The role of survival proteins involved in myocardial dysfunction after.

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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.