Ventricular but not atrial electro-mechanical delay of the embryonic heart is altered by anoxia-reoxygenation and improved by nitric oxide

Abstract

This work provides evidence that a NO-dependent pathway is involved in regulation of the ventricular excitation-contraction coupling in the anoxic-reoxygenated developing heart.

Left-ventricular electromechanical delay is prolonged in patients with postoperative atrial fibrillation

“…First, although LVEMD is reportedly prolonged by ischemia/reperfusion in normal rodents [15], it was not significantly prolonged postoperatively compared with the preoperative values in our study (Fig. 4).…”

“…We suggested here that LVEMD is one sensitive parameter for postoperative AF. Thus far, because the relationship between electromechanical delay and AF has been mainly described in animal models [14,15], clinical data are scarce. Roshanali et al identified the preoperative atrial electromechanical delay as a predictor for a post-coronary artery bypass graft AF [17].…”

“…# p value < 0.05 compared with the preoperative values. stress [15]. Further study is required to identify the mechanism for this difference in LVEMD between the non-AF and AF groups and it would provide new insights for the strategy for the prophylaxis of AF.…”

“…In an experimental ischemia/reperfusion model, electromechanical delay was reported to be prolonged by abnormality in calcium-handling proteins, which is considered one mechanism of AF [14,15]. We therefore hypothesized that postoperative electromechanical delay is correlated to AF after cardiac surgery and it could be a new parameter for it.…”

mitoKATP channel activation in the postanoxic developing heart protects E-C coupling via NO-, ROS-, and PKC-dependent pathways

“…Interestingly, the postischemic protection of embryonic ventricular myocytes afforded by mitoK ATP channel opening involves ROS and/or NO production (6,19). On the other hand, we recently found that inducible NO synthase (NOS) is strongly expressed in the embryonic myocardium and generates NO during anoxia-reoxygenation (38), improving recovery of excitation-contraction (E-C) coupling in the ventricle (21). However, the underlying protective mechanism involving the mitoK ATP channel remains to be explored in the whole developing heart.…”