Role of HTK solution in protecting cardiomyocytes against oxidative stress by upregulating Nrf2 during cardiac arrest and resuscitation: a rat model with a right thoracotomy.

IntroductionThe objective of this study was to establish a rat model for cardiopulmonary bypass (CPB) with cardiac arrest and resuscitation and to investigate the regulatory role of HTK solution in protecting cardiomyocytes against oxidative stress by upregulating Nrf2.Methods40 rats were randomly assigned to four groups: the control (Ctrl), the histidine-tryptophan-ketoglutarate (HTK), 4:1 blood cardioplegia (BC) and del Nido cardioplegia (DN) groups. The cardiopulmonary bypass (CPB) procedure was implemented and sustained for a duration of 1 hour.

A novel survival rat model of hyperkalemia and landiolol induced cardioplegic arrest and resuscitation via cardiopulmonary bypass.

Objective: A small animal model would be an effective tool for research on the pathophysiology of cardiopulmonary bypass (CPB). However, numerous CPB models do not involve myocardial arrest and resuscitation. The aim of this research is to establish an easily achievable myocardial arrest and resuscitation CPB model through hyperkalemia and landiolol, simulating clinical cardiac surgery.

Novel mutations of AXIN2 identified in a Chinese Congenital Heart Disease Cohort.

Congenital heart defects (CHDs), the most common congenital human birth anomalies, involves complex genetic factors. Wnt/β-catenin pathway is critical for cardiogenesis and proved to be associated with numerous congenital heart abnormities. AXIN2 has a unique role in Wnt/β-catenin pathway, as it is not only an important inhibitor but also a direct target of Wnt/β-catenin pathway.