Opening of the Mitochondrial Permeability Transition Pore Mediated Myocardial Damage After Perinatal Asphyxia in Neonatal Rats.

OBJECTIVES

This study investigated the mechanisms underlying myocardial damage after perinatal hypoxia.

METHODS

An intrauterine hypoxia-ischemia model (I/U HI) and a hypoxia/reoxygenation (H/R) model were established. Myocardial damage, mitochondrial function, and mitochondria permeability transition pore (MPTP) opening were determined. The results, presented as means ± SD, were analyzed using SPSS.

RESULTS

Intrauterine hypoxia induced cardiac damage, mitochondrial dysfunction, and MPTP opening in neonatal rats. H/R led to apoptosis and MPTP opening. cTnI and apoptosis-inducing factor (AIF) levels were positively correlated with the degree of MPTP opening. The larger degree of MPTP opening combined with the significant increases in the Ca2+, ROS, and decreases in mitochondrial membrane potential and ATP levels. The larger degree of MPTP opening combined with the stronger release of cytochrome c and AIF.

CONCLUSIONS

Increased MPTP opening may play a crucial role in perinatal asphyxia-induced myocardial damage in neonatal rats.