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.
PURPOSE: This study examines if ischemic postconditioning is preserved in hypertrophied myocardium of spontaneously hypertensiverats (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.
Authors: Matthias L Riess; Timothy R Matsuura; Jason A Bartos; Martin Bienengraeber; Mohammed Aldakkak; Scott H McKnite; Jennifer N Rees; Tom P Aufderheide; Mohammad Sarraf; Robert W Neumar; Demetris Yannopoulos Journal: Resuscitation Date: 2014-10-02 Impact factor: 5.262
Authors: Sandrine Lecour; Hans E Bøtker; Gianluigi Condorelli; Sean M Davidson; David Garcia-Dorado; Felix B Engel; Peter Ferdinandy; Gerd Heusch; Rosalinda Madonna; Michel Ovize; Marisol Ruiz-Meana; Rainer Schulz; Joost P G Sluijter; Linda W Van Laake; Derek M Yellon; Derek J Hausenloy Journal: Cardiovasc Res Date: 2014-10-24 Impact factor: 10.787