Key result
Ischemic postconditioning significantly reduced infarct size in normotensive rats, but this cardioprotective effect was completely lost in spontaneously hypertensive rats with myocardial hypertrophy.
Why the study?
Does ischemic postconditioning reduce infarct size in spontaneously hypertensive rats with hypertrophied myocardium compared to normotensive controls?
Does ischemic postconditioning reduce infarct size in spontaneously hypertensive rats with hypertrophied myocardium compared to normotensive controls?
Myocardial hypertrophy in spontaneously hypertensive rats completely abrogates the cardioprotective effects of ischemic postconditioning observed in normotensive controls.
Postconditioning protection lost in hypertrophied SHR hearts; leaves open translation to hypertensive patients with hypertrophy.
PURPOSE: This study examines if ischemic postconditioning is preserved in hypertrophied myocardium of spontaneously hypertensive rats (SHR). METHODS: Infarct sizes, hemodynamic, morphometric, and biochemical parameters were obtained from normotensive controls [Wistar-Kyoto (WKY) rats] and compared with SHRs. In open-chest rats, the infarct size was determined after 30 minutes of regional ischemia. Postconditioning was performed by 3 cycles of ischemia/reperfusion with 30 seconds each or 6 cycles of ischemia/reperfusion with 10 seconds each immediately after the infarction. RESULTS: Infarct size was comparable between control rats and SHRs. In WKY rats, postconditioning reduced the infarct size significantly. However, in SHRs, the postconditioning effect was completely lost for both postconditioning protocols. Even shortening of the ischemic period to 20 minutes did not restore the infarct sparing effect in SHRs. The phosphorylation of glycogen synthase kinase 3β increased 2.1-fold by ischemic postconditioning in WKY rats; however, this increase was completely absent in SHRs with both postconditioning protocols. CONCLUSIONS: Myocardial hypertrophy inhibits the protection by postconditioning in an experimental animal model. Future studies have to clarify whether this result can be extrapolated to patients with arterial hypertension and myocardial hypertrophy.
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Wagner et al. (2012) studied Myocardial hypertrophy and arterial hypertension. Ischemic postconditioning vs. No postconditioning was evaluated on Infarct size. Ischemic postconditioning significantly reduced infarct size in normotensive rats, but this cardioprotective effect was completely lost in spontaneously hypertensive rats with myocardial hypertrophy.
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