Myocardial interstitial levels of serotonin and its major metabolite 5-hydroxyindole acetic acid during ischemia-reperfusion

Du, Cheng-Kun; Zhan, Dong Yun; Akiyama, Tsuyoshi; Shishido, Toshiaki; Shirai, Masamitsu; Pearson, James T.

doi:10.1152/ajpheart.00471.2016

Cited by 15 publications

(25 citation statements)

References 35 publications

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“…Furthermore, estimated 5‐HT turnover rate during reperfusion indicated that turnover of the accumulated 5‐HT was dramatically suppressed by the inhibition of PMAT. This effect was not observed by inhibition of SERT (Du et al, ), moreover it was similar to the effect of MAO inhibition by pargyline as we reported previously (Du et al, ). We have also demonstrated MAO‐dependent production of hydroxyl radical in the heart during ischemia and reperfusion (Inagaki et al, ).…”

Section: Discussionsupporting

confidence: 91%

“…The first dialysate sampling was started from at least 2 hr after the probe implantation. Serotonin concentration in the dialysate sample was measured by electro‐chemical detection coupled with high performance liquid chromatography (HPLC‐ECD, Eicom) as described previously (Du et al, , ; Sonobe et al, ).…”

Section: Methodsmentioning

confidence: 99%

“…In our previous study using in vivo cardiac microdialysis technique in anesthetized rabbits (Sonobe et al, 2013) and rats (Du et al, 2017), we observed that local administration of SERT inhibitor fluoxetine had no effect on the clearance of accumulated 5-HT in the heart. This data implied the contribution of fluoxetine-resistant 5-HT transporters, such as extra-neuronal monoamine transporters (Furihata & Anzai, 2017), to remove 5-HT from the interstitial space.…”

mentioning

confidence: 89%

“…Dialysate from the myocardial interstitium was sampled and then analyzed using HPLC-ECD. A silk suture was passed around the coronary artery and occluded as necessary performance liquid chromatography (HPLC-ECD, Eicom) as described previously (Du et al, 2017Sonobe et al, 2013).…”

Section: Cardiac Microdialysis Techniquementioning

confidence: 99%

“…Serotonin (5‐hydroxytryptamine, 5‐HT) accumulates in the heart during cardiac ischemia (Du et al, ; Shimizu et al, ; Sonobe, Akiyama, Du, Zhan, & Shirai, ). The increased myocardial interstitial level of 5‐HT directly induces myocardial cell injury through 5‐HT receptor‐dependent coronary vasoconstriction (Golino et al, ; Métais, Bianchi, Li, Simons, & Sellke, ), platelet aggregation (Willerson, Golino, Eidt, Campbell, & Buja, ), and overactivation of afferent cardiac sympathetic nerves (Fu & Longhurst, ; Longhurst, Tjen‐A‐Looi, & Fu, ).…”

Section: Introductionmentioning

confidence: 99%

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Serotonin uptake via plasma membrane monoamine transporter during myocardial ischemia‐reperfusion in the rat heart in vivo

Sonobe

Akiyama

et al. 2019

Physiol Rep

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Serotonin (5‐HT) accumulates in the heart during myocardial ischemia and induces deleterious effects on the cardiomyocytes through receptor‐dependent and monoamine oxidase‐dependent pathways. We aimed to clarify the involvement of extra‐neuronal monoamine transporters in the clearance of 5‐HT during ischemia and reperfusion in the heart. Using a microdialysis technique in the anesthetized Wistar rat heart, we monitored myocardial interstitial 5‐HT and 5‐hydroxyindole acetic acid (5‐HIAA) concentration by means of electro‐chemical detection coupled with high‐performance liquid chromatography (HPLC‐ECD). Effects of inhibitors of the plasma membrane monoamine transporter (PMAT) and the organic cation transporter 3 (OCT3) (decynium‐22 and corticosterone) on the 5‐HT and 5‐HIAA concentrations during baseline, coronary occlusion, and reperfusion were investigated. Basal dialysate 5‐HT concentration were increased by local administration of decynium‐22, but not by corticosterone. Addition of fluoxetine, a serotonin transporter (SERT) inhibitor further increased the 5‐HT concentration upon during administration of decynium‐22. Decynium‐22 elevated the background level of 5‐HT during coronary occlusion and maintained 5‐HT concentration at a high level during reperfusion. Production of 5‐HIAA in the early reperfusion was significantly suppressed by decynium‐22. These results indicate that PMAT and SERT independently regulate basal level of interstitial 5‐HT, and PMAT plays a more important role in the clearance of 5‐HT during reperfusion. These data suggest the involvement of PMAT in the monoamine oxidase‐dependent deleterious pathway in the heart.

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Section: Discussionsupporting

confidence: 91%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 89%

Section: Cardiac Microdialysis Techniquementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Serotonin uptake via plasma membrane monoamine transporter during myocardial ischemia‐reperfusion in the rat heart in vivo

Sonobe

Akiyama

et al. 2019

Physiol Rep

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Monoamine oxidase-A, serotonin and norepinephrine: synergistic players in cardiac physiology and pathology

2018

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The mitochondrial enzyme monoamine oxidase A (MAO-A) is widely distributed in neuronal, myocyte and non-myocyte cardiac compartments. After the demonstrations that both cardiac neuronal and extraneuronal MAO-A contribute to the degradation of norepinephrine and serotonin, several studies attempted to determine the impact of MAO-A activity in the control of local concentration of the two biogenic amines and in their receptor-mediated effects. From the 2000s, an additional mechanism of action of MAO-A has been proposed. Such mechanism involves hydrogen peroxide (HO) production during substrate degradation. This finding stimulated a growing interest on the role of MAO-A-dependent oxidative stress in cardiac pathophysiology. Altogether, the results obtained by different groups showed that MAO-A played a key role in the regulation of physiological cardiac function and in the development of acute and chronic heart diseases through two mechanisms: the regulation of substrate concentrations and the intracellular production of reactive oxygen species. In this review, we will give an overview of the major results on the role of MAO-A in the field of cardiac diseases.

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Cardiomyocytes-specific deletion of monoamine oxidase B reduces irreversible myocardial ischemia/reperfusion injury

Heger

Hirschhäuser

Bornbaum

et al. 2021

Free Radical Biology and Medicine

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Myocardial interstitial levels of serotonin and its major metabolite 5-hydroxyindole acetic acid during ischemia-reperfusion

Cited by 15 publications

References 35 publications

Serotonin uptake via plasma membrane monoamine transporter during myocardial ischemia‐reperfusion in the rat heart in vivo

Serotonin uptake via plasma membrane monoamine transporter during myocardial ischemia‐reperfusion in the rat heart in vivo

Monoamine oxidase-A, serotonin and norepinephrine: synergistic players in cardiac physiology and pathology

Cardiomyocytes-specific deletion of monoamine oxidase B reduces irreversible myocardial ischemia/reperfusion injury

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