Noradrenaline reduces ischemia-induced arrhythmia in anesthetized rats: involvement of alpha1-adrenoceptors and mitochondrial K ATP channels.
INTRODUCTION: We have evaluated the part played by the mitochondrial ATP-sensitive potassium (mK(ATP)) channels on effect of alpha(1)-adrenoceptor activation by noradrenaline in ischemia-induced ventricular arrhythmia. METHODS AND RESULTS: Anesthetized rats were subjected to 25 minutes of regional i...
| Publicado en: | Journal of Cardiovascular Electrophysiology Vol. 19; no. 3; pp. 309 - 316 |
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| Autores principales: | , , , , |
| Formato: | Journal Article |
| Publicado: |
Wiley-Blackwell
Mar2008
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| Acceso en línea: | Ver este registro en EBSCOhost |
| fields | @attributes: recordID: 1 pdfLink: plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=105790696&site=ehost-live header: @attributes: shortDbName: ccm uiTerm: 105790696 longDbName: CINAHL Complete uiTag: AN controlInfo: bkinfo: dissinfo: jinfo: jid: 10453873 GSB jtl: Journal of Cardiovascular Electrophysiology issn: 10453873 maglogo: Y pubinfo: dt: Mar2008 vid: 19 iid: 3 pid: 480 pub: Wiley-Blackwell place: Malden, Massachusetts artinfo: ui: 105790696 2009988450 NLM18070031 105790696 ppf: 309 ppct: 7 formats: fmt: @attributes: type: P tig: atl: Noradrenaline reduces ischemia-induced arrhythmia in anesthetized rats: involvement of alpha1-adrenoceptors and mitochondrial K ATP channels. aug: au: Imani A Faghihi M Sadr SS Keshavarz M Niaraki SS affil: Department of Physiology, School of Medicine, Medical Sciences/University of Tehran, Tehran, IR Iran. sug: subj: Myocardial Ischemia Metabolism Norepinephrine Administration and Dosage Potassium Metabolism Receptors, Cell Surface Metabolism Receptors, Cell Surface Tachycardia, Ventricular Metabolism Adrenergic alpha-Agonists Administration and Dosage Animals Male Myocardial Ischemia Complications Myocardial Ischemia Drug Therapy Rats Tachycardia, Ventricular Drug Therapy Tachycardia, Ventricular Etiology Treatment Outcomes Male ab: INTRODUCTION: We have evaluated the part played by the mitochondrial ATP-sensitive potassium (mK(ATP)) channels on effect of alpha(1)-adrenoceptor activation by noradrenaline in ischemia-induced ventricular arrhythmia. METHODS AND RESULTS: Anesthetized rats were subjected to 25 minutes of regional ischemia, and infarct size (IS) and ischemia-induced ventricular arrhythmia were measured. Group I served as saline control with ischemia (n = 9). In group II (n = 9), the ischemic period was preceded by three short episodes of ischemia, followed by reperfusion. In group III, noradrenaline (2 microg/kg, IV, n = 9) was injected prior to ischemia. In group IV, an alpha(1)-adrenoceptor blocker (prazosin, 0.5 mg/kg, IV, n = 6) was administrated prior to noradrenaline injection. In Groups V and VI, rats received a specific mitochondrial K(ATP) channel inhibitor [5-hydroxydecanoic acid (5-HD), 10 mg/kg, IV, n = 6] prior to or after noradrenaline injection. Ischemic preconditioning (IPC) and noradrenaline markedly reduced incidences of ventricular fibrillation (VF) (0%, 0% vs. 55.5% in control, P < 0.05) and ventricular tachycardia (VT) (11%, 44.5% vs. 100% in control, P < 0.001 and P < 0.05), duration of VF + VT (3 +/- 1 seconds, 4.7 +/- 2.1 seconds vs. 52.9 +/- 6 seconds in control, P < 0.001), number of VF + VT episodes (1.7 +/- 1.7, 5.75 +/- 2.4 vs. 60.5 +/- 8 in control, P < 0.001), severity of arrhythmias (0.3 +/- 0.3, 1.7 +/- 0.5 vs. 3.9 +/- 0.3 in control rats, P < 0.001 and P < 0.01), and IS (13.6 +/- 1.8%, 18.2 +/- 1.5% vs. 49.6 +/- 2.4% in control, P < 0.001). Administration of prazosin or 5-HD prior to or after noradrenaline injection intensified incidences of VF (66.6%, 66.6% and 50%, P < 0.05) and VT (100%, 100%, and 100%, P < 0.05), duration of VF + VT episodes (70.2 +/- 10.5 seconds, 69.8 +/- 6.75 seconds, and 60.8 +/- 14.9 seconds, P < 0.001), number of VF + VT episodes (56 +/- 16.4, 67 +/- 11, and 45 +/- 3.5, P < 0.01, P < 0.001, and P < 0.05), severity of arrhythmias(3.8 +/- 0.3, 4 +/- 0.5, and 3.7 +/- 0.2, P < 0.01, P < 0.05, and P < 0.01), and IS (45.5 +/- 3%, 46.8 +/- 3.4%, and 43 +/- 2.5%, respectively, P < 0.001) compared with the noradrenaline-treated group. CONCLUSION: Prazosin or 5-HD treatment eliminated the beneficial effects of noradrenaline on arrhythmogenesis and infarct size. pubtype: Academic Journal doctype: Journal Article ougenre: Article language: English refInfo: holdings: @attributes: islocal: N |
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