Study On The Role Of Changes Of Brain Mitochondrial Permeability Transition Pore In Brain Damage And Its Mechanism After Cardiopulmonary Resuscitation In Rats

Accumulating evidence suggests that the mitochondrial permeability transition (MPT) is a common pathway leading to both necrotic and apoptotic cell death after ischemia/reperfusion. Opening of high conductance mitochondrial permeability transition pore (MPTP) in the mitochondrial inner membrane initiates the MPT. How inhibiting MPTP opening is a new effective strategy for the protection of cell from reperfusion injury. The study based on the animal model that cardiac arrest was induced by asphyxiation and ice-cold 0.5M Kcl in rats, investigates that if there exists the abnormal opening of mPTP in brain(spectrophotometric analysis) , the opening degree and the changing rules. Furthermore, we will investigate the relationship between the opening of MPTP and the energy dysmetabolism of neuroal cells, the role of MPTP in the cell apoptosis. We discuss the possible mechanism from several levels including entity , cell, mitochondrial and molecular. The major goal is to provide basis theory that MPTP is a new target for neuroprotection after cardiopulmonary resuscitation.