التفاصيل البيبلوغرافية
| العنوان: |
Argon preconditioning enhances postischaemic cardiac functional recovery following cardioplegic arrest and global cold ischaemia. |
| المؤلفون: |
Kiss, Attila, Shu, Huaqing, Hamza, Ouafa, Santer, David, Tretter, Eva Verena, Yao, Shanglong, Markstaller, Klaus, Hallström, Seth, Podesser, Bruno K, Klein, Klaus Ulrich |
| المصدر: |
European Journal of Cardio-Thoracic Surgery; Sep2018, Vol. 54 Issue 3, p539-546, 8p |
| مصطلحات موضوعية: |
ARGON, ISCHEMIA, CARDIOPLEGIC solutions, APOPTOSIS inhibition, CARDIAC surgery |
| مستخلص: |
OBJECTIVES Previous studies demonstrated that preconditioning with argon gas provided a marked reduction in inflammation and apoptosis and increased myocardial contractility in the setting of acute myocardial ischaemia–reperfusion (IR). There is substantial evidence that myocardial IR injury following cardioplegic arrest is associated with the enhancement of apoptosis and inflammation, which is considered to play a role in cardiac functional impairment. Therefore, the present study was designed to clarify whether preconditioning with argon gas enhances recovery of cardiac function following cardioplegic arrest. METHODS Sprague-Dawley rats were anaesthetized and ventilated and allocated to (i) the control group (control IR, n = 10) and (ii) the in vivo group (argon IR), which received 3 cycles of argon (50% argon, 21% oxygen and 29% nitrogen, n = 10) administered for 5 min interspersed with 5 min of a gas mixture (79% nitrogen and 21% oxygen). The hearts were excised and then evaluated in an erythrocyte-perfused isolated working heart system. Cold ischaemia (4°C) for 60 min was induced by histidine–tryptophan–ketoglutarate cardioplegia, followed by 40 min of reperfusion. Cardiac functional parameters were assessed. In left ventricular tissue samples, the expressions of extracellular-regulated kinase (ERK1/2), AKT serine/threonine kinase (Akt), jun N-terminal kinase (JNK), endothelial nitric oxide synthase (eNOS) and HMGB1: high-mobility group box 1 (HMGB1) protein were assessed by western blot, and high-energy phosphates were evaluated by high-performance liquid chromatography. RESULTS At the end of reperfusion, the rats preconditioned with argon showed significantly enhanced recovery of cardiac output (101 ± 6% vs 87 ± 11%; P < 0.01), stroke volume (94 ± 4% vs 80 ± 11%; P = 0.001), external heart work (100 ± 6% vs 81 ± 13%; P < 0.001) and coronary flow (90 ± 13% vs 125 ± 21%; P < 0.01) compared with the control IR group. These results were accompanied by a significant increase in the levels of myocardial phosphocreatine (23.71 ± 2.07 µmol/g protein vs the control IR group, 13.50 ± 4.75; P = 0.001) and maintained adenosine triphosphate levels (13.62 ±1.89 µmol/g protein vs control IR group adenosine triphosphate: 10.08 ± 1.94 µmol/g; P = 0.017). Additionally, preconditioning with argon markedly reduced the activation of JNK (0.11 ± 0.01 vs 0.25 ± 0.03; P = 0.005) and the expression of HMGB1 protein (0.52 ± 0.04 vs 1.5 ± 0.10; P < 0.001) following reperfusion. CONCLUSIONS Preconditioning with argon enhanced cardiac functional recovery in rat hearts arrested with histidine–tryptophan–ketoglutarate cardioplegia, thereby representing a potential novel cardioprotective approach in cardiac surgery. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
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