Effects of hyperthermal stress on the fibrinolytic system.

The effects of hyperthermal stress on the coagulation and fibrinolytic systems were examined in five healthy subjects who took a 3-min 47 degrees C hot-spring bath. After a 3-min 47 degrees C bath, the sublingual temperature was transiently increased about 1.8 degrees C, returning to the baseline level within 60 min. The plasma level of plasminogen activator inhibitor-1 antigen (PAI-1) was transiently increased 15 min after the start of bathing and returned to the pre-bathing level 360 min later. The plasma levels of tissue plasminogen activator antigen, alpha 2 plasmin inhibitor activity, plasmin-antiplasmin complex, thrombin-antithrombin III complex, and thrombomodulin antigen were not influenced by the bath. The in vivo result correlated well with the in vitro result that PAI-1 was released from cultured endothelial cells by heating. These findings suggest that the increase in plasma PAI-1 level may be due to the direct hyperthermal action of the very hot hot-spring bath on the endothelial cells and that acute hyperthermal stress may decrease the fibrinolytic capacity, leading to the occurrence of thrombotic events.

[1]  H. Kurabayashi,et al.  Dependence on very hot hot-spring bathing in a refractory case of atopic dermatitis. , 1994, Journal of medicine.

[2]  D. Collen,et al.  On the role of coagulation and fibrinolysis in atherosclerosis. , 1992, Annals of epidemiology.

[3]  H. Kurabayashi,et al.  A transient rise in plasma β-endorphin after a traditional 47°C hot-spring bath in Kusatsu-spa, Japan , 1992 .

[4]  P. Hufnagl,et al.  Hyperthermia stimulates plasminogen activator inhibitor type 1 expression in human umbilical vein endothelial cells in vitro. , 1991, The American journal of pathology.

[5]  G. Bergonzelli,et al.  Induction of plasminogen activator inhibitor 1 biosynthesis by hyperthermia , 1991, Journal of cellular physiology.

[6]  M. Nagao,et al.  A fibroblast-derived tumor cytotoxic factor/F-TCF (hepatocyte growth factor/HGF) has multiple functions in vitro. , 1991, Cell biology international reports.

[7]  T. Hayashi,et al.  One-step sandwich enzyme immunoassay for soluble human thrombomodulin using monoclonal antibodies. , 1990, Clinica chimica acta; international journal of clinical chemistry.

[8]  M. Rånby,et al.  Immunoreactivity of Tissue Plasminogen Activator and of Its Inhibitor Complexes , 1989, Thrombosis and Haemostasis.

[9]  H. Pelzer,et al.  Determination of Human Thrombin-Antithrombin III Complex in Plasma with an Enzyme-Linked Immunosorbent Assay , 1988, Thrombosis and Haemostasis.

[10]  M. Alessi,et al.  Measurement of plasminogen activator inhibitor 1 in biologic fluids with a murine monoclonal antibody-based enzyme-linked immunosorbent assay. , 1988, Blood.

[11]  M. Blombäck,et al.  PLASMINOGEN ACTIVATOR INHIBITOR IN PLASMA: RISK FACTOR FOR RECURRENT MYOCARDIAL INFARCTION , 1987, The Lancet.

[12]  青木延雄.  Evaluation of the assay for alpha 2PI and alpha 2PI-plasmin complex using the one-step sandwich method (EIA) , 1987 .

[13]  M. Blombäck,et al.  Increased plasma levels of a rapid inhibitor of tissue plasminogen activator in young survivors of myocardial infarction. , 1985, The New England journal of medicine.

[14]  J. Paramo,et al.  Generation in plasma of a fast-acting inhibitor of plasminogen activator in response to endotoxin stimulation. , 1985, The Journal of clinical investigation.

[15]  G. Claeson,et al.  Methods for the Determination of Plasmin, Antiplasmin and Plasminogen by Means of the Substrate S-2251 , 1977, Thrombosis and Haemostasis.