Remote vs. local ischaemic preconditioning in the rat heart: infarct limitation,suppression of ischaemic arrhythmia and the role of reactive oxygen species |
| |
| Authors: | Michael M. Galagudza Dmitry L. Sonin Timur D. Vlasov Dmitry I. Kurapeev Eugene V. Shlyakhto |
| |
| Affiliation: | 1. Institute of Experimental Medicine, Federal Almazov North‐West Medical Research Centre, St. Petersburg, Russian Federation;2. ITMO University, St. Petersburg, Russian Federation;3. Department of Pathophysiology, Pavlov First Saint Petersburg State Medical University, St. Petersburg, Russian Federation;4. Institute of Heart and Vessels, Federal Almazov North‐West Medical Research Centre, St. Petersburg, Russian Federation;5. Department of Internal Medicine, Pavlov First Saint Petersburg State Medical University, St. Petersburg, Russian Federation |
| |
| Abstract: | The unmet clinical need for myocardial salvage during ischaemia–reperfusion injury requires the development of new techniques for myocardial protection. In this study the protective effect of different local ischaemic preconditioning (LIPC) and remote ischaemic preconditioning (RIPC) protocols was compared in the rat model of myocardial ischaemia–reperfusion, using infarct size and ischaemic tachyarrhythmias as end‐points. In addition, the hypothesis that there is involvement of reactive oxygen species (ROS) in the protective signalling by RIPC was tested, again in comparison with LIPC. The animals were subjected to 30‐min coronary occlusion and 90‐min reperfusion. RIPC protocol included either transient infrarenal aortic occlusion (for 5, 15 and 30 min followed by 15‐min reperfusion) or 15‐min mesenteric artery occlusion with 15‐min reperfusion. Ventricular tachyarrhythmias during test ischaemia were quantified according to Lambeth Conventions. It was found that the infarct‐limiting effect of RIPC critically depends on the duration of a single episode of remote ischaemia, which fails to protect the heart from infarction when it is too short or, instead, too prolonged. It was also shown that RIPC is ineffective in reducing the incidence and severity of ischaemia‐induced ventricular tachyarrhythmias. According to our data, the infarct‐limiting effect of LIPC could be partially eliminated by the administration of ROS scavenger N‐2‐mercaptopropionylglycine (90 mg/kg), whereas the same effect of RIPC seems to be independent of ROS signalling. |
| |
| Keywords: | infarct size local ischaemic preconditioning myocardial ischaemia– reperfusion reactive oxygen species remote ischaemic preconditioning ventricular tachyarrhythmias |
|
|
