Increased myocardial vulnerability to ischemia-reperfusion injury in the presence of left ventricular hypertrophy
| Autor: | Barbara Faricelli, Søren Mølgaard, Max Salomonsson, Thomas Engstrøm, Marek Treiman |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Male medicine.medical_specialty Physiology Ischemia Myocardial Infarction Myocardial Reperfusion Injury 030204 cardiovascular system & hematology Left ventricular hypertrophy Incretins Rats Inbred WKY Severity of Illness Index Electron Transport Complex IV 03 medical and health sciences Electron Transport Complex III 0302 clinical medicine Internal medicine Rats Inbred SHR Severity of illness Internal Medicine medicine Animals cardiovascular diseases Myocardial infarction Left ventricle hypertrophy High prevalence business.industry Venoms Myocardium Heart medicine.disease Infarct size Rats 030104 developmental biology Hypertension cardiovascular system Cardiology Cytochromes Exenatide Hypertrophy Left Ventricular Cardiology and Cardiovascular Medicine business Peptides Reperfusion injury |
| Zdroj: | Journal of hypertension. 34(3) |
| ISSN: | 1473-5598 |
| Popis: | Despite its high prevalence among patients suffering myocardial infarction, the significance of left ventricle hypertrophy for infarct size is not known. We asked whether infarct size might be increased by this condition, and whether any such increase might be associated with an increased mitochondrial damage following coronary occlusion.Occlusion of the left descending artery in isolated, perfused hearts of SHR-SP (spontaneously hypertensive rat stroke-prone) (left ventricular hypertrophy) or Wistar-Kyoto (WKY) (control) rats was used, followed by reperfusion with or without exendin-4 (Exe-4), a glucagon-like peptide-1 receptor agonist. Infarct size relative to area-at-risk was determined. Separately, mitochondria were isolated after global ischemia. Activities of complexes III and IV and amounts of selected complex subunits and cytochromes a, b, c, and c1 were determined.Infarct size (ischemia 35 min and 120 min reperfusion) was 65.8% (±3.3%) and 37.1% (±3.4%) in the SHR-SP and WKY hearts, respectively (P 0.05). Exe-4 significantly decreased infarct size and hypercontracture in WKY, but not in SHR-SP, hearts. After ischemia 15 min in SHR-SP hearts, Exe-4 reduced the infarct (26.6%, ±3.8% to 9.3% ± 1.5%; P 0.05). Mitochondria from postischemic SHR-SP hearts showed a reduction of complex III (368.1 ± 37.5 to 175.8 ± 23.0 nmoles/min × mg; P 0.05) and complex IV (14.4 ± 0.22 to 5.8 ± 0.8 1/s × mg; P 0.05) activities and decreased amounts of cytochromes a, b, and c.Hearts from hypertensive (SHR-SP) rats with left ventricle hypertrophy appeared more vulnerable to ischemia-reperfusion injury, as supported by a more profound infarct development and an earlier loss of postconditioning by Exe-4. Mitochondrial complexes III and IV were identified among possible loci of this increased, hypertrophy-associated vulnerability. |
| Databáze: | OpenAIRE |
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