Cardiac and regional haemodynamic effects of histamine N-methyltransferase inhibitor metoprine in haemorrhage-shocked rats

Jochem, Jerzy

doi:10.1007/s00011-004-1268-y

Cited by 4 publications

(2 citation statements)

References 23 publications

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“…HNMT catalyzes the N ‐methylation of histamine thereby terminating its activity . In an experimental rat model of hypotension, central inhibition of HNMT, leads to activation of the histaminergic system and mobilization of compensatory cardiovascular mechanisms . HNMT activity gradually increases in both mouse and rat brain after birth and in mouse kidney the activity is about 60 times higher at maturation then at birth .…”

Section: Discussionmentioning

confidence: 99%

Validation of variants in SLC28A3 and UGT1A6 as genetic markers predictive of anthracycline‐induced cardiotoxicity in children

Visscher

Ross

Rassekh

et al. 2013

Pediatric Blood & Cancer

172

177

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Section: Discussionmentioning

confidence: 99%

Validation of variants in SLC28A3 and UGT1A6 as genetic markers predictive of anthracycline‐induced cardiotoxicity in children

Visscher

Ross

Rassekh

et al. 2013

Pediatric Blood & Cancer

172

177

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“…treatment rats were prepared 5-7 days before the experiment as previously described [6]. The right femoral artery was cannulated and three electrodes were implanted subcutaneously on the chest to measure MAP, PP and HR using the pressure transducer RMN-201 (Temed, Poland) and the electrocardiograph Diascope 2 (Unitra Biazet, Poland), respectively [8].…”

Section: Methodsmentioning

confidence: 99%

Influence of centrally acting amitriptyline and citalopram on histamine-induced cardiovascular effects in rats

2006

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Activation of the central histaminergic system mediates arachidonic-acid-induced cardiovascular effects

Altınbaş

Topuz

İlhan

et al. 2014

Can. J. Physiol. Pharmacol.

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The aim of this study was to explain the involvement of the central histaminergic system in arachidonic acid (AA)-induced cardiovascular effects in normotensive rats using hemodynamic, immunohistochemistry, and microdialysis studies. Intracerebroventricularly (i.c.v.) administered AA (0.25, 0.5, and 1.0 μmol) induced dose- and time-dependent increases in mean arterial pressure and decreased heart rate in conscious normotensive Sprague-Dawley rats. Central injection of AA (0.5 μmol) also increased posterior hypothalamic extracellular histamine levels and produced strong COX-1 but not COX-2 immunoreactivity in the posterior hypothalamus of rats. Moreover, the cardiovascular effects and COX-1 immunoreactivity in the posterior hypothalamus induced by AA (0.5 μmol; i.c.v.) were almost completely blocked by the H2 receptor antagonist ranitidine (50 and 100 nmol; i.c.v.) and partially blocked by the H1 receptor blocker chlorpheniramine (100 nmol; i.c.v.) and the H3-H4 receptor antagonist thioperamide (50 and 100 nmol; i.c.v.). In conclusion, these results indicate that centrally administered AA induces pressor and bradycardic responses in conscious rats. Moreover, we suggest that AA may activate histaminergic neurons and increase extracellular histamine levels, particularly in the posterior hypothalamus. Acting as a neurotransmitter, histamine is potentially involved in AA-induced cardiovascular effects under normotensive conditions.

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Cardiac and regional haemodynamic effects of histamine N-methyltransferase inhibitor metoprine in haemorrhage-shocked rats

Abstract: The results support the hypothesis that histaminergic system activation leads to mobilisation of compensatory mechanisms in haemorrhagic hypotension.

Cited by 4 publications

References 23 publications

Validation of variants in SLC28A3 and UGT1A6 as genetic markers predictive of anthracycline‐induced cardiotoxicity in children

Validation of variants in SLC28A3 and UGT1A6 as genetic markers predictive of anthracycline‐induced cardiotoxicity in children

Influence of centrally acting amitriptyline and citalopram on histamine-induced cardiovascular effects in rats

Activation of the central histaminergic system mediates arachidonic-acid-induced cardiovascular effects

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