Delayed exercise-induced protection against arrhythmias in dogs—effect of celecoxib

Nagy, Orsolya; Hajnal, A.; Parratt, J. R.; Végh, Ágnes

doi:10.1016/j.ejphar.2004.07.068

Cited by 7 publications

(7 citation statements)

References 9 publications

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“…This approach is founded on the fact that exercise is a potent stimulus of protection against IR-induced arrhythmias (14,15,21,29). Functional and clinically relevant outcome measures of exercise-induced cardioprotection research are needed in the search to discover protective mechanisms involved in this observed protection.…”

Section: Discussionmentioning

confidence: 99%

“…The clinical relevance of these in vivo animal studies is emphasized when ECG-related outcome measures are used as key dependent study variables (6,9,10,14,15,21,27). In this regard, application of clinically based ECG scoring systems for ventricular arrhythmias has revealed several important considerations for use in exercise-based cardioprotection studies.…”

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confidence: 99%

“…In this regard, application of clinically based ECG scoring systems for ventricular arrhythmias has revealed several important considerations for use in exercise-based cardioprotection studies. First, hearts exposed to even 3 d of moderate-intensity treadmill running and the associated habituation period are more resistant to IR-generated arrhythmias compared with sedentary counterparts (11,15,21,27). Second, the magnitude of exercise-mediated protection is most apparent when the major ventricular arrhythmias, including premature ventricular contractions (PVCs), ventricular tachycardia (VT), and ventricular fibrillation (VF), are analyzed collectively rather than individually (15,27).…”

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confidence: 99%

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Evaluation of Arrhythmia Scoring Systems and Exercise-Induced Cardioprotection

Miller

Hosick

Wrieden

et al. 2012

Medicine &Amp; Science in Sports &Amp; Exercise

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Introduction Exercise is protective against ventricular arrhythmias induced by ischemia (I), the condition of inadequate blood flow, and reperfusion (R), the reestablishment of blood flow. This protection is observed clinically and scientifically by decreased incidence in ECG abnormalities. Numerous scoring systems exist for the quantification of ventricular arrhythmia severity. On the basis of preventricular contractions, ventricular tachycardia, and ventricular fibrillation frequency, these scoring systems are intended to provide more robust ECG outcome indicators than individual arrhythmia variables. Scoring systems vary primarily on continuous versus discontinuous treatment of the data, which should be considered when matching these arrhythmia metrics to scientific applications. Purpose The aim of this investigation was to evaluate seven ECG scoring systems in the assessment of ventricular arrhythmia severity after IR in male Sprague–Dawley rats. Methods Animals remained sedentary or exercised (3 d of treadmill exercise for 60 min) before surgically induced IR. A subset of sedentary animals served as sham, undergoing surgical procedure without IR. ECGs were evaluated under blinded conditions by three trained individuals. Single arrhythmia data and the parametric score were analyzed by one-way ANOVA, whereas the Kruskal–Wallis was used to compare group means for all nonparametric scoring systems between groups. Results IR produced a significant arrhythmic response in exercised and sedentary rats as determined by all arrhythmia scoring systems. Four arrhythmia metrics resulted in significant differences between exercised and sedentary treatments (P < 0.001), whereas three metrics did not. Conclusions Continuous versus discontinuous treatment of the data may account for variation in scoring system outcomes. These data confirm that exercise protects against IR-induced arrhythmias, and care must be taken when selecting an arrhythmia scoring system for ECG evaluation.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Evaluation of Arrhythmia Scoring Systems and Exercise-Induced Cardioprotection

Miller

Hosick

Wrieden

et al. 2012

Medicine &Amp; Science in Sports &Amp; Exercise

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“…For example, acute increases in myocardial PKC activity is cardioprotective while prolonged activation or high levels of activation are deleterious to cardiac health [60,66]. Finally, cornerstones of IPC such as elevated myocardial cyclooxygenase-2 (COX-2) activity are not part of the protective response to exercise [69] indicating that many important mechanisms of IR injury resistance are unique to exercise versus ischemic preconditioning.…”

Section: Are Exercise and Ischemia Unique Forms Of Preconditioning?mentioning

confidence: 98%

Exercise Induced Cardioprotection: An Overview of a Unique Form of Preconditioning

Quindry¹,

Hamilton

2007

CCR

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Experimental models for the study of an ischemia reperfusion (IR) resistant myocardium include exercise, ischemia, and pharmacologic stimuli. While research utilizing all three of these models consistently demonstrates a cardioprotected phenotype, presently only exercise represents a viable intervention for humans. Nonetheless, knowledge gleaned from ischemic preconditioning research has contributed greatly to the progress in identifying mechanisms of exercise induced cardioprotection. Similarly, ongoing pharmacologic preconditioning investigations are a direct byproduct of ischemic preconditioning research. In this review we present a critical analysis of commonalities and differences between exercise, pharmacologic, and ischemic models of myocardial preconditioning. Specifically, we identify keys points that illustrate why exercise research may be valuable for translating ischemic preconditioning research into a viable intervention against IR injury. As part of this discussion, we first provide a brief introduction of the mechanisms responsible for IR mediated injury followed by a thorough discussion of exercise induced cardioprotection against IR injury.

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“…However, Nagy et al reported that COX II inhibition did not prevent exercise-induced cardioprotection against ventricular arrhythmias after coronary occlusion in dogs [81]. Accordingly, studies by Quindry et al [82, 83] revealed that exercise does not elevate cardiac COX-2 activity.…”

Section: Cyclooxygenase II and Exercise-induced Cardioprotectionmentioning

confidence: 99%

Molecular Mechanisms in Exercise-Induced Cardioprotection

Golbidi

Laher

2011

Cardiology Research and Practice

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Physical inactivity is increasingly recognized as modifiable behavioral risk factor for cardiovascular diseases. A partial list of proposed mechanisms for exercise-induced cardioprotection include induction of heat shock proteins, increase in cardiac antioxidant capacity, expression of endoplasmic reticulum stress proteins, anatomical and physiological changes in the coronary arteries, changes in nitric oxide production, adaptational changes in cardiac mitochondria, increased autophagy, and improved function of sarcolemmal and/or mitochondrial ATP-sensitive potassium channels. It is currently unclear which of these protective mechanisms are essential for exercise-induced cardioprotection. However, most investigations focus on sarcolemmal KATP channels, NO production, and mitochondrial changes although it is very likely that other mechanisms may also exist. This paper discusses current information about these aforementioned topics and does not consider potentially important adaptations within blood or the autonomic nervous system. A better understanding of the molecular basis of exercise-induced cardioprotection will help to develop better therapeutic strategies.

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Delayed exercise-induced protection against arrhythmias in dogs—effect of celecoxib

Cited by 7 publications

References 9 publications

Evaluation of Arrhythmia Scoring Systems and Exercise-Induced Cardioprotection

Evaluation of Arrhythmia Scoring Systems and Exercise-Induced Cardioprotection

Exercise Induced Cardioprotection: An Overview of a Unique Form of Preconditioning

Molecular Mechanisms in Exercise-Induced Cardioprotection

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