Abstract
The factors related to the initiation of fibrinolysis, especially with regard to the tissue-type plasminogen activator (tPA) and the plasminogen activator inhibitor-1 (PAI-1), were investigated in 15 patients who underwent hepatic resection, and the findings were compared between those with normal livers and those with diseased livers. It was found that tPA increased before hepatic division, whereas PAI-1 increased after hepatic division and reached a peak immediately following the operation. Plasminogen decreased during hepatectomy, reaching its lowest point on postoperative day 1, and increasing later. Decreased levels of both plasminogen and the α2-plasmin inhibitor were considered to be partly due to plasmin formation in the blood. Patients with a diseased liver tended to have higher intraoperative values of euglobulin lysis activity and higher postoperative values of plasminogen activator, but significantly lower postoperative values of α2-plasmin inhibitor than those with a normal liver. The results of this study suggest that activation of the fibrinolytic system occurs both during hepatectomy and in the early postoperative period, and that patients with a diseased liver are prone to develop hyperfibrinolysis during hepatectomy. Moreover, the increased levels of both tPA and PAI-1 can serve as one of the most sensitive markers for the vital reaction against surgical stress.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
References
Kambayashi J, Sakon M, Yokota M, Shiba E, Kawasaki T, Mori T (1990) Activation of coagulation and fibrinolysis during surgery analyzed by molecular markers. Thromb Res 60:157–167
Porte RJ, Bontempo FA, Knot EAR, Knot ERA, Lewis JH, Kang YG, Starzl TE (1989) Systemic effects of tissue plasminogen activator associated fibrinolysis and its relation to thrombin generation in orthotopic liver transplantation. Transplantation 47:978–984
Dzik WH, Arkin CF, Jenkins RL, Stump DC (1988) Fibrinolysis during liver transplantation in humans: role of tissue-type plasminogen activator. Blood 71:1090–1095
Plareti, De Rosa V, Fortunato G, Grauso F, Legnani C, Maccaferri M, Poggi M, Bianchini B, Bellusci R, Franceschelli N, Coccheri S (1988) Control of hemostasis during orthotopic liver transplantation. Fibrinolysis 2[Suppl III]:61
Ny T, Elgh F, Lund B (1984) The structure of the human tissue-type plasminogen activator gene: correlation of intron and exon structures to functional and structural domain. Proc Natl Acad Sci USA 81:5355–5359
Brommer EJP, Derkx FHM, Schalenkamp MADH, Dooijewaard G, Klaauw MM (1988) Renal and hepatic handling of endogenous tissue-type plasminogen activator (tPA) and inhibitor in man. Thromb Haemost 59:404
Levin EG (1983) Latent tissue plasminogen activator produced by human endothelial cells in culture: Evidence for an enzyme inhibitor complex. Proc Natl Acad Sci USA 80:6804–6808
Tygot G, Collen D, De Vreker R, Verstraete M (1968) Investigation on the fibrinolytic system in liver cirrhosis. Acta Haematol 50:265
Das PC, Cash JD (1969) Fibrinolysis at rest and after exercise in hepatic cirrhosis. Br J Haematol 17:431
Collen D (1982) On the regulation and control of fibrinolysis. Thromb Haemost 43:77
Smith D, Gilbert M, Owen WG (1985) Tissue plasminogen activator release in vitro in response to vasoactive agents. Blood 66:835
Loskutoff DJ, Sawdey M, Mimuro J (1989) Type 1 plasminogen activator inhibitor. In: Coller BS (ed) Progress in hemostasis and thrombosis. Saunders, Philadelphia, pp 87–115
Sprengers ED, Verheijen JH, Van Hinsberg VWM, Emeis JJ (1984) Evidence for the presence of two different fibrinolytic inhibitors in human endothelial cell conditioned medium. Biochim Biophys Acta 801:163–171
Erickson LA, Ginsberg MH, Loskutoff DJ (1984) Detection and partial characterization of an inhibitor of plasminogen activator in human platelet. J Clin Invest 74:1465–1472
Grosse H, Lobbes W, Frambach M, von Broen O, Ringe B, Barthels M (1991) The use of high dose aprotinin in liver transplantation: the influence on fibrinolysis and blood loss. Thromb Res 63:287–297
Neuhaus P, Bechstein WO, Lefebre B, Blumhardt G, Slama K (1989) Effect of aprotinin on intraoperative bleeding and fibrinolysis in liver transplantation. Lancet ii:924–925
Hynt BJ, Cottam S, Segal H, Ginsberg R, Potter D (1990) Inhibition by aprotinin of tPA-mediated fibrinolysis during orthotopic liver transplantation. Lancet ii:381
Levein EG, Marzec U, Anderson J, Harker LA (1984) Thrombin stimulates tissue plasminogen activator release from cultured human endothelial cells. J Clin Invest 74:1988–1995
Gelehrter TD, Sznycer-Laszuk R (1986) Thrombin induction of plasminogen activator-inhibitor in cultured human endothelial cells. J Clin Invest 77:165–169
Booth NA, Anderson JA, Bennett B (1984) Plasminogen activators in alcoholic cirrhosis: demonstration of increased tissue type and urokinase type activator. J Clin Pathol 37:772–777
Hersch SL, Kunelis T, Francis RB Jr (1987) The pathogenesis of accelerated fibrinolysis in liver cirrhosis: a critical role for tissue type plasminogen activator inhibitor. Blood 69:1315–1319
Kluft C, Verneijen JH, Jie AFH, Rijiken DC, Preston FE, Sueling HM, Jespersen J, Aasen AO (1985) The postoperative fibrinolytic shutdown: a rapidly reverting acute phase pattern for the fast-acting inhibitor of tissue-type plasminogen activator after trauma. Scand J Clin Lab Invest 45:605–610
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Shimada, M., Matsumata, T., Yamamoto, K. et al. Initiation of a fibrinolytic system in hepatic resection: The roles of tissue-type plasminogen activator and plasminogen activator inhibitor-1. Surg Today 24, 780–784 (1994). https://doi.org/10.1007/BF01636306
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/BF01636306