Long term effects of portocaval anastomosis in rats on brain levels of histamine and methylhistamine

Lozeva, V.; MacDonald, Ewen; Belcheva, A.; Hippeläinen, Mikko; Kosunen, H.; Fogel, Adam; Maśliński, Cz.; Tuomisto, Leena

doi:10.1007/bf01674393

Cited by 7 publications

(11 citation statements)

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“…Recently it was reported that increased amounts of the histamine catabolite, tele-methylhistamine, were found in some brain areas after several months of portocaval shunt [3]. Adaptation to PCA could involve cellular redistribution of brain histamine.…”

Section: Introductionmentioning

confidence: 99%

“…These high levels seem to result from accumulation of the amine produced in brain due to persistent saturation of histidine decarboxylase with L-histidine and no compensatory changes in histamine utilisation and catabolism [1,2]. Preliminary data [1] suggest that histamine is located in neurones.Recently it was reported that increased amounts of the histamine catabolite, tele-methylhistamine, were found in some brain areas after several months of portocaval shunt [3]. Adaptation to PCA could involve cellular redistribution of brain histamine.…”

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confidence: 99%

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An attempt to disclose brain histamine localisation in portocaval shunted rats

Fogel¹,

Sasiak²,

Andrzejewski³

1999

Inflammation Research

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IntroductionRats with portocaval anastomosis (PCA) exhibit 2-10 fold higher cerebral histamine concentrations than do control rats. These high levels seem to result from accumulation of the amine produced in brain due to persistent saturation of histidine decarboxylase with L-histidine and no compensatory changes in histamine utilisation and catabolism [1,2]. Preliminary data [1] suggest that histamine is located in neurones.Recently it was reported that increased amounts of the histamine catabolite, tele-methylhistamine, were found in some brain areas after several months of portocaval shunt [3]. Adaptation to PCA could involve cellular redistribution of brain histamine. We examined this possibility by a biochemical approach. Materials and methodsPCA rats (n = 18) and corresponding controls (SHAM, n = 12) were used 1.5 and 14 months after surgery performed according to Lee and Fisher [4]. The dissected brains were trimmed of cerebellum and brain stem. Subcellular fractionation of the brain was achieved by differential centrifugation using a modification of the Whittaker procedure [5]. Isolation of astrocyte-and neurone-enriched fractions was performed as described by Farooq and Norton [6] employing a discontinuous Ficoll gradient. Histamine concentrations were measured by radioenzymatic assay employing partially purified rat kidney histamine N-methyltransferase as described elsewhere [1] or RIA (Immunotech S.A., Marseille, France). The results are given as means ± SEM. Differences between groups were assessed with the unpaired t-test. Statistical evaluation was performed using an IBM PC with Prizma GraphPad Inc. USA software. Results and discussionShunted rats had significantly lower body and liver weights than their sham operated counterparts (body weight: 1.5 months after surgery 228 ± 20 g vs. 363 ± 26 g, p < 0.01; 14 months after surgery 324 ± 18 g vs. 504 ± 12 g, p < 0.001 and liver weight: 1.5 months after surgery 4.1 ± 0.46 g vs. 10.3 ± 1.89 g, p < 0.01; 14 months after surgery 6.1 ± 0.37 g vs. 14.9 ± 0.40 g, p < 0.001). The liver index (liver to body weight ratio ¥ 100), a measure of the organ atrophy, was approximately 35% smaller in PCA rats at 1.5 months after surgery and remained similar at 14 months, suggesting stabilised shunt conditions (p < 0.001).In the two groups of sham rats, the cerebral histamine distribution and histamine concentrations did not differ and therefore the values were combined as one control. The percent contribution of each subcellular fraction to the total tissue histamine content was very similar between sham and portocaval shunted rats (Fig. 1a). The higher histamine content in the cytosolic fraction indicates more loosely bound amine in shunted rats. When expressed in pmol/mg protein there is a clear difference in histamine levels between sham and PCA groups (Fig. 1b), which supports our previous findings [1,2]. However, the time since the establishment of the portocaval shunt did not have a significant effect, as the histamine values in the two groups overlapped due to h...

