieniem objawów DCS czy jałowej martwicy kości. Nadal, zatem poszukiwane są bardziej czułe i specyficzne parametry do oceny bezpieczeństwa dekompresji. W badaniach przyżyciowych i autopsyjnych osób z wypadków nurkowych stwierdzano przypadki krwotoków, które nie powstały na skutek urazów czy też koincydencji innych jednostek chorobowych. Opisane przypadki nie zostały jednak wystarczająco wnikliwie zbadane pod kątem zaburzeń układu hemostazy. W artykule przedstawiono wyniki badań, których celem było określenie wpływu ekspozycji hiperbarycznych i dekompresji na wybrane parametry hemostazy. Badania zostały przeprowadzone u 39 zdrowych ochotników. 8 nurków poddano krótkotrwałej ekspozycji powietrznej odpowiadającej głębokości 30 m, 16 saturowanej ekspozycji powietrznej odpowiadającej głębokości 18 m oraz 15 saturowanej eksopzycji heliokosowej równej nurkowaniu na 30 m.
EN
Introduction: Diving and decompression performed strictly according to the decompression tables, corrected by the Doppler assessment of desaturation process do not fully assure divers from the development of DCS or bone necrosis. Thus more sensitive and specific safety parameters of decompression have been still seeking. Haemorrhages are implicated in the pathogenesis of some cases of DCS without coincidence with trauma or other pathology. Bleeding complications occurring after diving reported in some papers has not been sufficiently investigated and thus could not be directly correlated to the enhanced fibrinolysis. The aim of our study was to measure the effect of hyperbaric expositions and decompression on the markers of hemostasis. Material and methods: 36 healthy divers underwent hyperbaric exposures. Divers were subjected to short term exposures to the pressure of 400 kPa (corresponding water depth - 30 m) with 24 min plateau and continuous decompression with air as a breathing medium (8 divers) or saturated exposures to the pressure of 200 kPa(corresponding water depth - 18 m) with air as a breathing medium (16 divers) or saturated exposures to the pressure of 400 kPa with heliox as a breathing medium (15 divers). The divers were monitored for Doppler-detected venous gas bubbles as a risk factor for DCS. Blood samples were taken before exposure and after decompression.
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2005
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tom 52
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nr 2
EN
Platelets play a key role not only in physiological haemostasis, but also under pathological conditions such as thrombosis. Platelet activation may be initiated by a variety of agonists including thrombin, collagen, thromboxane or adenosine diphosphate (ADP). Although ADP is regarded as a weak agonist of blood platelets, it remains an important mediator of platelet activation evoked by other agonists, which induce massive ADP release from dense granules, where it occurs in molar concentrations. Thus, ADP action underlies a positive feedback that facilitates further platelet aggregation and leads to platelet plug formation. Additionally, ADP acts synergistically to other, even weak, agonists such as serotonin, adrenaline or chemokines. Blood platelets express two types of P2Y ADP receptors: P2Y1 and P2Y12. ADP-dependent platelet aggregation is initiated by the P2Y1 receptor, whereas P2Y12 receptor augments the activating signal and promotes platelet release reaction. Stimulation of P2Y12 is also essential for ADP-mediated complete activation of GPIIb-IIIa and GPIa-IIa, and further stabilization of platelet aggregates. The crucial role in blood platelet biology makes P2Y12 an ideal candidate for pharmacological approaches for anti-platelet therapy.
