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Wpływ nurkowania na PAI - 1 I ALFA2-antyplazminy oraz aktywność fibrynolityczna

Treść / Zawartość
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Warianty tytułu
EN
Decreased levels of PAI-1 and alpha2-antiplasmin contribute to enhanced fibrynolitic activity in divers
Języki publikacji
PL
Abstrakty
PL
Praca mówi o nie zbadanych dotychczas dokładnie powiązaniach choroby dekompresyjnej z zagadnieniami hemostazy a szczególnie fibrynolizy. Badany był wpływ ekspozycji hiperbarycznej na główne składniki systemu fibrynolizy. Dwie grupy młodych mężczyzn poddawane były ekspozycjom hierbarycznym do ciśnienia 400 kPa - grupa I - i 700 kPa - grupa II. Stosowano dekompresję powietrzna. Po ekspozycji badano nurków na obecność objawów choroby dekompresyjnej, a także poszukiwano pęcherzyków gazu w naczyniach żylnych metoda Dopplera. 15 minut po zakończeniu dekompresji pobierano krew do badań koagulologicznych. Badano stężenie i aktywność t-PA i PAI-1, stężenie PAP i alfa2-antyplazminy. W grupach badawczych nie stwierdzono wykładników choroby dekompresyjnej ani nadmiernej ilości pęcherzyków wewnątrznaczyniowych. Stwierdzono miedzy innymi spadek poziomu alfa2-antyplazminy, spadek stężenia i aktywności PAI-1. Nie zaobserwowano zmian w zakresie czynnika XII jak i t-PA. Ekspozycja hiperbaryczna i dekompresja indukuje fibrynolize, nawet bez obecności pęcherzyków gazowych.
EN
There are a number of reported cases of decompression sickness (DCS) with haemorrhages. These cases have not been sufficiently investigated and thus bleeding complications could not be directly correlated to the enhanced fibrinolysis. The effect of hyperbaric exposition and decompression on the main components of fibrynolitic system have been measured. Two groups of 25 male divers each, were subjected to hyperbaric exposures to the pressure of either 400 kPa - group I - or 700 kPa - group II followed by a staged decompression. The divers were monitored for clinical symptoms of DCS and checked for Doppler-detected venous gas bubbles. Venous blood was drawn from divers before exposition and 15 minutes after decompression. The concentrations and activities of t-PA and PAI-1 as well as concentrations of PAP and alpha2-antiplasmin and activity of factor XIIa were measured. In all groups of divers no cases of DCS as well as detectable gas bubbles were noted. We observed elevated concentration of PAP, decreased concentration of alpha2-AP, decreased PAI-1 concentration and activity. There were no significant changes in factor XIIa activity as well a of t- PA concentration and activity. Hyperbaric exposition and decompression induce activation of fibrynolisis, even in the absence of detectable gas bubbles. Fibrynolitic activity increases mainly due to decrease of PAI-1 concentration and activity. Further clinical trials are necessary for the estimation of the importance of activation of fibrynolisis with decreased level of PAI-1 and alpha2-AP as possible risk factor for bleeding in divers.
Rocznik
Tom
Strony
33--42
Opis fizyczny
Bibliogr. 35 poz., tab.1, wykr.4
Twórcy
autor
autor
  • Regional Centre for Transfusion Medicine, Skłodowskiej 23 PL - 15-950 Białystok, Poland, piotr.radziwon@wp.pl
Bibliografia
  • 1. Nishi RY. Doppler evaluation of decompression tables.str.297-316; In: Lin YC, Shida KK, eds. Man the sea. San Pedro, CA. Best Publishing Company 1990.
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  • 9. Boussuges A, Succo E, Bordet JC, Sainty JM. Activation of coagulation in decompression illness.; 69:129-132 ;Aviat Space Environ Med 1998.
  • 10. Olszanski R, Radziwon P, Baj Z, Kaczmarek P, Giedrojc J, Galar M, Kłoczko J. Changes i the extrinsic and intrinsic coagulation pathways in humans after decompression following saturation diving.;12:1-6; Blood Coagul Fibrinolysis 2001.
  • 11. Balk M, Goldman JM. Alveolar hemorrhage as a manifestation of pulmonary barotrauma after scuba diving;19:930-934; Ann Emerg Med 1990.
  • 12. Boussuges A, Pinet C, Thomas P, Bergmann E, Sainty JM, Vervloet D. Haemoptysis after breath-hold diving.;13:697-699; Eur Respir J 1999.
  • 13. Chen JC, Kucharczyk W. Nontraumatic orbital subperiosteal hematoma in scuba diver: CT and MR findings; 12:504-506; J Comput Assist Tomogr 1988.
