Role of Ammonia and Nitric Oxide in the Decrease in Plasma Prolactin Levels in Prehepatic Portal Hypertensive Male Rats

Scorticati, Camila; Perazzo, Juan Carlos; Rettori, Valéria; McCann, Samuel M.; Laurentiis, Andrea De

doi:10.1159/000097260

Cited by 6 publications

(4 citation statements)

References 61 publications

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“…Also, the increase in NOS activity and/or content in AP induced NO produc�� tion that directly inhibited PRL secretion from the AP, without the participation of the dopaminergic system. These results demonstrate the alteration of the neuroen�� docrine axis in a model of MHE and opens an interesting area of study that remains largely unexplored [161] .…”

Section: Neuroendocrine Axismentioning

confidence: 63%

“…�corticati et al [161] studied plasma prolactin (PRL) levels in our laboratory and the involvement of hyperammone�� mia, nitric oxide (NO) and dopaminergic and adrenergic systems in the control of this hormone secretion in a male rat model of mHE. The authors conducted in vivo studies to determine plasma ammonia and PRL levels, dopamine (DA), dihydroxyphenylacetic acid (DOPAC), epinephrine and norepinephrine content in medial basal hypothalamus (MBH) and anterior pituitary (APs).…”

Section: Neuroendocrine Axismentioning

confidence: 99%

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Hepatic encephalopathy: An approach to its multiple pathophysiological features

Perazzo¹,

Tallis²,

Delfante³

et al. 2012

WJH

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Hepatic encephalopathy (HE) is a neuropsychiatric complex syndrome, ranging from subtle behavioral abnormalities to deep coma and death. Hepatic encephalopathy emerges as the major complication of acute or chronic liver failure. Multiplicity of factors are involved in its pathophysiology, such as central and neuromuscular neurotransmission disorder, alterations in sleep patterns and cognition, changes in energy metabolism leading to cell injury, an oxidative/nitrosative state and a neuroinflammatory condition. Moreover, in acute HE, a condition of imminent threat of death is present due to a deleterious astrocyte swelling. In chronic HE, changes in calcium signaling, mitochondrial membrane potential and long term potential expression, N-methyl-D-aspartate-cGMP and peripheral benzodiazepine receptors alterations, and changes in the mRNA and protein expression and redistribution in the cerebral blood flow can be observed. The main molecule indicated as responsible for all these changes in HE is ammonia. There is no doubt that ammonia, a neurotoxic molecule, triggers or at least facilitates most of these changes. Ammonia plasma levels are increased two-to three-fold in patients with mild to moderate cirrhotic HE and up to ten-fold in patients with acute liver failure. Hepatic and inter-organ trafficking of ammonia and its metabolite, glutamine (GLN), lead to hyperammonemic conditions. Removal of hepatic ammonia is a differentiated work that includes the hepatocyte, through the urea cycle, converting ammonia into GLN via glutamine synthetase. Under pathological conditions, such as liver damage or liver blood by-pass, the ammonia plasma level starts to rise and the risk of HE developing is high. Knowledge of the pathophysiology of HE is rapidly ex-HE is rapidly ex-HE is rapidly expanding and identification of focally localized triggers has led the development of new possibilities for HE to be considered. This editorial will focus on issues where, to the best of our knowledge, more research is needed in order to clarify, at least partially, controversial topics.

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Section: Neuroendocrine Axismentioning

confidence: 63%

Section: Neuroendocrine Axismentioning

confidence: 99%

Hepatic encephalopathy: An approach to its multiple pathophysiological features

Perazzo¹,

Tallis²,

Delfante³

et al. 2012

WJH

View full text Add to dashboard Cite

show abstract

“…It showed that both the globus pallidus and AP could be involved in young CPSS patients. Studies in rats with portosystemic hepatic encephalopathy showed that although plasma catecholamines such as E and NE contents were significantly increased, there was no significant change in hypothalamic-APdopaminergic activity (25).…”

Section: Discussionmentioning

confidence: 96%

Quantitative Brain MRI Signal Differences in Children with Congenital Portosystemic Shunt Based on 3D T1-Weighted Sequence

Zhou,

Guo,

Zhu

et al. 2024

I J Radiol

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Background: Different degrees of T1-weighted (T1W) signal intensities in certain locations on brain magnetic resonance imaging (MRI) are characteristic features of neurological involvement in congenital portosystemic shunt (CPSS). Long-term accumulation of manganese (Mn) as a biomarker can lead to irreversible brain damage. Objectives: The aim of this study was to utilize quantitative brain MRI indicators to characterize brain signal differences in various regions in children with congenital portosystemic shunt. This may contribute to diagnosis, prognosis, and treatment decisions. Patients and Methods: This was a case-control study. Thirty-two patients diagnosed with CPSS based on at least one of the following imaging studies—abdominal ultrasound, Digital Subtraction Angiography (DSA), and Computed Tomography (CT)—and who underwent brain MRI prior to interventional treatment or surgery were included as the Case Group in this study. The age of these patients varied from 22 months to 15 years. Brain MRI of thirty children aged 2 to 15 years, identified without liver or structural diseases, were selected as the Control Group. The brain imaging protocol included an axial spin-echo T1-weighted image (T1WI), an axial T2-weighted image (T2WI), an axial diffusion-weighted imaging (DWI), an axial T2-fluid attenuated inversion recovery (FLAIR) sequence, and a sagittal gradient-echo 3D T1W thin-slice sequence, which can be reconstructed into axial and coronal planes. We utilized quantitative MRI assessment based on the 3D T1-weighted sequence to evaluate intracranial signal differences. The quantitative index was categorized into two types: Globus pallidus-to-frontal subcortical white matter Index (GFI) and anterior pituitary-to-pons Index (API). GFI and API were measured and statistically analyzed on the 3D T1W sequence between the Case Group and the Control Group. GFI of the Case Group was also measured and analyzed between the 3D T1W sequence and the standard T1W sequence. Correlation analysis was applied between the GFI ratios and ammonia levels, as well as between the API ratios and ammonia levels in the Case Group. The duration of the study was more than three months. Results: Significant differences in GFI and API were observed in the Case Group compared with the Control Group (P < 0.01). There was also a statistical difference in GFI between the 3D T1W sequence and the standard T1W sequence (P < 0.01). However, the GFI and API ratios were not correlated with ammonia levels (P > 0.05). The Pearson correlation values were 0.147 and 0.190, respectively. Conclusion: There was a correlation between different brain signals and congenital portosystemic shunt. Quantitative MRI assessment based on the 3D T1-weighted sequence could be used to evaluate these brain signal differences. A longitudinal study with multiple measurements would be beneficial for more accurately assessing such differences, enabling timely interventions, reducing complications, and avoiding lifelong drug therapy.

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“…Other alterations that have been described in this experimental model could also be related to the establishment of a low grade cerebral inflammatory response. These include, for example, an altered blood-brain barrier permeability [ 129 ], neuro-endocrine alterations [ 46 , 130 , 131 ] with a decreased uptake and an increased release of norepinephrine [ 130 ], an upregulation of tyrosin hydroxilase activity [ 132 ], as well as astrogliosis and angiogenesis in the hippocampus [ 133 ]. These functional, biochemical and morphological alterations may possibly help characterize portal hypertensive encephalopathy.…”

Section: Extra-splanchnic Alterations In Portal Hypertensionmentioning

confidence: 99%