IKs protects from ventricular arrhythmia during cardiac ischemia and reperfusion in rabbits by preserving the repolarization reserve
| Autor: | Shenming Wang, Yesong Wang, Long-Yun Peng, Xiuren Gao, Xiao-gang Guo, Yingying Zhu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2012 |
| Předmět: |
Male
Potassium Channels Time Factors Myocardial Ischemia Infarction Action Potentials lcsh:Medicine Stimulation Cardiovascular Biochemistry Acetamides Pericardium lcsh:Science Benzodiazepinones Multidisciplinary Potassium channel medicine.anatomical_structure Epinephrine Anesthesia Reperfusion Injury KCNQ1 Potassium Channel Cardiology cardiovascular system Medicine Female Rabbits medicine.drug Research Article medicine.medical_specialty Drugs and Devices Heart Ventricles Ischemia Down-Regulation Model Organisms Internal medicine Receptors Adrenergic beta medicine Animals cardiovascular diseases Biology business.industry lcsh:R Proteins Arrhythmias Cardiac medicine.disease Blockade Gene Expression Regulation lcsh:Q business Reperfusion injury Delayed Rectifier Potassium Channels |
| Zdroj: | PLoS ONE, Vol 7, Iss 2, p e31545 (2012) PLoS ONE |
| ISSN: | 1932-6203 |
| Popis: | INTRODUCTION: The function of the repolarization reserve in the prevention of ventricular arrhythmias during cardiac ischemia/reperfusion and the impact of ischemia on slowly activated delayed rectifier potassium current (I(Ks)) channel subunit expression are not well understood. METHODS AND RESULTS: The responses of monophasic action potential duration (MAPD) prolongation and triangulation were investigated following an L-768,673-induced blockade of I(Ks) with or without ischemia/reperfusion in a rabbit model of left circumflex coronary artery occlusion/reperfusion. Ischemia/reperfusion and I(Ks) blockade were found to significantly induce MAPD90 prolongation and increase triangulation at the epicardial zone at 45 min, 60 min, and 75 min after reperfusion, accompanied with an increase in premature ventricular beats (PVBs) during the same period. Additionally, I(Ks) channel subunit expression was examined following transient ischemia or permanent infarction and changes in monophasic action potential (MAP) waveforms challenged by β-adrenergic stimulation were evaluated using a rabbit model of transient or chronic cardiac ischemia. The epicardial MAP in the peri-infarct zone of hearts subjected to infarction for 2 days exhibited increased triangulation under adrenergic stimulation. KCNQ1 protein, the α subunit of the I(Ks) channel, was downregulated in the same group. Both findings were consistent with an increased incidence of PVBs. CONCLUSION: Blockade of I(Ks) caused MAP triangulation, which precipitated ventricular arrhythmias. Chronic ischemia increased the incidence of ventricular arrhythmias under adrenergic stimulation and was associated with increased MAP triangulation of the peri-infarct zone. Downregulation of KCNQ1 protein may be the underlying cause of these changes. |
| Databáze: | OpenAIRE |
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