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Status: Bibliographieeintrag

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Verfasst von:Gries, André [VerfasserIn]   i
 Böttiger, Bernd W. [VerfasserIn]   i
 Dörsam, Joachim [VerfasserIn]   i
 Bauer, Harald [VerfasserIn]   i
 Weimann, Jörg [VerfasserIn]   i
 Bode, Christoph [VerfasserIn]   i
 Martin, Eike [VerfasserIn]   i
 Motsch, Johann [VerfasserIn]   i
Titel:Inhaled nitric oxide inhibits platelet aggregation after pulmonary embolism in pigs
Verf.angabe:André Gries, M.D., Bernd W. Böttiger, M.D., Joachim Dörsam, M.D., Harry Bauer, M.D., Jörg Weimann, M.D., Christoph Bode, M.D., Eike Martin, M.D., Johann Motsch, M.D.
E-Jahr:1997
Jahr:February 1997
Umfang:7 S.
Fussnoten:Presented in part at the Third Congress of the European Society of Anaesthesiology, Paris, France, May 1-3, 1995 ; Gesehen am 01.12.2017
Titel Quelle:Enthalten in: Anesthesiology
Ort Quelle:Hagerstown, Md. : Lippincott Williams & Wilkins, 1940
Jahr Quelle:1997
Band/Heft Quelle:86(1997), 2, Seite 387-393
ISSN Quelle:1528-1175
Abstract:BACKGROUND: Inhaled nitric oxide (NO) is reported to prolong bleeding time in animals and humans and to inhibit platelet aggregation in persons with acute respiratory distress syndrome. In pulmonary embolism (PE), inhibition of platelet aggregation appears useful because further thrombus formation may lead to right ventricular dysfunction that results in circulatory failure. In the present study, the effect of inhaled NO on platelet aggregation after acute massive PE was investigated. METHODS: After acute massive PE was induced in 25 anesthetized pigs by injecting microspheres, 5, 20, 40, and 80 parts per million inhaled NO were administered stepwise for 10 min each in 11 animals (NO group). In the control group (n = 14). NO was not administered. Adenosine diphosphate-induced initial and maximal platelet aggregation were measured before PE (10), immediately after induction of PE (PE), at the end of each 10-min NO inhalation interval (t10-t40), and 15 min after cessation of NO inhalation (t55) in the NO group, and at corresponding times in the control group, respectively. RESULTS: Two animals in the control group and one in the NO group died within 10 min after PE induction and were excluded from analysis. Peaking at t40 and t55, respectively, initial (-13 +/- 6%; P < 0.05) and maximal (+44 +/- 17%; P < 0.05) platelet aggregation increased significantly after PE in the control group. In contrast, NO administration after PE led to a significant decrease in initial (maximum decrease, -9 +/- 3% at t40; P < 0.05) and maximal (maximum decrease, -15 +/- 7% at t30; P < 0.05) platelet aggregation. In the NO group, platelet aggregation had returned to baseline levels again at t55. In addition, NO administration significantly decreased mean pulmonary artery pressure and significantly increased end-tidal carbon dioxide concentration and mean systemic blood pressure. CONCLUSIONS: Inhaled NO has a systemic and rapidly reversible inhibitory effect on platelet aggregation after acute massive PE in pigs. This may be beneficial in treating acute massive PE.
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Volltext: http://anesthesiology.pubs.asahq.org/article.aspx?articleid=2027407
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Animals
 Nitric Oxide
 Administration, Inhalation
 Blood Pressure
 Platelet Aggregation
 Platelet Aggregation Inhibitors
 Pulmonary Embolism
 Swine
K10plus-PPN:1565952073
Verknüpfungen:→ Zeitschrift

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