Kaljusto Mari-Liis, Mori Tomohisa, Mohammad Husain Rizvi Syed, Galagudza Michael, Frantzen Marthe-Lise, Valen Guro, Vaage Jarle
Department of Cardiothoracic Surgery, Ullevål University Hospital, Oslo, Norway.
Scand Cardiovasc J. 2006 Dec;40(6):334-41. doi: 10.1080/14017430601007587.
For subsequent studies on the molecular mechanisms of postconditioning, we aimed to identify a robust postconditioning protocol in rat and mouse heart.
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.
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).
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.
为了后续关于后适应分子机制的研究,我们旨在确定一种适用于大鼠和小鼠心脏的可靠后适应方案。
对离体大鼠心脏采用不同的后适应方案(研究1和2)。将这种保护作用与预处理进行比较。在两个不同实验室对体内的大鼠(研究3)进行后适应处理。对离体小鼠心脏(研究4)和体内的小鼠(研究5)进行后适应处理。
后适应并不能保护离体灌注的大鼠心脏,然而,预处理可改善心脏功能并减小梗死面积。在一个实验室中,后适应对体内大鼠心脏有一定的保护倾向(p = 0.10),而在另一个实验室中则观察到了保护作用(梗死面积51±11% 对比对照组62±3%,p = 0.01)。后适应处理的小鼠心脏,无论是在离体状态(16±9% 对比对照组33±18%,p = 0.02)还是在体内状态(21±5% 对比42±7%,p < 0.001)均受到保护。
大鼠心脏不太适合用于后适应机制的研究。结果表明预处理和后适应的信号通路有所不同。小鼠心脏受到后适应的强烈保护,基因工程小鼠可能对后适应研究有用。