Adenosine triphosphate-dependent potassium channel modulation and cardioplegia-induced protection of human atrial muscle in an in vitro model of myocardial stunning
| Autor: | Benedetto Marino, Sandra Picard, Paolo Emilio Puddu, Ugo Papalia, Francesco Monti, Pietro Paolo Campa, Giovanni Ruvolo, Saverio La Francesca, Katsunori Iwashiro, Anna Criniti |
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| Rok vydání: | 2000 |
| Předmět: |
Pulmonary and Respiratory Medicine
Adult Male medicine.medical_specialty Dihydropyridines Cardiotonic Agents Potassium Channels Potassium chemistry.chemical_element Atrial Function Right In Vitro Techniques Sodium Chloride Potassium Chloride Contractility Glibenclamide Calcium Chloride Adenosine Triphosphate Internal medicine Dobutamine Glyburide medicine Potassium Channel Blockers Humans Benzopyrans Magnesium Cardioplegic Solutions Aged Myocardial Stunning Myocardial stunning business.industry Hypoxia (medical) Middle Aged medicine.disease Adenosine Myocardial Contraction Potassium channel Cell Hypoxia Bicarbonates chemistry Cardiology Heart Arrest Induced Surgery Female medicine.symptom Cardiology and Cardiovascular Medicine business medicine.drug |
| Zdroj: | Scopus-Elsevier |
| ISSN: | 0022-5223 |
| Popis: | Objectives: Although adenosine triphosphate–dependent potassium channel openers have been shown to enhance cardioplegic protection in animal myocardium, there is a lack of data on human cardiac tissues. We aimed at determining, on human atrial muscle, whether adenosine triphosphate– dependent potassium channels are involved in protection caused by high-potassium cardioplegia and whether adenosine triphosphate–dependent potassium channel activation might improve cardioplegic protection in an in vitro model of myocardial stunning. Methods: Human atrial trabeculae were obtained from adult patients undergoing cardiac operations. In an organ bath at 37°C, the preparations were subjected to 60 minutes of hypoxia at a high stimulation rate either in Tyrode solution (control, n = 17) or in St Thomas’ Hospital solution without additives (n = 6) or associated with 100 nmol/L bimakalim (n = 7) or 1 μmol/L glibenclamide (n = 7), followed by 60 minutes of reoxygenation and 15 minutes of positive inotropic stimulation with 1 μmol/L dobutamine. Results: Atrial developed tension was reduced by hypoxia to 27% ± 5% of baseline and incompletely recovered after reoxygenation to 38% ± 7%, whereas dobutamine restored contractility to 74% ± 7% of basal values. St Thomas’ Hospital solution with or without bimakalim improved developed tension after reoxygenation and dobutamine (P < .0001 vs control), whereas glibenclamide inhibited these protective effects of cardioplegic arrest (P = .001 vs St Thomas’ Hospital solution). After reoxygenation, the protective effect of bimakalim disappeared at a high pacing rate (400- and 300-ms cycle length) but recovered during dobutamine superfusion. Conclusions: Adenosine triphosphate–dependent potassium channels are likely involved in the cardioprotective effects of cardioplegia in human atrial trabeculae and adenosine triphosphate–dependent potassium channel activation with bimakalim used as an additive to cardioplegia enhanced protection. (J Thorac Cardiovasc Surg 2000;119:842-8) |
| Databáze: | OpenAIRE |
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