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Ischaemic preconditioning does not protect hypertrophied myocardium against ischaemia
J A Moolman1, S Genade, E Tromp
1Department of Internal Medicine, University of Stellenbosch.
Insights
Genetic hypertension in rats prevents the protective effects of ischaemic preconditioning on the heart. This suggests caution when considering preconditioning for patients with conditions like left ventricular hypertrophy.
Area of Science:
- Cardiovascular Research
- Ischaemic Physiology
Background:
- Ischaemic preconditioning is a potent endogenous mechanism protecting against myocardial infarction.
- Understanding its efficacy in hypertensive conditions is crucial for clinical application.
Purpose of the Study:
- To investigate the protective potential of ischaemic preconditioning in the myocardium of genetically hypertensive rats.
- To compare the response to preconditioning between hypertensive and normotensive rat hearts.
Main Methods:
- Male genetically hypertensive (GH) and normotensive (WAG) Wistar rats (12 months old) were used.
- Isolated perfused hearts underwent a preconditioning protocol (3x5 min global ischemia/5 min reperfusion).
- Hearts were subsequently subjected to 25 min global ischemia followed by 30 min reperfusion.
Main Results:
- Genetically hypertensive rats exhibited higher heart and body mass compared to controls.
- Normotensive WAG hearts showed protective effects of preconditioning on post-ischaemic function and creatine phosphate levels.
- Genetically hypertensive GH hearts did not demonstrate protective effects from ischaemic preconditioning.
Conclusions:
- The myocardium of genetically hypertensive rats is resistant to the protective effects of ischaemic preconditioning.
- The underlying mechanism for this failure in preconditioning is currently unknown.
- Findings suggest caution regarding the clinical use of preconditioning in patients with angina pectoris and left ventricular hypertrophy.
Objectives:
Because ischaemic preconditioning elicits a potent endogenous protective mechanism against the development of myocardial infarction, it is important to explore its utilisation in clinical situations. The aim of this study was to examine whether the myocardium of rats with genetic hypertension could be protected by ischaemic preconditioning.
Methods:
Male New Zealand genetically hypertensive rats (GH-Wistar-derived) and normotensive Wistar controls (WAG-Wistar-derived), aged 12 months, were used. Isolated perfused hearts were preconditioned by 3 periods of 5 minutes' global ischaemia, interspersed with 5 minutes' reperfusion, and subsequently subjected to 25 minutes' global ischaemia, followed by 30 minutes' reperfusion.
Results:
Heart and body mass were significantly higher in GH rats. Although the heart/body mass ratios of GH rats were higher than those of WAG rats, the difference was not significant. The reperfusion coronary flow pattern during the preconditioning protocol differed markedly between the 2 groups. Only normotensive WAG hearts demonstrated protective effects of preconditioning on post-ischaemic function and tissue creatine phosphate content, while the GH hearts could not be preconditioned.
Conclusions:
An explanation for the failure of preconditioning in GH hearts is not yet available. The data caution against implementation of preconditioning in patients with angina pectoris and left ventricular hypertrophy.