Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

The thrombolytic paradox.

H M Hoffmeister1, S Szabo, U Helber

  • 1Medizinische Klinik, Abteilung Innere Medizin III, Eberhard-Karls-Universität, Tübingen, Germany.

Thrombosis Research
|September 25, 2001
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Interdisciplinary consensus on indications for transfemoral transcatheter aortic valve implantation (TF-TAVI) : Joint Consensus Document of the Arbeitsgemeinschaft Leitende Kardiologische Krankenhausärzte e.V. (ALKK) and cooperating Cardiac Surgery Departments.

Clinical research in cardiology : official journal of the German Cardiac Society·2019
Same author

[Certification in cardiology : Contra: The concept should be improved].

Herz·2018
Same author

[Recommendations for extracorporeal cardiopulmonary resuscitation (eCPR) : Consensus statement of DGIIN, DGK, DGTHG, DGfK, DGNI, DGAI, DIVI and GRC].

Der Anaesthesist·2018
Same author

[Recommendations for extracorporeal cardiopulmonary resuscitation (eCPR) : Consensus statement of DGIIN, DGK, DGTHG, DGfK, DGNI, DGAI, DIVI and GRC].

Medizinische Klinik, Intensivmedizin und Notfallmedizin·2018
Same author

[Hemorrhage under direct oral anticoagulants : Occurrence and treatment in intensive care patients].

Medizinische Klinik, Intensivmedizin und Notfallmedizin·2018
Same author

[New oral anticoagulants : What you need to know-questions and answers].

Medizinische Klinik, Intensivmedizin und Notfallmedizin·2017
Same journal

Heatstroke-induced coagulopathy: A scoping review of therapeutic strategies and outcome reporting.

Thrombosis research·2026
Same journal

Mapping thrombus habitat: Non-contrast MRI radiomics and pixel-tile histomics approach to track venous thrombosis evolution in mice.

Thrombosis research·2026
Same journal

A study protocol for a randomised controlled trial evaluating the safety and efficiency of the YEARS algorithm versus computed tomography pulmonary angiography only for suspected acute pulmonary embolism in patients with cancer: the Hydra Study.

Thrombosis research·2026
Same journal

Associating the phenotypic expression of platelets with disease type through image-based single-cell profiling.

Thrombosis research·2026
Same journal

The mechanisms of contractile dysfunction following chronic limited platelet activation in (pro)thrombotic conditions.

Thrombosis research·2026
Same journal

Molecular basis of the E69Q and R383W heterozygous F2 variants identified in the proband associated with severe hemostatic defects.

Thrombosis research·2026
See all related articles

Thrombolytic drugs can paradoxically increase blood clotting by activating the coagulation system. This "thrombolytic paradox" is linked to non-fibrin-specific drugs and systemic plasmin activation, not fibrin-specific agents like tenecteplase.

Area of Science:

  • Biochemistry
  • Hematology
  • Pharmacology

Background:

  • Patients with acute myocardial infarction often have a hypercoagulative state.
  • Thrombolytic drugs aim to dissolve clots but can also activate coagulation pathways.

Purpose of the Study:

  • To investigate the mechanism behind paradoxical thrombin activation during thrombolytic therapy.
  • To test the hypothesis that plasmin-mediated activation of the contact phase causes this procoagulant effect.

Main Methods:

  • Evaluation of various thrombolytic regimens in vitro.
  • Assessment of thrombin activation and systemic plasmin activation.
  • Comparison of fibrin-specific (tenecteplase) and non-fibrin-specific (streptokinase) drugs.

Main Results:

Related Experiment Videos

  • Non-fibrin-specific thrombolytics, like streptokinase, caused significant thrombin activation and contact phase activation.
  • Fibrin-specific tenecteplase did not induce additional thrombin activation.
  • The "thrombolytic paradox" correlated with the degree of systemic plasmin activation.

Conclusions:

  • Plasmin-mediated activation of the factor XII/kallikrein system is the cause of the thrombolytic paradox.
  • Fibrin specificity is crucial in preventing paradoxical thrombin activation during thrombolysis.