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Gewählte Publikation:

Korn, P; Kröner, A; Schirnhofer, J; Hallström, S; Bernecker, O; Mallinger, R; Franz, M; Gasser, H; Wolner, E; Podesser, BK.
Quinaprilat during cardioplegic arrest in the rabbit to prevent ischemia-reperfusion injury.
J THORAC CARDIOVASC SURG 2002 124: 352-360. Doi: 10.1067/mtc.2002.121676 [OPEN ACCESS]
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Co-Autor*innen der Med Uni Graz
Hallström Seth
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Abstract:
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 microg/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 micromol/g vs 1.81 +/- 0.12 micromol/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.
Find related publications in this database (using NLM MeSH Indexing)
Analysis of Variance -
Angiotensin-Converting Enzyme Inhibitors - pharmacology
Animals - pharmacology
Blood Gas Analysis - pharmacology
Cardioplegic Solutions - pharmacology
Heart Arrest, Induced - methods
Hemodynamic Processes - methods
Isoquinolines - pharmacology
Mitochondria, Heart - ultrastructure
Myocardial Reperfusion Injury - prevention and control
Rabbits - prevention and control
Research Support, Non-U.S. Gov't - prevention and control
Tetrahydroisoquinolines - prevention and control

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