Myocardial Serotonin during Ischemia under Conditions of Ischemic Preconditioning

Naumenko, S. E.; Latysheva, T. V.; Gilinskii, M. A.

doi:10.1007/s10517-014-2590-1

Cited by 2 publications

(2 citation statements)

References 9 publications

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“…The authors hypothesized that serotonin released by mast cells and sympathetic nerve endings could be responsible for deleterious effects resulting from 5‐HT2A receptor activation during myocardial ischemia, whereas extracardiac serotonin, on the contrary, could elicit protective vasodilatation in the I/R injury context. Naumenko et al reported peak serotonin levels in the myocardial interstitium immediately after preconditioning in a rat model. Serotonin interstitial concentrations increased during ischemia and reperfusion in both preconditioned and control rats, with a more pronounced increase observed in the control group.…”

Section: Discussionmentioning

confidence: 99%

Metabolic Signature of Remote Ischemic Preconditioning Involving a Cocktail of Amino Acids and Biogenic Amines

Barca

Bakhta

Kalakech

et al. 2016

JAHA

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BackgroundRemote ischemic preconditioning (RIPC) is an attractive therapeutic procedure for protecting the heart against ischemia/reperfusion injury. Despite evidence of humoral mediators transported through the circulation playing a critical role, their actual identities so far remain unknown. We sought to identify plasmatic RIPC‐induced metabolites that may play a role.Methods and ResultsRat plasma samples from RIPC and control groups were analyzed using a targeted metabolomic approach aimed at measuring 188 metabolites. Principal component analysis and orthogonal partial least‐squares discriminant analysis were used to identify the metabolites that discriminated between groups. Plasma samples from 50 patients subjected to RIPC were secondarily explored to confirm the results obtained in rats. Finally, a combination of the metabolites that were significantly increased in both rat and human plasma was injected prior to myocardial ischemia/reperfusion in rats. In the rat samples, 124 molecules were accurately quantified. Six metabolites (ornithine, glycine, kynurenine, spermine, carnosine, and serotonin) were the most significant variables for marked differentiation between the RIPC and control groups. In human plasma, analysis confirmed ornithine decrease and kynurenine and glycine increase following RIPC. Injection of the glycine and kynurenine alone or in combination replicated the protective effects of RIPC seen in rats.ConclusionsWe have hereby reported significant variations in a cocktail of amino acids and biogenic amines after remote ischemic preconditioning in both rat and human plasma.Clinical Trial RegistrationURL: http://www.clinicaltrials.gov. Unique identifier: NCT01390129.

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Section: Discussionmentioning

confidence: 99%

Metabolic Signature of Remote Ischemic Preconditioning Involving a Cocktail of Amino Acids and Biogenic Amines

Barca

Bakhta

Kalakech

et al. 2016

JAHA

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“…Myocardial ischemia refers to a decrease in blood perfusion in the heart, resulting in conditions such as hypoxia and abnormal energy metabolism [15,16]. CHD is the main cause of myocardial ischemia.…”

Section: Discussionmentioning

confidence: 99%

Xuan Bi Tong Yu Fang Promotes Angiogenesis via VEGF‐Notch1/Dll4 Pathway in Myocardial Ischemic Rats

Dong

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Objective. To investigate the effect of Xuan Bi Tong Yu Fang (XBTYF) on angiogenesis via the vascular endothelial growth factor- (VEGF-) Notch1/delta-like 4 (Dll4) pathway. Materials and Methods. Sixty Sprague-Dawley rats were randomly divided into six groups: control, sham-operated, myocardial ischemia model, and XBTYF treatment at 3.2, 1.6, and 0.8 g/kg. Electrocardiography was performed to evaluate the successful establishment of the model. Hematoxylin-eosin staining and transmission electron microscopy were carried out to observe the morphology and mitochondrial structure in myocardial cells, respectively. TUNEL staining was performed to assess the degree of cell apoptosis. The expression of VEGF-A, Notch1, Dll4, Bcl2, Bax, caspase 3, caspase 9, and cytochrome-c (Cyt-c) was observed by western blot. Results. XBTYF inhibited changes to the morphology and mitochondrial structure in cardiomyocyte and reduced cell apoptosis. Compared with the model group, XBTYF at all doses (3.2, 1.6, and 0.8 g/kg) reduced the expression of Notch1, Dll4, Bax, caspase 3, caspase 9, and Cyt-c, whereas expression of VEGF-A and Bcl2 was increased. Conclusion. XBTYF attenuated mitochondrial damage and cell apoptosis while promoting the angiogenesis of cardiomyocyte. The associated mechanism may be related to the VEGF-Notch1/Dll4 pathway.

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Myocardial Serotonin during Ischemia under Conditions of Ischemic Preconditioning

Cited by 2 publications

References 9 publications

Metabolic Signature of Remote Ischemic Preconditioning Involving a Cocktail of Amino Acids and Biogenic Amines

Metabolic Signature of Remote Ischemic Preconditioning Involving a Cocktail of Amino Acids and Biogenic Amines

Xuan Bi Tong Yu Fang Promotes Angiogenesis via VEGF‐Notch1/Dll4 Pathway in Myocardial Ischemic Rats

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