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  • 1
    Electronic Resource
    Electronic Resource
    REQUIREMENTS FOR THROMBORESISTANCE OF SURFACE-HEPARINIZED MATERIALS (1983)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 416 (1983), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1983.tb35210.x
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  • 2
    Electronic Resource
    Electronic Resource
    186. Hämodynamische und respiratorische Veränderungen bei reaktiven Thrombocytenausschwemmungen (1971)
    Springer
    Langenbeck's archives of surgery 329 (1971), S. 634-635 
    Details
    ISSN: 1435-2451
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Zufuhr von Thrombin in den rechten Vorhof von Hunden führte zu einer Erhöhung des Gefäßwiderstandes im kleinen Kreislauf and zu einer Erhöhung des Trachealdruckes. Gleichzeitig mit diesen Veranderungen sieht man eine Senkung der Trombocytenzahl. Die Hunde wurden such mit dem Schlangen giftpräparat Reptilas defibriniert. Die Reaktionen nach Zufuhr von Thrombin waren genau diesselben in diesen Hunden wie in normalen Hunden. Suspensionen von gereinigten Blutzellen wurden mit Thrombin inkubiert. Die Überstände, die man nach Zentrifugierung erhielt, verursachten eine Vasoconstriction in isolierten durchgeströmten Lungenlappen. Diese Vasoconstriction konnte mit dem. Serotoninantagonist Methysergid aufgehoben werden. Die Aktivität der Überstände war mit dem Gehalt von Trombocyten in den Suspensionen korreliert. In vivo wurde der resistenserhöhende Effekt von Thrombin im kleinen Kreislauf such mit Methysergid gehemmt. Dieser Serotoninantagonist hatte aber keinen Effekt auf die Senkung der Thrombocytenzahl. Zufuhr von Protamin führt such zu einer Senkung der Plättchenzahl and man sicht genau dieselben hämodynamischen and respiratorischen Veranderungen wie man nach Zufuhr von Thrombin sieht. Die hämodynamischen and vor allem die respiratorischen Veranderungen nach Thrombin and Protamin konnten mit Acetyl salicylsäure gehemmt werden. Acetylsalicylsäure hatte keinen Effekt auf die Sen kung der Thrombocytenzahl. Das Resultat dieser Versuche ist, daß Thrombin eine Vasoconstriction im kleinen Kreislauf and eine Bronchoconstriction auslöst. Diese Veranderungen sind zu einem großen Teil durch Serotonin verursacht, das aus Plättchen freigesetzt wird. Die mechanische Blockierung der Gefäße durch Fibrin oder Plättchenaggregate ist von geringerer Bedeutung. Protamin verursacht ähnliche hämodynamische and respiratorische Veranderungen wie Thrombin.
    Notes: Summary The introduction of thrombin into the right atrium of dogs led to an increase of vascular resistance in the pulmonary circulation and a rise of the tracheal pressure. At the same time there is a reduction in the number of thrombocytes. Dogs were also defibrinated with the snake venom preparation Reptilas. The reactions after the administration of thrombin were exactly the same in these dogs as in normal dogs. Suspensions of washed blood cells were incubated with thrombin. The supernatant fluid obtained after centrifuging caused vasoconstriction in isolated perfused lung lobes. This vasoconstriction could be neutralised by the serotonin antagonist, methysergid. The activity of the supernatant fluid correlated with the thrombocyte content of the suspension. In vivo the resistance-increasing effect of thrombin in the pulmonary circulation was also inhibited by methysergid. This serotonin antagonist however had no effect on the reduction of thrombocytes. The administration of protamine also leads to a fall in platelets and the same haemo dynamic and respiratory changes are seen as after thrombin administration. The haemodynamic and, above all, the respiratory changes after thrombin andprotamine could be inhibited by acetylsalicylic acid. Acetylsalicylic acid had no effect on the reduction of thrombocytes. These experiments show that thrombin causes vaso constriction in the pulmonary circulation and bronchoconstriction. These changes are largely caused by serotonin liberated from platelets. Mechanical blockage of vessels by fibrin or platelet aggregates is of little importance. Protamine causes haemodynamic and respiratory changes similar to those caused by thrombin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01770612
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  • 3
    Electronic Resource
    Electronic Resource
    An improved microsurgical course for a mixed group of surgeons (1981)
    Springer
    World journal of surgery 5 (1981), S. 285-292 
    Details
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé Tout bon chirurgien, s'il est décidé à apprendre la microchirurgie, peut en acquérir les principes, même si les cours organisés dans ce but reçoivent des participants de formation et d'expérience très variable et même si les ouvrages de référence sont peu nombreux. Pour la formation de base, il faut un texte valable, un programme d'application pratique de qualité et un instructeur entraîné. Les moyens audiovisuels sont fort utiles. Il est possible d'apprendre en quelques jours toutes les techniques, depuis la plus simple, l'anastomose vasculaire, jusqu'aux plus complexes, comme la transplantation d'organe chez les rongeurs. Les cours de 7 à 10 jours devraient être répétés chaque année pour permettre aux participants de perfectionner leur maîtrise technique. De plus, pendant ce cours annuel, une journée, ou une demi-journée, peut être consacrée à un programme scientifique de microchirurgie qui stimule les jeunes et permet les échanges d'information scientifique et clinique.
