Delayed anti-arrhythmic effect of nitroglycerin in anesthetized rats: Involvement of CGRP, PKC and mKATP channels

Anti-Apoptotic Effect of Hyperbaric Oxygen Preconditioning on a Rat Model of Myocardial Infarction

“…As was reported, ischemia preconditioning induces a biphasic tolerance against subsequent insult, with an early phase that lasts for 2 to 3 h and a delayed phase that initiates about 24 h later and continues up to 72 h [27,28]. Choi's group, using HBO in the isolated rat hearts [5], also showed a similar biphasic effect.…”

Delayed Cardioprotective Effects of Hyperoxia Preconditioning Prolonged by Intermittent Exposure

“…Increasing the protection of tissues against a prolonged ischemic injury has a great interest in clinical realm. Since Murry et al in 1986 [23], it has been reported that preconditioning by sublethal stimulus induces a biphasic tolerance against a subsequent lethal insult: with an early phase that lasts for 2 to 3 h and a delayed phase that initiates about 24 h later and continues up to 72 h [19,24]. Several studies using infusion of low concentrations of oxygen radicals [3,4,6,25] and administration of antioxidants [26][27][28] have demonstrated that ROS acts as the trigger of preconditioning process.…”

Mitochondria are sources of metabolic sink and arrhythmias

“…A protective role for mitoK ATP channel activation against arrhythmias has been inferred by experiments demonstrating that mitoK ATP channel blockers consistently abolished the anti-arrhythmic phenotype provided by preconditioning stimuli, such as ischemic preconditioning (Vegh & Parratt, 2002; Rajesh et al , 2004), adenosine (Headrick et al , 2003), delta opioid agonists (Fryer et al , 2000; Fischbach et al , 2003), estrogen (Das & Sarkar, 2006), 3-nitropropionic acid (Basgut et al , 2008), nitroglycerin (Baharvand et al , 2009), noradrenaline (Imani et al , 2008), or endothelin receptor agonists (Das et al , 2007). It is important to note, however, that mitoK ATP channel blockade during other preconditioning stimuli; namely, bradykinin (Driamov et al , 2004), low-flow ischemia (Driamov et al , 2004), peroxynitrite (Kiss et al , 2008), and estradiol (Tsai et al , 2002) failed to attenuate the anti-arrhythmic protection of these stimuli.…”