Moderate stress by cardiac pacing may induce both short term and long term cardioprotection

Szekeres, L.; Papp, Julius Gy.; Szilvássy, Zoltán; Udvary, Éva; Végh, Ágnes

doi:10.1093/cvr/27.4.593

Cited by 39 publications

(13 citation statements)

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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].…”

Section: Characteristics Of Delayed Preconditioningmentioning

confidence: 85%

“…Preceding the publication of the first studies describing delayed IPC [3,4], Szekeres and co-workers [5] described a delayed cardioprotective effect with cardiac pacing. 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.…”

Section: Characteristics Of Delayed Preconditioningmentioning

confidence: 99%

“…Kuzuya and co-workers [4] demonstrated myocardial infarct size reduction using an in vivo canine model either immediately or 24 h following a standard IPC stimulus, but failed to observe an infarct-limiting effect at 3 or 12 h following the IPC stimulus, confirming the presence of a bi-phasic cardioprotective response to IPC. Interestingly, an earlier study in the same year by Szekeres and co-workers [5] had reported using an in vivo rabbit model that a period of cardiac pacing provided cardioprotection which waned after 1 h and re-appeared at 24 and 48 h but not at 72 h. Interestingly, 10 years earlier in 1983, Szekeres and coworkers reported that prostacyclin elicited a delayed antiischemic effect 24-48 h later (reviewed in [6]). In this article, we review the phenomenon of delayed preconditioning, the mechanisms underlying its beneficial effects (including several novel concepts) and its potential for clinical application.…”

Section: Introductionmentioning

confidence: 99%

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

Hausenloy

Yellon

2010

Cardiovasc Drugs Ther

137

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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Section: Characteristics Of Delayed Preconditioningmentioning

confidence: 85%

Section: Characteristics Of Delayed Preconditioningmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Hausenloy

Yellon

2010

Cardiovasc Drugs Ther

137

118

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“…Acute and rapid artificial pacing has also been shown to induce preconditioning in various adult animal models (12,17,18,46,47, 53). Pacing rates used in these studies are clearly higher than the physiological intrinsic rates of the species under consideration, resulting in transient myocardial ischemia, which is most likely the principal cause of preconditioning.…”

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confidence: 99%

Ectopic pacing at physiological rate improves postanoxic recovery of the developing heart

Rosa

Maury²,

Terrand

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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Recently, rapid and transient cardiac pacing was shown to induce preconditioning in animal models. Whether the electrical stimulation per se or the concomitant myocardial ischemia affords such a protection remains unknown. We tested the hypothesis that chronic pacing of a cardiac preparation maintained in a normoxic condition can induce protection. Hearts of 4-day-old chick embryos were electrically paced in ovo over a 12-h period using asynchronous and intermittent ventricular stimulation (5 min on-10 min off) at 110% of the intrinsic rate. Sham (n ϭ 6) and paced hearts (n ϭ 6) were then excised, mounted in vitro, and subjected successively to 30 min of normoxia (20% O2), 30 min of anoxia (0% O2), and 60 min of reoxygenation (20% O2). Electrocardiogram and atrial and ventricular contractions were simultaneously recorded throughout the experiment. Reoxygenation-induced chrono-, dromo-, and inotropic disturbances, incidence of arrhythmias, and changes in electromechanical delay (EMD) in atria and ventricle were systematically investigated in sham and paced hearts. Under normoxia, the isolated heart beat spontaneously and regularly, and all baseline functional parameters were similar in sham and paced groups (means Ϯ SD): heart rate (190 Ϯ 36 beats/min), P-R interval (104 Ϯ 25 ms), mechanical atrioventricular propagation (20 Ϯ 4 mm/s), ventricular shortening velocity (1.7 Ϯ 1 mm/s), atrial EMD (17 Ϯ 4 ms), and ventricular EMD (16 Ϯ 2 ms). Under anoxia, cardiac function progressively collapsed, and sinoatrial activity finally stopped after ϳ9 min in both groups. During reoxygenation, paced hearts showed 1) a lower incidence of arrhythmias than sham hearts, 2) an increased rate of recovery of ventricular contractility compared with sham hearts, and 3) a faster return of ventricular EMD to basal value than sham hearts. However, recovery of heart rate, atrioventricular conduction, and atrial EMD was not improved by pacing. Activity of all hearts was fully restored at the end of reoxygenation. These findings suggest that chronic electrical stimulation of the ventricle at a near-physiological rate selectively alters some cellular functions within the heart and constitutes a nonischemic means to increase myocardial tolerance to a subsequent hypoxia-reoxygenation. chick embryo; hypoxia-reoxygenation; preconditioning; arrhythmias; excitation-contraction coupling IN THE ADULT HEART, it is well established that the deleterious consequences of prolonged ischemia can be minimized if this condition is preceded by a short episode(s) of ischemia, the so-called classical preconditioning (30). Cardioprotection is measured in terms of a decrease in infarct size, a delay in ultrastructural damage, a reduction in myocardial stunning, and a diminution in incidence and severity of ischemia-reperfusion-induced arrhythmias. Preconditioning can also be induced by numerous nonischemic stimuli, such as exercise, heat stress, endotoxins or cytokines, catecholamines, pharmacological agents, adenosine, reactive oxygen species (ROS), and nitric ...