  • 14. Green S.M, Rothrock SG, Green EA. Tympanometric evaluation of middle ear barotraumas during recreational scuba diving.;14:411-415. Int J Sports Med 1993.
  • 15. Josefsen R, Wester K. Cerebellar hemorrhage – a rare, but serious complication in decompression disease.;119:3901-3902; Tidsskr Nor Laegeforen 1999.
  • 16. Sheridan MF, Hetherington HH, Hull JJ. Inner ear barotrauma from scuba diving. 78:181,184,186-187; Ear Nose Throat J 1999.
  • 17. Hida K, Iwasaki Y, Akino M. Spontaneous spinal hemorrhage during scuba diving. Case illustration.;96(suppl. 3):351 ; J Neurosurg 2002.
  • 18. Nguyen MH, Ernsting KS, Proctor DD. Massive variceal bleeding caused by scuba diving.;95:3677-3678; AmJ Gastroenterol 2000.
  • 19. Townsley MI, Parker JC, Longenecker GL, Perry ML, Pitt RM, Taylor AE. Pulmonary embolism: analysis of endothelial pore sizes in canine lung.;255:H1075– H1083; Am J Physiol 1988.
  • 20. Moosavi H, Utell MJ, Hyde RW, Fahey PJ, Peterson BT, Donnelly J, Jensen KD. Lung ultrastructure in non-cardiogenic pulmonary edema induced by air embolism in dogs. 45:456–464; Lab Invest 1981.
  • 21. Erdmann AJ III, Vaughan TR Jr, Brigham KL, Woolverton WC, Staub NC. Effect of increased vascular pressure on lung fluid balance in unanesthetized sheep. 37:271–284; Circ Res 1975.
  • 22. Busch C, Lindquist O, Saldeen T. Respiratory insufficiency in the dog induced by pulmonary microembolism and the inhibition of fibrinolysis: effect of defibrinogenation, leucopenia and thrombocytopenia. 140:255–266; Acta Chir Scand 1974.
  • 23. Ohkuda K, Nakahara K, Binder A, Staub NC. Venous air emboli in sheep: reversible increasein lung microvascular permeability. 51:887–894; J Appl Physiol 1981.
  • 24. Lee WH, Hairston P. Structure effects on blood proteins at the gas-blood interface. 30:1615–1620; Fed Proc1971.
  • 25. Ward CA, Koheil A, McCullough D, Johnson WR, Fraser WD. Activation of complement at plasma-air or serum-air interface of rabbits. 60:1651–1658. J Appl Physiol 1986.
  • 26. Stevens DM, Gartner SL, Pearson RR, Flynn ET, Mink RB, Robinson DH, Dutka AJ. Complem ent activation during saturation diving. 20:279–288;Undersea Hyperb Med 1993.
  • 27. Thorsen T, Dalen H, Bjerkvig R, Holmsen H. Transmission and scanning electron microscopy of N2 microbubble-activated human platelets in vitro.14:45–58; Undersea Biomed Res 1987.
  • 28. Warren BA, Philp RB, Inwood MJ. The ultrastructural morphology of air embolism: platelet adhesion to the interface and endothelial damage. 54:163–172; Br J Exp Pathol 1973.
  • 29. Olszanski R, Radziwon P, Baj Z, Kaczmarek P, Giedrojc J, Galar M, Kloczko J. Changes in the extrinsic and intrinsic coagulation pathways in humans after decompression following saturation diving. 12:1-6; Blood Coagul Fibrin 2001.
  • 30. Slivka SR, Loskutoff DJ. Platelets stimulate endothelial cells to synthesize type 1 plasminogen activator inhibitor. Evaluation of the role of transforming growth factor beta. 77:1013- 1019; Blood 1991.
  • 31. Radziwon P, Olszanski R, Baj Z, Kloczko J, Klos R, Konarski M, Siermontowski P. The use of Heliox instead of air diminishes the effect of hyperbaric expositions and decompression on blood platelets but not on leukocytes. 14(suppl. I):95-98; Polish Journal of Environmental Studies 2005.
  • 32. Plow EF. The major fibrinolytic proteases of human leukocytes. 630:47-56; Biochim Biophys Acta 1980.
  • 33. Machovich R, Owen WG. An elastase-dependent pathway of plasminogen activation; 28:4517-4522;Biochemistry 1989.
  • 34. Machovich R, Himer A, Owen WG. Neutrophil proteases in plasminogen activation; 1:273-277; Blood Coagul Fibrinolysis 1990.
  • 35. Brower MS, Harpel PC. Proteolytic cleavage inhibitor and C1 inactivator by human 257:9849- 9854; J Biol Chem 1982.
Typ dokumentu
Bibliografia
Identyfikator YADDA
bwmeta1.element.baztech-article-BAT1-0027-0019
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