Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Trescher, K; Dzilic, E; Kreibich, M; Gasser, H; Aumayr, K; Kerjaschki, D; Pelzmann, B; Hallström, S; Podesser, BK.
The nitric oxide donor, S-nitroso human serum albumin, as an adjunct to HTK-N cardioplegia improves protection during cardioplegic arrest after myocardial infarction in rats.
Interact Cardiovasc Thorac Surg. 2015; 20(3):387-394
Doi: 10.1093/icvts/ivu383
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- Führende Autor*innen der Med Uni Graz
- Hallström Seth
- Co-Autor*innen der Med Uni Graz
- Pelzmann Brigitte
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- Abstract:
- Currently available cardioplegic solutions provide excellent protection in patients with normal surgical risk; in high-risk patients, however, such as in emergency coronary artery bypass surgery, there is still room for improvement. As most of the cardioplegic solutions primarily protect myocytes, the addition of substances for protection of the endothelium might improve their protective potential. The nitric oxide donor, S-nitroso human serum albumin (S-NO-HSA), which has been shown to prevent endothelial nitric oxide synthase uncoupling, was added to the newly developed histidine-tryptophan-ketoglutarat (HTK-N) cardioplegia in an isolated heart perfusion system after subjecting rats to acute myocardial infarction (MI) and reperfusion. In male Sprague-Dawley rats, acute MI was induced by ligation for 1 h of the anterior descending coronary artery. After 2 h of in vivo reperfusion hearts were evaluated on an isolated erythrocyte-perfused working heart model. Cold ischaemia (4°C) for 60 min was followed by 45 min of reperfusion. Cardiac arrest was induced either with HTK (n = 10), HTK-N (n = 10) or HTK-N + S-NO-HSA (n = 10). In one group (HTK-N + S-NO-HSA plus in vivo S-NO-HSA; n = 9) an additional in vivo infusion of S-NO-HSA was performed. Post-ischaemic recovery of cardiac output (HTK: 77 ± 4%, HTK-N: 86 ± 7%, HTK-N + S-NO-HSA: 101 ± 5%, in vivo S-NO-HSA: 93 ± 8%), external heart work (HTK: 79 ± 5%, HTK-N: 83 ± 3%, HTK-N + S-NO-HSA: 101 ± 8%, in vivo S-NO-HSA: 109 ± 13%), coronary flow (HTK: 77 ± 4%, HTK-N: 94 ± 6%, HTK-N + S-NO-HSA: 118 ± 15%, in vivo S-NO-HSA: 113 ± 3.17%) [HTK-N + S-NO-HSA vs HTK P < 0.001; HTK-N + S-NO-HSA vs HTK-N P < 0.05] and left atrial diastolic pressure (HTK: 122 ± 31%, HTK-N: 159 ± 43%, HTK-N + S-NO-HSA: 88 ± 30, in vivo S-NO-HSA: 62 ± 10%) [HTK-N + S-NO-HSA vs HTK P < 0.05; in vivo S-NO-HSA vs HTK-N P < 0.05] were significantly improved in both S-NO-HSA-treated groups compared with HTK and HTK-N, respectively. This was accompanied by better preservation of high-energy phosphates (adenosine triphosphate; energy charge) and ultrastructural integrity on transmission electron microscopy. However, no additional benefit of in vivo S-NO-HSA infusion was observed. Addition of the NO donor, S-NO-HSA refines the concept of HTK-N cardioplegia in improving post-ischaemic myocardial perfusion. HTK-N with S-NO-HSA is a possible therapeutic option for patients who have to be operated on for acute MI. © The Author 2014. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.
- Find related publications in this database (using NLM MeSH Indexing)
- Animals -
- Cardiac Output - drug effects
- Cardiac Output - physiology
- Cardioplegic Solutions - pharmacology
- Disease Models, Animal -
- Glucose - pharmacology
- Heart Arrest - etiology
- Heart Arrest - prevention & control
- Heart Arrest, Induced - methods
- Male -
- Mannitol - pharmacology
- Myocardial Infarction - complications
- Myocardial Infarction - physiopathology
- Myocardial Infarction - therapy
- Nitric Oxide Donors - pharmacology
- Nitroso Compounds - pharmacology
- Potassium Chloride - pharmacology
- Procaine - pharmacology
- Rats -
- Rats, Sprague-Dawley -
- Serum Albumin - pharmacology
- Serum Albumin, Human -
- Treatment Outcome -
- Find related publications in this database (Keywords)
- Myocardial infarction
- Induced heart arrest
- Reperfusion injury