Myocardial Energy Transport and Heart Failure

Portman, Michael A.; Zhang, Jianyi

doi:10.2174/1573403052952347

Cited by 5 publications

(4 citation statements)

References 94 publications

(150 reference statements)

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“…In addition, some authors also suggest the synchrony between CK kinetic and ATP level [43,44] . Therefore, preserved myocardial CK activity and improved ATPases activity after atorvastatin + isoproterenol treatment are in concurrence with earlier reports.…”

Section: Discussionmentioning

confidence: 99%

Effect of Atorvastatin Treatment on Isoproterenol-Induced Myocardial Infarction in Rats

Trivedi¹,

Balaraman²,

Majithiya³

et al. 2006

Pharmacology

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In the present study, chronic treatment of atorvastatin was evaluated on isoproterenol-induced myocardial infarction. Male Sprague-Dawley rats (200 ± 25 g) were randomized into the following four groups: (1) control group, (2) isoproterenol-treated group, (3) atorvastatin-treated group, and (4) isoproterenol- and atorvastatin-treated group. Various serum and tissue parameters as well as histopathological studies were carried out in all groups. Isoproterenol administration produced severe myocardial damage and oxidative stress in rats. Atorvastatin treatment reduced myocardial infarction which has been reflected by improvement in serum parameters, ATPase activities and histopathological lesions. However, it could not reduce oxidative stress and hypertrophy induced by isoproterenol. Hence, it can be concluded that atorvastatin may protect myocardial infarction induced by isoproterenol independent of its antioxidant properties.

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Section: Discussionmentioning

confidence: 99%

Effect of Atorvastatin Treatment on Isoproterenol-Induced Myocardial Infarction in Rats

Trivedi¹,

Balaraman²,

Majithiya³

et al. 2006

Pharmacology

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“…Previous studies indicate differences in energy metabolism in cardiac chambers (1,3,26,39,40) and show linkage between bioenergetic deficit and decompensation of heart performance (11,12,15,29,33,43,44,53,56) with potential benefit afforded by angiotensin-converting enzyme inhibitors (29). The bioenergetic profile of the failing atrium versus ventricle, especially in large animal models that closely mimic human heart failure, has, however, not been fully established, and it remains unknown whether strategies that inhibit RAAS would prevent metabolic distress imposed with disease (2,8,33).…”

mentioning

confidence: 99%

“…The bioenergetic profile of the failing atrium versus ventricle, especially in large animal models that closely mimic human heart failure, has, however, not been fully established, and it remains unknown whether strategies that inhibit RAAS would prevent metabolic distress imposed with disease (2,8,33). Thus the objectives of the present study were to characterize the bioenergetic response to pressure and volume overload of atria and ventricles in experimental congestive heart failure (CHF) and to establish the effectiveness of pharmacotherapy in preserving cardiac energetic parameters, including phosphotransfer enzyme function, using the prototypic vasopeptidase inhibitor omapatrilat.…”

mentioning

confidence: 99%

Bioenergetic protection of failing atrial and ventricular myocardium by vasopeptidase inhibitor omapatrilat

Mei

Dzeja²,

Redfield³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Deficient bioenergetic signaling contributes to myocardial dysfunction and electrical instability in both atrial and ventricular cardiac chambers. Yet, approaches capable to prevent metabolic distress are only partially established. Here, in a canine model of tachycardia-induced congestive heart failure, we compared atrial and ventricular bioenergetics and tested the efficacy of metabolic rescue with the vasopeptidase inhibitor omapatrilat. Despite intrinsic differences in energy metabolism, failing atria and ventricles demonstrated profound bioenergetic deficiency with reduced ATP and creatine phosphate levels and compromised adenylate kinase and creatine kinase catalysis. Depressed phosphotransfer enzyme activities correlated with reduced tissue ATP levels, whereas creatine phosphate inversely related with atrial and ventricular load. Chronic treatment with omapatrilat maintained myocardial ATP, the high-energy currency, and protected adenylate and creatine kinase phosphotransfer capacity. Omapatrilat-induced bioenergetic protection was associated with maintained atrial and ventricular structural integrity, albeit without full recovery of the creatine phosphate pool. Thus therapy with omapatrilat demonstrates the benefit in protecting phosphotransfer enzyme activities and in preventing impairment of atrial and ventricular bioenergetics in heart failure.

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“…In fact, a better preservation of myocardial adenine nucleotides and PCr may be of critical importance for maintaining cell membrane integrity and ion homeostasis, thus preventing irreversible damage of cardiomyocytes during reperfusion. [25] Various studies point out an emerging role of apelin in stimulation of glucose utilization in normal and insulin-resistant mice. [26] In the heart and skeletal muscle, apelin effects on glucose uptake and oxidation are attributed to the activation of eNOS, AMP-activated protein kinase (AMPK) and Akt-dependent pathways.…”

Section: Discussionmentioning

confidence: 99%

Effects of structural analogues of apelin-12 in acute myocardial infarction in rats

Писаренко

Serebryakova

Студнева

et al. 2013

J Pharmacol Pharmacother

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Objective:To examine cardioprotective effects of Ρ-terminal fragment of adipokine apelin-12 (A12), its novel structural analogue [MeArg1, NLe10]-A12 (I), and [d-Ala12]-A12 (II), a putative antagonist of APJ receptor, employing in vivo model of ischemia/reperfusion (I/R) injury.Materials and Methods:Peptides were synthesized by the automatic solid phase method using Fmoc technology. Anesthetized open-chest male Wistar rats were subjected to left anterior descending (LAD) coronary artery occlusion and coronary reperfusion. Hemodynamic variables and electrocardiogram (ECG) were monitored throughout the experiment. Myocardial injury was assessed by infarct size (IS), activity of necrosis markers in plasma, and metabolic state of the area at risk (AAR).Results:Intravenous injection of A12, I, or II at the onset of reperfusion led to a transient reduction of the mean arterial pressure. A12 or I administration decreased the percent ratio of IS/AAR by 40% and 30%, respectively, compared with control animals which received saline. Both peptides improved preservation of high-energy phosphates, reduced lactate accumulation in the AAR, and lowered CK-MB and LDH activities in plasma at the end of reperfusion compared with these indices in control. Treatment with II did not significantly affect either the IS/AAR, % ratio, or activities of both markers of necrosis compared with control. The overall metabolic protection of the AAR in the treated groups increased in the following rank: II < A12 < I.Conclusions:The structural analogue of apelin-12 [MeArg1, NLe10]-A12 may be a promising basis to create a new drug for the treatment of acute coronary syndrome.

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Myocardial Energy Transport and Heart Failure

Cited by 5 publications

References 94 publications

Effect of Atorvastatin Treatment on Isoproterenol-Induced Myocardial Infarction in Rats

Effect of Atorvastatin Treatment on Isoproterenol-Induced Myocardial Infarction in Rats

Bioenergetic protection of failing atrial and ventricular myocardium by vasopeptidase inhibitor omapatrilat

Effects of structural analogues of apelin-12 in acute myocardial infarction in rats

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