Exercise induces early and late myocardial preconditioning in dogs

Domenech, Raúl; Macho, Pilar; Schwarze, Hermann; Pecchi, Gina

doi:10.1016/s0008-6363(02)00334-6

Cited by 101 publications

(100 citation statements)

References 21 publications

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“…Experiments in pigs 14 and dogs 15 showed that brief episodes of tachycardia that do not induce ischemia before a prolonged coronary occlusion decrease the infarct size (Figure) by a mechanism similar to that of ischemic preconditioning and that is mediated through modifications of sarcoplasmic reticulum and mitochondrial ATPsensitive potassium channels. 16,17 Subsequent experiments in rats 18 and in dogs 19 showed, as expected, that brief episodes of exercise also induced preconditioning of the infarct size. Interestingly, exercise induces early as well as late preconditioning and the magnitude of reduction in infarct size observed in dogs is much larger than that obtained with ischemic and tachycardia preconditioning (Figure).…”

Section: Benefits Of Exercisementioning

confidence: 55%

Preconditioning

Domenech

2006

Circulation

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Case presentation: A 45-yearold man with coronary artery disease is found to be in good condition after his annual medical checkup, and his doctor advises him to continue with the same drugs, a prudent diet, entertainment, and regular exercise; however, the patient is afraid that he will not have time to exercise regularly. Benefits of ExerciseClinicians have learned about the beneficial effects of several factors that may prevent a myocardial infarction (MI), including avoidance of smoking; treatment of high blood pressure, diabetes, dyslipidemia, and obesity; and regular performance of exercise. This last factor is based on epidemiological observations such as a decrease in the incidence of MI in men who perform heavy work 1,2 ; however, it is only in the last few years that the beneficial effect of exercise has obtained plausible explanations of its own, that is, apart from its effect on other risk factors. There are at least 3 distinct mechanisms for this benefit: (1) Improvement of endothelial function, thereby preventing atherosclerosis and coronary occlusion 3 ; (2) prevention of remodeling after MI through the expression of oxidative metabolism-related genes 4 ; and (3) delaying acute ischemic injury after a coronary occlusion by preconditioning.Since the discovery of ischemic preconditioning by Murry et al 5 in 1986, studies have appeared in the literature searching for its mechanisms and for alternative ways to trigger it. The concept that 1 or 2 episodes of brief ischemia (Ϸ5 minutes in duration each), induced a few minutes or a few hours (early preconditioning) or 24 to 72 hours (late preconditioning or second window) before a prolonged coronary occlusion, followed by reperfusion substantially decreases the speed of the ischemic injury and limits infarct size is firmly established in all animal species studied in the experimental laboratory. 6 It is one of the most powerful means of protecting the myocardium with the exception of early reperfusion. Several lines of evidence in coronary patients suggest but do not prove that the human myocardium is also protected by ischemic preconditioning. For example, preinfarction angina is associated with a smaller infarct size; a lower incidence of congestive heart failure, shock, and ventricular arrhythmias; and decreased mortality. [7][8][9] The ST-segment elevation observed during angioplasty decreases after subsequent occlusions, 10 which suggests that each occlusion provides preconditioning for the ischemic effect of the next one. Protocols of ischemic preconditioning before coronary artery bypass grafting preserve ATP levels during the subsequent global ischemic period 11 and decrease serum levels of troponin T, thereby suggesting a smaller infarct size. 12 Finally, the progressive decrease in the magnitude of ischemia during several consecutive episodes of exercise in patients with demand angina (warm-up phenomenon) suggests the preconditioning effect of each episode. 13 The protective effect of ischemic preconditioning can be reproduced by several drugs,...

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Section: Benefits Of Exercisementioning

confidence: 55%

Preconditioning

Domenech

2006

Circulation

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“…The velocity on the treadmill was 15 m/min and the exercise duration was for 10-20 min/day. The EP protocol was designed with minor modifications of the protocol described by Domenech et al 10 and Parra et al 6 On the seventh day, animals were randomly assigned to 10 experimental groups (n=25 rats per group):…”

Section: Experimental Protocolmentioning

confidence: 99%

Exercise Preconditioning-Induced Early and Late Phase of Cardioprotection Is Associated With Protein Kinase C Epsilon Translocation

