OBJECTIVE: For subsequent studies on the molecular mechanisms of postconditioning, we aimed to identify a robust postconditioning protocol in rat and mouse heart. DESIGN: Isolated rat hearts were subjected to different postconditioning protocols (study 1 and 2). The protection was compared to preconditioning. Rats (study 3) in vivo in two different laboratories were postconditioned. Isolated mouse hearts (study 4) and mice in vivo (study 5) were postconditioned. RESULTS: Postconditioning did not protect isolated, perfused rat hearts, however, preconditioning improved function and reduced infarct size. Postconditioning tended to protect rat hearts in vivo in one laboratory (p = 0.10), whereas protection was seen in the other laboratory (infarct size 51+/-11% vs controls 62+/-3%, p = 0.01). Postconditioned mouse hearts were protected, both ex vivo (16+/-9% vs controls 33+/-18%, p = 0.02) and in vivo (21+/-5% vs 42+/-7%, p < 0.001). CONCLUSIONS: Rat hearts are less suitable for studies of mechanisms of postconditioning. The results suggest that the signaling pathways differ between pre- and postconditioning. Mouse hearts were strongly protected by postconditioning, and genetically engineered mice may be useful for postconditioning research.
OBJECTIVE: For subsequent studies on the molecular mechanisms of postconditioning, we aimed to identify a robust postconditioning protocol in rat and mouse heart. DESIGN: Isolated rat hearts were subjected to different postconditioning protocols (study 1 and 2). The protection was compared to preconditioning. Rats (study 3) in vivo in two different laboratories were postconditioned. Isolated mouse hearts (study 4) and mice in vivo (study 5) were postconditioned. RESULTS: Postconditioning did not protect isolated, perfused rat hearts, however, preconditioning improved function and reduced infarct size. Postconditioning tended to protect rat hearts in vivo in one laboratory (p = 0.10), whereas protection was seen in the other laboratory (infarct size 51+/-11% vs controls 62+/-3%, p = 0.01). Postconditioned mouse hearts were protected, both ex vivo (16+/-9% vs controls 33+/-18%, p = 0.02) and in vivo (21+/-5% vs 42+/-7%, p < 0.001). CONCLUSIONS:Rat hearts are less suitable for studies of mechanisms of postconditioning. The results suggest that the signaling pathways differ between pre- and postconditioning. Mouse hearts were strongly protected by postconditioning, and genetically engineered mice may be useful for postconditioning research.
Authors: Regina Ye; Hani Jneid; Mahboob Alam; Barry F Uretsky; Dan Atar; Masafumi Kitakaze; Sean M Davidson; Derek M Yellon; Yochai Birnbaum Journal: Cardiovasc Drugs Ther Date: 2022-02-16 Impact factor: 3.727
Authors: Michael D Goodman; Sheryl E Koch; Geraldine A Fuller-Bicer; Karyn L Butler Journal: Am J Physiol Heart Circ Physiol Date: 2008-08-15 Impact factor: 4.733
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