Abstract 16: Significant Role of Action Potential Duration Dispersion and Connexin 43 in Lethal Arrhythmogenesis in Hemorrhagic Shock Heart: Optical Mapping Analysis
Prolonged low mean systemic blood pressure<40 mmHg in hemorrhagic shock causes irreversible heart dysfunction despite successful resuscitation. This “Shock Heart Syndrome” associates with lethal arrhythmias leading to adverse prognosis. To investigate mechanisms of lethal arrhythmogenesis, we performed optical mapping analysis (OM), electrophysiological study (EPS) and connexin 43 (Cx43) expression in Sprague-Dawley rat’s heart (n=32) obtained from 30% hemorrhagic shock model with repetitive bleedings (prolonged shock>30 min). Rats were divided into not resuscitated (No-R) and resuscitated by washed red blood cell (wRBC), normal saline (NS) and 5% albumin (5%alb) groups. Hearts were excised, perfused with Tyrode solution and stained with voltage-sensitive dye di-4-ANEPPS (15μmol/L). Ventricular fibrillation (VF) was induced by burst pacing stimulus to multiple sites in left ventricle (LV) and OM was performed. CX43 expression quantity was measured in LV myocardium by immunohistochemistry. Spontaneous VF was observed in No-S and VF was induced in all rats resuscitated by NS and 5%alb and their OM showed conduction delay and impaired action potential duration (APD) dispersion (APDd), defined as APDd = maximum APD - minimum APD, in LV. However, all rats rescued by wRBC had normal OM findings and no VF was induced. CX43 decreased in No-R, NS, 5%alb but not in wRBC. Conclusions; LV myocardial conduction disturbance accompanying impaired APD dispersion and CX43 damage is possible mechanism in lethal arrhythmogenetic electrophysiological property in shock heart syndrome.
- © 2012 by American Heart Association, Inc.