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J Thorac Cardiovasc Surg 2002;124:352-360
© 2002 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology (CSP)

Quinaprilat during cardioplegic arrest in the rabbit to prevent ischemia-reperfusion injury

From the Department of Cardiothoracic Surgery, AKH Wien, Vienna^a; the Ludwig Boltzmann Institute for Heart Research, Vienna^b; and the Department of Histology and Embryology II, University of Vienna, Austria.^c

Supported by funds from the Ludwig Boltzmann Institute for Heart Research and Hans und Blanca Moser Stiftung, both in Vienna, Austria. Quinaprilat was generously provided by Dr R. Bakovic-Alt, Gödecke AG, Freiburg, Germany. Statistical analysis was conducted in cooperation with Meinhard Ploner, PhD, Department of Cardiothoracic Surgery, AKH Wien, Vienna, Austria.

Received for publication Jan 26, 2000. Revisions requested Feb 23, 2000; revisions received Oct 19, 2001. Accepted for publication Oct 24, 2001. Address for reprints: Bruno K. Podesser, MD, Associate Professor of Cardiac Surgery, Ludwig Boltzmann Institute for Cardiosurgical Research, c/o Institute of Biomedical Research, Allgemeines Krankenhaus Wien, Waehringer Guertel 18-20, 1090 Vienna, Austria (E-mail: B.K.Podesser{at}cardiovascular-research.at).

Objectives: This study evaluated intracardiac angiotensin-converting enzyme inhibition as an adjuvant to cardioplegia and examined its effects on hemodynamic, metabolic, and ultrastructural postischemic outcomes.
Methods: The experiments were performed with an isolated, erythrocyte-perfused, rabbit working-heart model. The hearts excised from 29 adult New Zealand White rabbits (2950 ± 200 g) were randomly assigned to four groups. Two groups received quinaprilat (1 µg/mL), initiated either with cardioplegia (n = 7) or during reperfusion (n = 7). The third group received L-arginine (2 mmol/L) initiated with cardioplegia (n = 7). Eight hearts served as a control group. Forty minutes of preischemic perfusion were followed by 60 minutes of hypothermic arrest and 40 minutes of reperfusion.
Results: All treatments substantially improved postischemic recovery of external heart work (62% ± 6%, 69% ± 3%, and 64% ± 5% in quinaprilat during cardioplegia, quinaprilat during reperfusion, and L-arginine groups, respectively, vs 35% ± 5% in control group, P < .001) with similarly increased external stroke work and cardiac output. When administered during ischemia, quinaprilat significantly improved recovery of coronary flow (70% ± 8%, P = .028 vs quinaprilat during reperfusion [49% ± 5%] and P = .023 vs control [48% ± 6%]). L-Arginine (55% ± 7%) showed no significant effect. Postischemic myocardial oxygen consumption remained low in treatment groups (4.6 ± 1.2 mL · min^-1 · 100 g^-1, 6.0 ± 2.2 mL · min^-1 · 100 g^-1, and 4.7 ± 1.6 mL · min^-1 · 100 g^-1 in quinaprilat during cardioplegia, quinaprilat during reperfusion, and L-arginine groups, respectively, vs 4.2 ± 0.8 mL · min^-1 · 100 g^-1 in control group), even though cardiac work was markedly increased. High-energy phosphates, which were consistently elevated in all treatment groups, showed a significant increase in adenosine triphosphate with quinaprilat during ischemia (2.24 ± 0.14 µmol/g vs 1.81 ± 0.12 µmol/g in control group, P = .040). Ultrastructural grading of mitochondrial damage revealed best preservation with quinaprilat during ischemia (100% [no damage], P = .001 vs control).
Conclusion: These experimental findings have clinical relevance regarding prevention of postoperative myocardial stunning and low coronary reflow in patients undergoing heart surgery.

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