Delayed Cardiac Protection Against Harmful Consequences of Stress can be Induced in Experimental Atherosclerosis in Rabbits

Szekeres, L.; Szilvássy, Zoltán; Ferdinándy, Péter; Nágy, I.; Karcsú, Sarolta; Csáti, S.

doi:10.1006/jmcc.1997.0418

Cited by 32 publications

(14 citation statements)

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“…1,24 Therefore, the findings are difficult to evaluate because the animal model was not one of pure hypercholesterolemia and because the significance of the end points selected is unclear. In addition, unlike the present study, neither of these investigations 22,23 used ischemia as the PC stimulus. The clinical relevance of tachycardia and lipopolysaccharide as PC stimuli is uncertain.…”

Section: Tang Et Al Hypercholesterolemia and Ischemic Pc 2153mentioning

confidence: 76%

“…With regard to the effect of hypercholesterolemia on late PC induced by stimuli other than ischemia, only 2 reports 22,23 are available besides our recent study. 9 In the first report, Szekeres et al 22 concluded that the protection induced by rapid ventricular pacing against the hemodynamic and electrophysiological changes caused by subsequent rapid overpacing was still present in cholesterol-fed rabbits, but a greater PC stimulus was required. These results were interpreted to suggest that hypercholesterolemia elevates the threshold for the PC response.…”

Section: Tang Et Al Hypercholesterolemia and Ischemic Pc 2153mentioning

confidence: 96%

“…In another study, Szilvassy et al 23 reported that the delayed protective effect induced by lipopolysaccharide against the hemodynamic and electrophysiological changes caused by ventricular overpacing was not abrogated in cholesterol-fed conscious rabbits. In both of these studies, 22,23 however, the experiments were performed in hypercholesterolemic rabbits with atherosclerotic lesions, which may have confounded the effects of hypercholesterolemia per se (ie, the presence of obstructive vascular disease may have caused ischemia); furthermore, the end points used were ST-segment elevation, left ventricular end-diastolic pressure, and shortening of the ventricular effective refractory period, not infarct size. These end points are not commonly used in studies of PC.…”

Section: Tang Et Al Hypercholesterolemia and Ischemic Pc 2153mentioning

confidence: 99%

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Hypercholesterolemia Abrogates Late Preconditioning via a Tetrahydrobiopterin-Dependent Mechanism in Conscious Rabbits

et al. 2005

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Background-Although the late phase of ischemic preconditioning (PC) is known to confer cardioprotection in healthy animal models, it is unknown whether this phenomenon exists in the presence of hypercholesterolemia. The goal of this study was to determine whether the infarct-sparing effect of late PC is affected by hypercholesterolemia and, if so, whether a tetrahydrobiopterin (BH 4 )-dependent mechanism is responsible for the loss of late PC. Methods and Results-Conscious rabbits fed a normal diet or a 1% cholesterol diet for 6 weeks were subjected to ischemic PC (six 4-minute coronary occlusion/4-minute reperfusion cycles) and, 24 hours later, underwent a 30-minute occlusion followed by 3 days of reperfusion. A total of 125 rabbits were used. In normocholesterolemic rabbits, ischemic PC reduced infarct size, an effect that was abrogated by administration of the BH 4 synthesis inhibitor N-acetylserotonin (15 mg/kg IV) before the 30-minute occlusion. In hypercholesterolemic rabbits, however, ischemic PC failed to reduce infarct size. Myocardial BH 4 levels in the ischemic zone increased 24 hours after ischemic PC in normocholesterolemic rabbits but not in hypercholesterolemic rabbits. In addition, in normocholesterolemic rabbits, pretreatment with N-acetylserotonin completely abolished the ischemic PC-induced increase in myocardial BH 4 levels. Conclusions-This study demonstrates that (1) hypercholesterolemia abrogates both the infarct-sparing effect of late PC and the concomitant upregulation of myocardial BH 4 , and (2)

