China
Africa
Explore chapters and articles related to this topic
Coronary Vascular Endothelium, Preconditioning and Arrhythmogenesis
Published in Malcolm J. Lewis, Ajay M. Shah, Endothelial Modulation of Cardiac Function, 2020
There is abundant evidence that the endothelium plays a significant role in modulating coronary vasomotor tone through the synthesis and metabolism of various vasoactive substances (Vane and Botting, 1994; Bassenge, 1995; Gryglewski et al., 1995). Rather more recently, it has been recognised that endocardial endothelial and coronary vascular endothelial cells communicate with cardiac myocytes to modulate contractility through the release of various endothelium-derived substances which include nitric oxide and endothelin, a subject extensively reviewed elsewhere in this volume. In this chapter we summarise the evidence that endothelium-derived substances also modify, in a protective fashion, the life-threatening ventricular arrhythmias that arise during a period of myocardial ischaemia and reperfusion. In particular, we summarise the evidence that the pronounced antiarrhythmic effects of ischaemic preconditioning are due, in part, to the elaboration of such substances. In this context we define ischaemic preconditioning as “the increased tolerance of the myocardium to ischaemic injury after it has been ‘primed’ by much shorter periods of ischaemia”. These can be induced, for example, by partial or complete coronary artery occlusion or by cardiac pacing.
Unbiased research
Published in C. P. Khare, Evidence-based Ayurveda, 2019
In this study, the effect of garlic (Allium sativum) extract on ischemic preconditioning and ischemia-reperfusion induced cardiac injury has been studied. Hearts from adult albino rats of Wistar strain were isolated and immediately mounted on Langendorff’s apparatus for retrograde perfusion. After 15 minutes of stabilization, the hearts were subjected to four episodes of 5 min ischemia, interspersed with 5 min reperfusion (to complete the protocol of ischemic preconditioning), 30 min global ischemia, followed by 120 min of reperfusion. In the control and treated groups, respective interventions were given instead of ischemic preconditioning. The magnitude of cardiac injury was quantified by measuring Lactate Dehydrogenase and creatine kinase concentration in the coronary effluent and myocardial infarct size by macroscopic volume method.
Preclinical Models
Published in George C. Kagadis, Nancy L. Ford, Dimitrios N. Karnabatidis, George K. Loudos, Handbook of Small Animal Imaging, 2018
Irene Cuadrado, Jesús Egido, Jose Luis Zamorano, Carlos Zaragoza
The method has been further modified to analyze ischemic preconditioning of the heart. In this method, the left coronary artery is repeatedly occluded to subject the heart to several rounds of brief ischemia and reperfusion, followed by permanent occlusion. This approach has identified several ischemia-induced genes that confer tolerance to a subsequent ischemic event (Xuan et al. 2007).
Targeting circadian PER2 as therapy in myocardial ischemia and reperfusion injury
Published in Chronobiology International, 2021
Yoshimasa Oyama, Lori A Walker, Tobias Eckle
Interestingly, the discovery of light elicited PER2 was initially based on studies investigating adenosine signaling in cardioprotection. Extracellular adenosine signaling is an essential cellular adaptive mechanism (Fredholm 2007; Ohta and Sitkovsky 2001; Sitkovsky et al. 2004; Thiel et al. 2005). In the extracellular space, adenosine originates from 5ʹ-adenosine monophosphate (AMP) via ecto-5ʹ-nucleotidase (CD73) mediated phosphohydrolysis. Adenosine then signals through four well-described adenosine receptors, the ADORA1, ADORA2A, ADORA2B, or ADORA3 (Fredholm 2007; Hasko et al. 2008). During hypoxia or ischemia, extracellular adenosine production and signaling increase significantly (Eckle et al. 2008b, 2007). Enhanced activation of adenosine receptors can then mediate endothelial barrier protective or anti-inflammatory effects (Eckle et al. 2008a; Eltzschig et al. 2004; Rosenberger et al. 2009). These adenosine signaling effects are ultimately organ protective during ischemia (Hart et al. 2008; Lappas et al. 2006; Linden 2006; Yang et al. 2005). On the other side, genetic ablation of ADORA2B signaling abolishes ischemic-preconditioning elicited cardioprotection (Eckle et al. 2008c; Eltzschig 2009; Kohler et al. 2007). Interestingly, ischemic preconditioning, where short non-lethal ischemic periods precede a more extended ischemic period, has been described as the most potent cardioprotective mechanism discovered at the bench. Regardless, these studies implicate adenosine signaling events as a central mechanism in cardioprotection.
Remote ischemic postconditioning as well as blood plasma from double-conditioned donor ameliorate reperfusion syndrome in skeletal muscle
Published in Journal of Plastic Surgery and Hand Surgery, 2020
Rastislav Burda, Radoslav Morochovič, Miroslava Némethová, Jozef Burda
Conditioning procedures are the most powerful cardioprotective interventions in animal experiments. However, ischemic preconditioning cannot be used to reduce infarct size in patients with acute myocardial infarction because its occurrence is not predictable [1]. The decisive factor for activation of ischemic tolerance is combination of two stresses [2,3]. This phenomenon is a two-stage process; the first tier is obligatory in any case; however, for full tolerance activation the application of the second stress is absolutely necessary as well. A great advantage is that the two stresses need not be of the same nature (cross tolerance). This cross tolerance not only enables the first stress to have the form of planned stress (preconditioning), but it can be a pathological event as well, and then planned stress can be used as the second stress, i.e. postconditioning (hundreds of publications confirm this fact).
Neuroprotective and tumoricidal activities of cardiac glycosides. Could oleandrin be a new weapon against stroke and glioblastoma?
Published in International Journal of Neuroscience, 2018
İlhan Elmaci, Ebru Emekli Alturfan, Salih Cengiz, Aysel Ozpinar, Meric A. Altinoz
Ischemic preconditioning spares the brain from ischemic injury, where a brief period of ischemia protects from a longer damaging ischemic episode [16]. As ischemic preconditioning is unlikely to be used in the clinic, pharmacological preconditioning (PP) is actively being investigated. Kaur et al. analyzed the possible neuroprotective effect of PP with digoxin and its likely mechanisms [22]. Bilateral carotid artery occlusion (BCAO) of 17 min followed by reperfusion for 24 h was performed to produce ischemia and reperfusion (I/R) induced cerebral injury in male mice [22]. They assessed cerebral infarct size with triphenyltetrazolium staining, memory performance with elevated plus maze test and the motor deficits with inclined beam walking test, rota rod test and lateral push test [22]. Digoxin (0.08 mg/kg, i.p.) treatment was employed 24 h before surgery in a separate group of animals to induce PP. BCAO followed by reperfusion caused a cerebral infarct with impairment of memory and motor coordination. Digoxin treatment significantly decreased the cerebral infarct size and prevented I/R induced cognitive and motor deficits. Using specific inhibitors, they demonstrated that digoxin mediated neuroprotection involves L-type calcium channels, ryanodine receptors and Na+/Ca2+ exchanger [22].