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Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

An attempt to disclose brain histamine localisation in portocaval shunted rats

Fogel¹,

Sasiak²,

Andrzejewski³

1999

Inflammation Research

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“…Possibly, the inherent level of turnover rate and release of brain histamine of individual animals would determine their propensity to release neurotransmitter when H3 histamine autoreceptors are pharmacologically blocked. In fact, both enhancement of thioperamide-induced histamine release (Anttila et al, 1995) and increased levels of t-methylhistamine are seen in PCA-operated rats (Fogel et al, 1994;Lozeva et al, 1995). The slightly larger EEG activity change in PCA rats with thioperamide may be a physiological consequence related to intensified release of brain histamine in PCA rats.…”

Section: Discussionmentioning

confidence: 86%

“…In contrast to transient changes of histaminergic activity induced by thioperamide, the portocaval anastomosis (PCA) operation of the liver not only permanently elevates the brain histamine level (Fogel et al, 1991(Fogel et al, , 1994Imura et al, 1986;Lozeva et al, 1995; but also permanently renders animals more liable to release histamine by thioperamide (Anttila et al, 1995). Hence, those plausible histaminergic modes of actions described above were examined both in unoperated controls and in PCA-operated rats.…”

Section: Introductionmentioning

confidence: 98%

Histaminergic modulation of neocortical spindling and slow-wave activity in freely behaving rats

Valjakka

Vartiainen

Kosunen

et al. 1996

J. Neural Transmission

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Histaminergic H3 receptor antagonists stimulate neuronal histamine release and could consequently have a number of physiological effects in the brain. The effects of H3 receptor blockade, induced by systemically administered thioperamide, were assessed on the frontal cortex electroencephalographic (EEG) properties in freely behaving rats. The relationship of EEG activity variables to endogenous brain histaminergic markers was also examined, both in controls and in portocaval anastomosis (PCA)-operated rats (which show increased levels of brain histamine and t-methylhistamine). Thioperamide reduced the incidence of thalamus-regulated EEG spindles, while it slightly increased their amplitude. It furthermore reduced the spectral power of low-frequency (1.5-5Hz) EEG, which effect was equally distributed over the spindle and non-spindle EEG states. These EEG effects were accompanied by increased motor activity of the animals. Both the low-frequency EEG activity and spindle incidence correlated inversely with the histamine level of the brain (hypothalamus and cerebellum excluded) while t-methylhistamine level correlated with the degree of thioperamide-induced reduction of slow-wave EEG activity. The present results provide evidence for the involvement of endogenous brain histamine level, histamine release (as assessed by t-methylhistamine level) and H3 receptors in the histaminergic regulation of neocortical synchronization patterns assumed to be linked to arousal control.

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The effect of in vivo deprenyl on cerebral amine system in rats with portocaval shunts

Fogel¹,

Andrzejewski²,

Sasiak³

et al. 2000

Inflamm. res.

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There is an excessive formation of amine neuromediators in the brain after portocaval shunt which is counterbalanced by enhanced degradation (serotonin, dopamine, methylhistamine) and/or deposition (histamine) [1][2][3]. In normal rat brains, serotonin, adrenaline and noradrenaline are metabolised predominantly by MAO-A, whereas the preferred substrates for MAO-B are phenylethylamine and methylhistamine. The Km of rat brain MAO-B enzyme towards serotonin is about ten times higher than that of MAO-A. Thus, at low substrate concentrations the metabolism of 5HT is essentially due to MAO-A [4]. The situation may however be different at the high amine levels that may be saturable for MAO-B. To address this possibility, rats with portocaval anastomosis (PCA) were treated with an irreversible monoamine oxidase B (MAO-B) inhibitor, deprenyl [5]. Materials and methodsPortocavally shunted (PCA) rats and corresponding controls (SHAM) were operated according to Lee and Fisher [6]. Animal procedures complied with Polish legislation concerning animal experimentation and were approved by the local care committee. From 5 th to 26 th day after surgery groups of 5 -7 rats were treated twice a week with a dose of 0.5 mg/kg deprenyl HCL (RBI Natick, USA) s.c. and were sacrificed on the 28 th day. To estimate amine concentrations and MAO-A and MAO-B activities, brain and liver samples were collected. The dissected brains were trimmed of cerebellum and brain stem and divided into two partshypothalamus and the rest of the brain.Indole and catechol compounds were examined by HPLC with electrochemical detection, brain and hepatic histamine by radioenzymatic and column chromatographic assays, respectively. Enzyme activities were measured with radiometric methods [1,2].The results are given as means ± SEM. Differences between groups were assessed with the unpaired Student's t-test. Statistical evaluation was performed using an IBM PC with Prizma GraphPad Inc. USA software. Fig. 1. The effect of deprenyl treatment on brain amine system in portocaval shunted (PCA) rats. The data are given as means ± SEM for groups of 5 -7 rats. The results have been normalised to the values for non drug treated animals (100 %). 5-HIAA-5-hydroxyindoleacetic acid; 5HT-serotonin;

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Long term effects of portocaval anastomosis in rats on brain levels of histamine and methylhistamine

Cited by 7 publications

References 6 publications

An attempt to disclose brain histamine localisation in portocaval shunted rats

An attempt to disclose brain histamine localisation in portocaval shunted rats

Histaminergic modulation of neocortical spindling and slow-wave activity in freely behaving rats

The effect of in vivo deprenyl on cerebral amine system in rats with portocaval shunts

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