Yoon Sung Kim

The potential mechanism of the detrimental effect of defibrillation prior to cardiopulmonary resuscitation in prolonged cardiac arrest model

Defibrillation is no longer universally recommended as initial intervention for the reversal of ventricular fibrillation (VF) after a prolonged and untreated cardiac arrest. We sought to examine this issue in an animal model where a prolonged untreated VF was induced. The aim of this study was to investigate the potential mechanism of the detrimental effect of defibrillation prior to cardiopulmonary resuscitation (CPR) in prolonged cardiac arrest model. VF was electrically induced in 32 domestic male swine weighing 40±3 kg and remained untreated for 15 minutes. The animals were then randomly allocated to either the initial defibrillation group or the chest compression group. Mean aortic pressure, right atrial pressure and coronary perfusion pressure (CPP) were continuously measured during the performance. The dimensions of the left ventricle (LV) were assessed by echocardiographic methods. The CPP induced by CPR after defibrillation was significantly lower in the initial defibrillation group than in the chest compression group; 1 minute after defibrillation (9±3 mmHg vs. 14.8±7 mmHg (P<0.05)), and after 5 minutes 16±5 mmHg vs. 21.7±1 mmHg (P<0.05). The LV volumes were reduced from 18±2 mmHg to 14±1 mmHg after defibrillation (P<0.05). In brief, this study showed that the conducting defibrillation prior to chest compression may cause a contracture of the LV, resulting in lowering CPP, thus dropping the efficiency of chest compression in a prolonged cardiac arrest model.

Delta neutrophil index: A reliable marker to differentiate perforated appendicitis from non-perforated appendicitis in the elderly

Delta neutrophil index (DNI) is a new inflammatory marker and the present study aimed to evaluate the predictive value of the DNI for the presence of a perforation in elderly with acute appendicitis.

Ischemic preconditioning induces neuroprotection cause by a transient global ischemia via maintaining the expression of p63.

p63 is a transcription factor of p53 gene family, which are involved in development, differentiation and cell response to stress; however, their roles in ischemic preconditioning (IPC) in the brain are not clear.

Ischemic preconditioning maintains immunoreactivities of glucokinase and glucokinase regulatory protein in neurons of the gerbil hippocampal CA1 region following transient cerebral ischemia.

Glucokinase (GK) plays a key role in the control of blood glucose homeostasis. In the present study, we investigated the effect of ischemic preconditioning (IPC) on immunoreactivities of GK and its regulatory protein (GKRP) following 5 min of transient cerebral ischemia in gerbils.