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Section: Tang Et Al Hypercholesterolemia and Ischemic Pc 2153mentioning

confidence: 76%

Section: Tang Et Al Hypercholesterolemia and Ischemic Pc 2153mentioning

confidence: 96%

Section: Tang Et Al Hypercholesterolemia and Ischemic Pc 2153mentioning

confidence: 99%

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Hypercholesterolemia Abrogates Late Preconditioning via a Tetrahydrobiopterin-Dependent Mechanism in Conscious Rabbits

et al. 2005

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“…The interaction of hyperlipidemia with late preconditioning has been examined in only a few studies. In a conscious rabbit model of rapid cardiac pacing-induced demand ischemia, the authors were able to induce late cardioprotection in hyperlipidemic animals only when the number of cycles of preconditioning ischemia was increased compared with that applied in normolipidemic animals to induce late cardioprotection (Szekeres et al, 1997). This finding shows that the threshold stress to trigger cardioprotection is increased in experimental hyperlipidemia.…”

Section: Cardioprotection By Pre-and Postconditioning In Hyperlipidemiamentioning

confidence: 86%

Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning

Ferdinándy¹,

Schulz²,

Baxter³

2007

Pharmacol Rev

648

615

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“…Taken together, it is likely that hyperlipidemia modifies the effect of preconditioning to some extent but that the net result of this effect is critically dependent on the strength of the cardioprotective signals. This also applies to late preconditioning (199) and postconditioning (73). In fact, the same rabbit in the ischemia-reperfusion model was used to show the loss of the infarct limitation in response to late preconditioning (204).…”

Section: Comorbidities and Cardioprotection: Prevailing Knowledge Intmentioning

confidence: 99%

Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective measures

Shoji

Komuro

Kitakaze

2011

American Journal of Physiology-Heart and Circulatory Physiology

328

270

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Sanada S, Komuro I, Kitakaze M. Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective measures. Am J Physiol Heart Circ Physiol 301: H1723-H1741, 2011. First published August 19, 2011; doi:10.1152/ajpheart.00553.2011.-Heart diseases due to myocardial ischemia, such as myocardial infarction or ischemic heart failure, are major causes of death in developed countries, and their number is unfortunately still growing. Preliminary exploration into the pathophysiology of ischemia-reperfusion injury, together with the accumulation of clinical evidence, led to the discovery of ischemic preconditioning, which has been the main hypothesis for over three decades for how ischemia-reperfusion injury can be attenuated. The subcellular pathophysiological mechanism of ischemia-reperfusion injury and preconditioninginduced cardioprotection is not well understood, but extensive research into components, including autacoids, ion channels, receptors, subcellular signaling cascades, and mitochondrial modulators, as well as strategies for modulating these components, has made evolutional progress. Owing to the accumulation of both basic and clinical evidence, the idea of ischemic postconditioning with a cardioprotective potential has been discovered and established, making it possible to apply this knowledge in the clinical setting after ischemia-reperfusion insult. Another a great outcome has been the launch of translational studies that apply basic findings for manipulating ischemia-reperfusion injury into practical clinical treatments against ischemic heart diseases. In this review, we discuss the current findings regarding the fundamental pathophysiological mechanisms of ischemiareperfusion injury, the associated protective mechanisms of ischemic pre-and postconditioning, and the potential seeds for molecular, pharmacological, or mechanical treatments against ischemia-reperfusion injury, as well as subsequent adverse outcomes by modulation of subcellular signaling mechanisms (especially mitochondrial function). We also review emerging translational clinical trials and the subsistent clinical comorbidities that need to be overcome to make these trials applicable in clinical medicine. calcium overload; reactive oxygen species; mitochondria; transition pore; comorbidities; clinical trials WHAT DO WE KNOW ABOUT ischemia-reperfusion injury? Because the morbidity and mortality due to ischemic heart diseases have come to the fore in developed countries and are still increasing, it is critically important, both scientifically and socially, to know how cardioprotection is achieved in ischemic myocardium. In fact, in the clinical setting, the application of coronary thrombolysis or immediate percutaneous coronary intervention for faster recanalization has been shown to dramatically improve the outcomes of patients with acute or chronic myocardial ischemia due to impaired coronary blood supply. This finding is founded on the premise that a shorter period of index ischemia...

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Delayed Cardiac Protection Against Harmful Consequences of Stress can be Induced in Experimental Atherosclerosis in Rabbits

Cited by 32 publications

References 0 publications

Hypercholesterolemia Abrogates Late Preconditioning via a Tetrahydrobiopterin-Dependent Mechanism in Conscious Rabbits

Hypercholesterolemia Abrogates Late Preconditioning via a Tetrahydrobiopterin-Dependent Mechanism in Conscious Rabbits

Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning

Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective measures

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