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“…Most studies do not compare metabolic and functional effects of single and repeated cycles of IP. It was reported that compared to single IP, multiple IP does not improve myocardial protection [1,4,8] and even abolishes its beneficial effect [9,10]. This hinders the study of IP mechanisms and its use in clinical practice.…”

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confidence: 99%

Energy metabolism disturbances induced by multiple ischemic preconditioning worsen the recovery of cardiac function in reperfusion

1997

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Single ischelnic preconditioning improves functional recovery of isolated rat heart subjected to global ischemia and reperfusion. Two preconditioning cycles abolish this protective effect, while 4 cycles impair functional recovery of the heart. These phenomena are due to the fact that repetitive ischemic preconditioning reduces the content of phosphocreatine and adenine nucleotides in the heart before long-term ischemia, which prevents the recove13, of energy metabolism and induces additional damage to cardiomyocyte membranes during reperfusion.Key Words: rat heart; preconditioning; pump function; energy metabolism Repeated ischemia and reperfusion episodes protect the hem~ against prolonged ischemic and reperfusion stress. This so-called ischemic preconditioning (IP) is related to a decrease in the rate of phosphocreatine (Per) and ATP utilization and glycogenolysis during long-term ischelnia. This inhibits accumulation of catabolites and the development of acidosis in ischemized tissue and promotes recovery of oxidative respiration and cardiac function during subsequent reperfusion [7]. Most studies do not compare metabolic and functional effects of single and repeated cycles of IP. It was reported that compared to single IP, multiple IP does not improve myocardial protection [1,4,8] and even abolishes its beneficial effect [9,10]. This hinders the study of IP mechanisms and its use in clinical practice. The aim of the present study was to compare the effects of shlgle and multiple IP on functional and metabolic parameters of isolated working heart subjected to global ischemia. The study is focused on the assessment of cardiac function during reperfusion and determination of adenine MATERIALS AND METHODSHearts were isolated under urethane llarcosis (1.6-2.0 g/kg) flom Wistar rats weighing 250-300 g. The hearts were perfused by the method of R. Neely against constant Idling and resistance pressures of 20 and 90 cm H20 , respectively, with a I~'ebs--Henseleit bicarbonate buffer contahahag (in raM): 118 NaCI, 4.7 KC1, 3.0 CaC12, 0.5 Na2-EDTA , 1.2 KH2PO 4, 1.2 MgSO4, 25.0 NaHCO3, and 11.0 glucose, p H 7.4+ 0.1 at 37~ and oxygenated ~vith 95% O~ and 5% CO 2. Left ventricle pressure, coronary flow, and aortal pressure and output were recorded. Volume work was calculated as the product of cardiac output and mean aortal pressure; contractile fnnction was calculated as the product of developed pressure of the left ventricle and heart rate.In the control series the hea1~s were perfused for 50 lnin in a working regime for recording the initial parameters and then subjected to 15-rain global ischelnia and 30-rain reperfusion. The 50-min perfusion period was replaced with 3 types of IP. In the IP-I

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Moderate stress by cardiac pacing may induce both short term and long term cardioprotection

Abstract: The results suggest that brief periods of rapid pacing induce both short term and long term cardioprotection, as shown by reduced electrophysiological and haemodynamic consequences of subsequent pacing periods. Endogenous prostanoids might play a role in the short term cardioprotection.

Cited by 39 publications

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

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

Ectopic pacing at physiological rate improves postanoxic recovery of the developing heart

Energy metabolism disturbances induced by multiple ischemic preconditioning worsen the recovery of cardiac function in reperfusion

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