The role of survival proteins involved in myocardial dysfunction after.

本研究采用大鼠脑死亡模型，探讨了脑死亡后心肌功能障碍的发生机制。通过用300 μ l盐水对插入动物硬膜下腔的4Fr Fogarty导管进行分级膨胀来产生脑死亡。本研究旨在检测脑死亡后心肌功能障碍中磷脂酰肌醇3-激酶（PI 3 K）-Akt信号通路的变化。PI 3 K抑制剂Wortmannin可改善脑死亡后EF和LV dp/dt max及存活率。另一项使用蛋白质印迹的研究表明，脑死亡增加Akt的磷酸化，减少磷蛋白的磷酸化，渥曼青霉素抑制Akt的磷酸化，逆转磷蛋白磷酸化的减少。此外，渥曼青霉素不影响SERCA的水平。这些数据表明，心肌PI 3 k-Akt信号磷酸化和磷酰胺磷酸化的减少可能参与脑死亡后的心肌功能障碍。

We examined the mechanism involved in myocardial dysfunction following brain death using rat-brain-death-model. Brain death was produced by graded inflation of a 4Fr Fogarty catheter inserted into the animal's subdural space by 300 ul of saline. The study was designed to examine the Phosphatidylinositol 3-kinase (PI3K)-Akt signaling involved in the myocardial dysfunction after brain death. Wortmannin, an inhibitor of PI3K, improved EF and LV dp/dt max and survival rate after brain death. Another study using Western blotting showed that brain death increased phosphorylation of Akt and decreased phosphorylation of phosphoramban and wortmannin suppressed the phosphorylation of Akt and reversed the decreased phosphorylation of phosphoramban. In addition, wortmannin did not affect of level of SERCAs. These data indicate that myocardial PI3k-Akt-signaling phosphorylation and reduction of phosphorylation of phosphoramban may be involved in the myocardial dysfunction following brain death.