Hao

Shen

et al. 2014

Circ J

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1636HAO Z et al. Circulation JournalOfficial Journal of the Japanese Circulation Society http://www. j-circ.or.jp the EP-induced early phase of cardioprotection requires PKCδ translocation. 8 In this study, which was performed by the present team, short-term adaptation of adult rats to EP was found to markedly increase the expression of PKCδ and phosphorylation of PKCδ. However, the PKCε responsible for EP has not been identified. In the present study, it was hypothesized that EP caused an increase in PKCε expression and translocation of PKCε, and that the PKC inhibitor, chelerythrine (CHE), suppressed these events, thus attenuating the EP-mediated cardioprotection. Methods Ethical ApprovalAdult (8-week-old) male Sprague-Dawley rats (Sippr BK, Shanghai, China) were housed at a constant temperature (22±2°C) on a 12-h light/dark cycle. They were fed ad libitum on standard laboratory rat chow and had free access to tap water. The investigation conforms to the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (NIH Publication no. 85-23, revised 1996) and was schemia/reperfusion (I/R) is one of the major causes of myocardial injury. Over the years, investigators have studied many approaches regarding the protection of the heart against I/R injury. Specifically, cardioprotection of ischemic preconditioning (IP) 1 and remote IP 2,3,4 were described as the immediate adaptation of the heart to brief sublethal ischemia but it lacking practical utility for providing protection to human. Recently, researchers have found that, like IP, exercise preconditioning (EP), which here refers to brief episodes of exercise, can also enhance the tolerance of the heart to subsequent ischemic insult. 5,6 It is demonstrated here that EP has 2 distinct protective phases, the early phase, which occurs immediately after the exercise, and a late phase, which peaks 24 h after exercise. 6-9 Although the powerful cardioprotective effect of EP has been proved, the intracellular mechanisms involved in this EP-conferred cardioprotection remain unclear. Recent evidence supports the contention that acute exercise directly enhances myocardial tolerance to ischemia in the hearts of rats through a protein kinase C (PKC)-mediated mechanism. 5 However, studies investigating the role of isoform-specific alterations in PKC after EP are still rare. One recent study clearly demonstrated that Background: Exercise preconditioning (EP) can provide powerful protection to the heart. Evidence supports the contention that EP directly enhances myocardial tolerance to ischaemia through a protein kinase C (PKC)-mediated mechanism. However, studies investigating the role of isoform-specific PKC after EP are lacking.

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“…These authors reported in conscious rabbits that a brief episode of cardiac pacing (500 beats per minute for 5 min) reduced post-pacing ST-segment elevation and decreased left ventricular end-diastolic pressure for up to 1 h following which the beneficial effects disappeared and re-appeared 24 and 48 h later, with the beneficial effect finally disappearing again after 72 h [5], a timeline which closely matched delayed IPC. Exercise has also been reported to elicit delayed preconditioning with myocardial infarct-size reduction 24 h later in both rats [9] and dogs [10]. In terms of the elucidating the mechanisms underlying delayed preconditioning much of the work has focused on ischemia rather than pacing or exercise as the stimulus for delayed cardioprotection.…”

Section: Characteristics Of Delayed Preconditioningmentioning

confidence: 99%

The Second Window of Preconditioning (SWOP) Where Are We Now?

Hausenloy

Yellon

2010

Cardiovasc Drugs Ther

138

118

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A standard ischemic preconditioning (IPC) stimulus of one or more brief episodes of non-lethal myocardial ischemia and reperfusion elicits a bi-phasic pattern of cardioprotection. The first phase manifests almost immediately following the IPC stimulus and lasts for 1-2 h, after which its effect disappears (termed classical or early IPC). The second phase of cardioprotection appears 12-24 h later and lasts for 48-72 h (termed the Second Window of Protection [SWOP] or delayed or late IPC). The cardioprotection conferred by delayed IPC is robust and ubiquitous but is not as powerful as early IPC. Although there are some similarities in the mechanisms underlying early and delayed IPC, one of the major distinctions between the two is the latter's requirement for de novo protein synthesis of distal mediators such as iNOS and COX-2 which mediate the cardioprotection 24 h after the IPC stimulus. The phenomenon of delayed IPC has been demonstrated in man using a variety of experimental models. However, its clinical application has been limited by the same factors which affect early IPC- i.e. the need to intervene before the onset of myocardial ischemia, thereby restricting its potential clinical utility to planned settings of acute myocardial ischemia-reperfusion injury such as coronary artery bypass graft surgery, cardiac transplantation and percutaneous coronary intervention. In this article, the focus will be on the origins of delayed IPC, the mechanisms underlying its delayed cardioprotective effect, and the potential areas for its clinical application.

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Exercise induces early and late myocardial preconditioning in dogs

Cited by 101 publications

References 21 publications

Preconditioning

Preconditioning

Exercise Preconditioning-Induced Early and Late Phase of Cardioprotection Is Associated With Protein Kinase C Epsilon Translocation

The Second Window of Preconditioning (SWOP) Where Are We Now?

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