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    Adriamycin-induced Cardiomyopathy in the Dog:
    an Appropriate Model for Research on Partial Left Ventriculectomy? (2002)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Christiansen, Stefan
    Redmann, Klaus
    Scheld, Hans H
    Jahn, Uli R
    Stypmann, Jörg
    Fobker, Manfred
    Gruber, Achim D (WE 12)
    Hammel, Dieter
    Quelle
    The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation; 21(7) — S. 783–790
    ISSN: 1053-2498
    Sprache
    Englisch
    Verweise
    Pubmed: 12100904
    Kontakt
    Institut für Tierpathologie

    Robert-von-Ostertag-Str. 15
    Gebäude 12
    14163 Berlin
    +49 30 838 62450

    Abstract / Zusammenfassung

    To evaluate the adriamycin-induced cardiomyopathy in the dog for research on partial left ventriculectomy (PLV).

    An intracoronary catheter was introduced into the left main stem via the first diagonal branch in a retrograde fashion in 6 adult FBI (Foxhound Boehringer Ingelheim) dogs weighing 30 to 35 kg. The catheter was connected to a percutaneous access port that was used for weekly adriamycin administration (10 mg over a 1-hour period for 5 times). Follow-up examinations (transthoracic echocardiography, hemodynamic parameters, cardiopulmonary status, and neurohormones) were done before, 1 week after the last adriamycin administration, and 6 weeks later. After the last measurements, all dogs were euthanized with saturated potassium chloride under general anesthesia and the hearts were excised for histologic examinations. All data were calculated as mean values and standard error of the mean. Differences were calculated by the Wilcoxon signed rank test for paired and unpaired data. p values less than 0.05 were considered significant.

    Central venous pressure (2.2 +/- 0.8 vs 5.2 +/- 0.4 mm Hg, p = 0.03), mean pulmonary artery pressure (8.6 +/- 1.1 vs 12.4 +/- 0.5 mm Hg, p = 0.03), pulmonary wedge pressure (2.6 +/- 0.9 vs 7.0 +/- 0 mm Hg, p = 0.03), left ventricular endsystolic diameter (2.5 +/- 0.2 vs 3.1 +/- 0.4 cm, p = 0.03), and enddiastolic (4.5 +/- 0.2 vs 4.9 +/- 0.2 cm, p = 0.03) diameter increased significantly after adriamycin administration, whereas cardiac output (4.0 +/- 0.3 vs 3.3 +/- 0.1 liter/min, p = 0.03), stroke volume index (66.0 +/- 7.4 vs 54.0 +/- 3.9 ml/beat/m(2), p = 0.03), and ejection fraction (61.1 +/- 5.1 vs 37.7 +/- 5.7%, p = 0.03) decreased markedly. These changes were accompanied by a significant decline of oxygen delivery (1130 +/- 170 vs 790 +/- 65 ml/min, p = 0.03), which led to an enhanced oxygen extraction (0.12 +/- 0.01 vs 0.24 +/- 0.01, p = 0.03). Consequently, venous oxygen saturation (82.7 +/- 4.1 vs 71.3 +/- 2.5%, p = 0.03) decreased. Troponin I (0.02 +/- 0.025 vs 1.7 +/- 0.6 ng/ml, p = 0.03) and the anti-diuretic hormone (1.9 +/- 0.9 vs 20.0 +/- 1.9 pg/ml, p = 0.03) increased significantly after adriamycin administration. Deterioration of cardiac function continued after termination of adriamycin administration, albeit slower than during adriamycin administration. All hearts had severe histologic alterations, which were characteristic of adriamycin-induced toxicity: cytoplasmic vacuolation, myocyte degeneration, and increased fibrosis.

    The adriamycin-induced cardiomyopathy in the dog is similar to the dilated cardiomyopathy in humans and may be an appropriate model for PLV.