    Notes: Abstract Although the participants in the various microsurgical courses were of varied backgrounds and experience, and published materials that can serve as an adequate text are limited, the principles of microsurgery can be learned by skilled surgeons determined to become microsurgeons. Fundamental training depends upon the proper text and suitable models for practice under the guidance of a properly trained microsurgeon instructor. In particular, audiovisual aids are of substantial value. Techniques from the fundamental, simple vascular anastomosis to highly sophisticated organ transplantation in rodents may be mastered in a course of several days' duration. A 7- to 10-day course should be repeated annually to enable participants to polish their skills. Further, during an annual course, a half to whole day can be set aside for a microsurgical scientific program to allow exchange of scientific and clinical information, and to stimulate junior participants.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01658317
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  • 4
    Electronic Resource
    Electronic Resource
    Synthetic arterial grafts cause prolonged increase in the in vivo formation of thromboxane and prostacyclin in humans (1987)
    Springer
    Research in experimental medicine 187 (1987), S. 175-184 
    Details
    ISSN: 1433-8580
    Keywords: Thromboxane ; Prostacyclin ; Metabolites ; Synthetic arterial grafts ; Humans
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To evaluate the in vivo production of thromboxane A2 and prostacyclin their major urinary metabolites were measured in patients following graft replacement of the abdominal aorta. Specific methods based on gas chromatography-mass spectrometry were used to measure the urinary excretion of 2,3-dinor-TxB2 and 2,3-dinor-6-keto-PGF1α. The excretion of these metabolites increased tenfold and almost fortyfold during post-operative Day 1 and remained elevated 6–10 days p.o. In a group undergoing cholecystectomy smaller changes of shorter duration were seen. It is concluded from this study that synthetic grafts cause prolonged increase in the in vivo formation of thromboxane A2 and prostacyclin. The reason for the increased TxA2 formation is probably platelet interaction with the foreign surface, whereas the increase of PGI2 could be part of a vascular defense against induced thrombotic activity. Those increases may have pathophysiologic implications.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01852081
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  • 5
    Electronic Resource
    Electronic Resource
    Thrombin uptake and inhibition on endothelium and surfaces with a stable heparin coating: A comparative in vitro study (1986)
    Hoboken, NJ : Wiley-Blackwell
    Journal of Biomedical Materials Research 20 (1986), S. 235-246 
    Details
    ISSN: 0021-9304
    Keywords: Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine , Technology
    Notes: The endothelial lining and two differently heparin-coated surfaces were compared in vitro regarding thrombin uptake and inhibition. One heparin surface was based on stabilized ionic binding of heparin, the other on covalent binding of partially degraded heparin. Both heparin surfaces have previously been shown to have pronounced thromboresistant properties. The two heparinized polyethylene surfaces and the endothelial surface of segments of the porcine aorta were studied. After exposure to the surfaces, thrombin disappeared from the solution and appeared bound to the surfaces. The disappearance rate of thrombin from the solution was the same on exposure to the endothelium and the covalently bonded heparin surface, but less following exposure to the ionically bonded heparin surface. The thrombin activity appearing on the endothelium was lower than on the heparin surfaces, indicating that the endothelium exerted a slow thrombin inhibiting capacity. On exposure of the thrombin-loaded endothelium to plasma, thrombin was rapidly inhibited. Thrombin bound to the covalently bonded heparin surface was inhibited at a slower rate than on the ionically bonded surface, but still faster than the rate at which free thrombin was inhibited in nonheparinized plasma. It is concluded that the endothelium and stabilized heparin coatings bind thrombin and accelerate its inhibition by plasma.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jbm.820200212
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