Acute myocardial infarction enhances the portal venous histamine level in dogs

Gyöngyösi, Mariann; Kaszaki, József; Wolfárd, Antal; Mojzes, L.; Németh, József; Jambrik, Z.

doi:10.1007/s000110050183

Cited by 5 publications

(5 citation statements)

References 25 publications

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“…Our finding of an elevation in serum histamine after AMI is consistent with previous studies 8 9 10 12 . The degranulation of mast cells 16 17 18 and activation of sympathetic nerves 30 were reported to be responsible for the immediate elevation of histamine after the onset of AMI, but mast cells are able to provide only a temporary pulse of histamine release.…”

Section: Discussionsupporting

confidence: 93%

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Histamine deficiency exacerbates myocardial injury in acute myocardial infarction through impaired macrophage infiltration and increased cardiomyocyte apoptosis

Deng

Hong

Lin

et al. 2015

Sci Rep

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Histamine is a biogenic amine that is widely distributed and has multiple functions, but the role it plays in acute myocardial infarction (AMI) remains unclear. In this study, we investigated the origin and contribution of endogenous histamine to AMI. Histidine decarboxylase (HDC) is the unique enzyme responsible for histamine generation. Using HDC-EGFP bacterial artificial chromosome (BAC) transgenic mice in which EGFP expression is controlled by the HDC promoter, we identified HDC expression primarily in CD11b+Gr-1+ immature myeloid cells (IMCs) that markedly increase in the early stages of AMI. Deficiency of histamine in HDC knockout mice (HDC−/−) reduced cardiac function and exacerbated the injury of infarcted heart. Furthermore, administering either an H1 receptor antagonist (pyrilamine) or an H2 receptor antagonist (cimetidine) demonstrated a protective effect of histamine against myocardial injury. The results of in vivo and in vitro assays showed that histamine deficiency promotes the apoptosis of cardiomyocytes and inhibits macrophage infiltration. In conclusion, CD11b+Gr-1+ IMCs are the predominant HDC-expressing sites in AMI, and histamine plays a protective role in the process of AMI through inhibition of cardiomyocyte apoptosis and facilitation of macrophage infiltration.

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Section: Discussionsupporting

confidence: 93%

“…Histamine is a biogenic amine which is widely distributed and has many functions 4 5 6 7 . Several studies have found that the levels of histamine in the serum and myocardium increased significantly in acute myocardial infarction (AMI) 8 9 10 11 12 . Mast cells have been considered to be the primary cellular source of histamine.…”

mentioning

confidence: 99%

Histamine deficiency exacerbates myocardial injury in acute myocardial infarction through impaired macrophage infiltration and increased cardiomyocyte apoptosis

Deng

Hong

Lin

et al. 2015

Sci Rep

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“…All dogs had baseline histamine concentrations that were within the range reported in the literature. 4,21 The assay used for plasma histamine concentration in our study is a verified method. 22 It is possible that IV administration of hydromorphone could induce histamine release from mast cells.…”

Section: Discussionmentioning

confidence: 87%

Effects of hydromorphone or oxymorphone, with or without acepromazine, on preanesthetic sedation, physiologic values, and histamine release in dogs

Smith

Yu²,

Bjorling³

et al. 2001

javma

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“…Histamine is a biogenic amine, which is widely distributed and possesses many biological functions 24 – 27 . There are growing researches including ours reporting that histamine in the serum and myocardium increased significantly after AMI 26 , 28 – 31 . Recent work demonstrated that histamine deficiency exacerbates AMI-induced cardiomyocyte apoptosis, indicating that endogenous histamine might exhibit a protective effect during MI 30 .…”

Section: Introductionmentioning

confidence: 94%

Histamine deficiency aggravates cardiac injury through miR-206/216b-Atg13 axis-mediated autophagic-dependant apoptosis

et al. 2018

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Histamine is a widely distributed biogenic amine involved in the regulation of an array of biological processes. Serum histamine level is markedly elevated in the early stages of acute myocardial infarction, whereas the role it plays remains unclear. Histidine decarboxylase (HDC) is the unique enzyme responsible for histamine production, and cardiac injury is significantly aggravated in HDC knockout mice (HDC−/−), in which histamine is deficient. We also observed that autophagy was highly activated in cardiomyocytes of HDC−/− mice post acute myocardial infarction (AMI), which was abolished by compensation of exogenous histamine. The in vivo and in vitro results showed that acting through histamine 1 receptor, histamine increased miR-206 and miR-216b, which worked in concert to target to Atg13, resulting in the reduction of autophagy activation under hypoxia and AMI condition. Further study revealed that Atg13 interacted with FADD to promote the activation of caspase-8 and cell apoptosis. Taken together, these data unveil a novel intracellular signaling pathway involved in histamine regulating myocardial autophagy and apoptosis under hypoxia and AMI condition, which might help to more comprehensively evaluate the usage of histamine receptor antagonists and to develop new therapeutic targets for myocardial infarction.

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Acute myocardial infarction enhances the portal venous histamine level in dogs

Abstract: Histamine is released into the gastrointestinal tract during acute myocardial ischemia and reperfusion, but the release of the vasoactive drug has no effect on systemic hemodynamics.

Cited by 5 publications

References 25 publications

Histamine deficiency exacerbates myocardial injury in acute myocardial infarction through impaired macrophage infiltration and increased cardiomyocyte apoptosis

Histamine deficiency exacerbates myocardial injury in acute myocardial infarction through impaired macrophage infiltration and increased cardiomyocyte apoptosis

Effects of hydromorphone or oxymorphone, with or without acepromazine, on preanesthetic sedation, physiologic values, and histamine release in dogs

Histamine deficiency aggravates cardiac injury through miR-206/216b-Atg13 axis-mediated autophagic-dependant apoptosis

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