EN
Activated blood platelets shed microparticles with procoagulant activity that probably participate in normal hemostasis. We have isolated spontaneously formed microparticles from human blood and analysed them for ultrastructure, antigenic profile, and biochemical composition. In transmission electron microscopy microparticles appeared as regular vesicles with a mean diameter of 300 nm (50-600 nm). In flow cytometry almost all microparticles reacted with fluorescein isothiocyanate (FITC) labeled antibody to platelet glycoprotein complex IIb-IIIa (GpIIb-IIIa) and with FITC-annexin V but only 40-50% of microparticles reacted with FITC-antibody to platelet glycoprotein Ib (GpIb). The latter result was confirmed by double labeling of microparticles with FITC-antibody to GpIIb-IIIa and phycoerythrin (PE) labeled antibody to GpIb. Large microparticles reacted better with anti-GpIb than the small ones. A decreased level of GpIb was also demonstrated by SDS/polyacrylamide gel electrophoresis of microparticles. Compositional studies indicated, that in terms of cholesterol and protein contents, microparticles resembled platelets rather than platelet membranes as previously thought. They are, however, deficient in certain components. Thus, in comparison to platelets, microparticles had reduced contents of sialic acid (by 56.4%), galactosamine (by 48.2%), glucosamine (by 22.4%), galactose by (11.8%) and fucose (by 21.6%). Mannose content was increased by 11.8%. Total phospholipids in microplatelets were lower by 17.8%. Glycerophospholipids only were affected with phosphatidylserine being decreased as much as by 43.2%. Neutral glycosphingolipids, gangliosides and ceramides in microparticles were reduced by half. We conclude that the biochemical composition of microparticles probably reflects previous activation of progenitor platelets
EN
This study compared the antihrombotic effect of plasma angiotensin converting enzyme inhibitors (ACE-Is): captopril (CAP), enalapril (ENA) and Tissue ACE-Is: perindopril (PER), quinapril (QUIN) in experimental venous and arterial thrombosis. Normotensive Wistar rats were treated p.o. with CAP (75 mg/kg), ENA (20 mg/kg), PER (2 mg/kg) and QUIN (3 mg/kg) for 10 days. The influence of ACE-Is on coagulation and fibrinolytic systems as well as platelet function was evaluated. The hypotensive effect of ACE-Is was equal in all groups. QUIN mantained the final carotid blood flow at the highest value in comparison to PER and plasma ACE-Is. The arterial thrombus weight was reduced in PER and QUIN groups while venous thrombus weight was also reduced after CAP. Tissue andplasma ACE-Is caused the inhibition of platelet adhesion and aggregation. A reduction of fibrin generation, prolongation of prothrombin time (PT), activated partial thromboplastin time (APTT) and shortening of euglobulin clot lysis time (ECLT) were observed after PER and QUIN treatment. In conclusion, given in equipotent hypotensive doses, Tissue ACE-Is exerted more pronounced antithrombotic effect than plasma ACE-Is in experimental thrombosis. The differences between Tissue and plasma ACE-Is in terms of their more pronounced inhibition of experimental thrombosis may be related to the intensified activation of fibrinolysis and inhibition of coagulation.
PL
W 18 spośród 26 badanych napojów alkoholowych występują związki chemiczne hamujące agregację płytek i refrakcję skrzepu krwi oraz upośledzające lub zwiększające zużycie protrombiny.
EN
The influence of some strong drinks containing different amounts of ethanol (beer, vodka, brandy), or ethanol and acetaldehyde on collagen-, ADP-, and trombin-induced platelet aggregation, clot retraction, and prothrombin consumption was determined. Non-distilled drinks containing ethanol and the accompanying compounds, distillates of those drinks containing ethanol and accompanying volatile compounds, and the postdistillation residue with its accompanying compounds were analysed. Chemical compounds inhibiting platelet aggregation were found in 18 of the 26 examined strong drinks. They also inhibit clot retraction and reduce or increase prothrombin consumption. Ethanol and, even more evidently, acetaldehyde inhibit platelet aggregation. Both compounds inhibit also clot retraction. Ethanol decreases, and acetaldehyde increases prothrombin consumption.
PL
Określono wpływ 26 napojów alkoholowych, ich destylatów i pozostałości podestylacyjnych na aktywność fibrynolityczną i kazeinolityczną euglobulin osoczowych i plazminy.
EN
The effect of strong drinks containing different amounts of alcohol (beer, wine, vodka, brandy) on fibrinolytic and caseinolytic activity of euglobulins and plasmin was assessed. Non-distilled drinks containing ethanol and the accompanying compounds, distillates of those drinks containing ethanol and accompanying volatile compounds, and the post-distillation residue with its accompanying compounds were analysed. Chemical compounds inhibiting fibrinolytic activity of euglobulins were found only in 6, and those decreasing fibrinolytic activity of plasmin in 2 of the 27 examined strong drinks. These compounds did not decrease caseinolytic activity of euglobulins or plasmin. They are found in non-distilled drinks and post-distillation residue. Ethanol slightly inhibits fibrinolytic and caseinolytic activity of euglobulins and plasmin in very high concentrations, which are beyond the concentration range of usual strong drinks.
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