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Expression of classical mediators in hearts of rats with hepatic dysfunction
Dagmar Jarkovska1,2, Monika Bludovska1,3, Eliska Mistrova1,2
1a Biomedical Center, Faculty of Medicine in Pilsen, Charles University, alej Svobody 1655/76, Pilsen 323 00, Czech Republic.
Insights
Experimental liver injury in rats alters heart nerve function. Bile duct ligation reduced key enzymes for noradrenaline synthesis in the heart, suggesting impaired cardiac nervous control in hepatic dysfunction.
Area of Science:
- Cardiovascular Physiology
- Hepatology
- Neuroendocrinology
Background:
- Liver cirrhosis significantly impacts cardiovascular function, affecting heart innervation and systemic circulation.
- Key neurotransmitter synthesis enzymes like choline acetyltransferase (ChAT) and those involved in noradrenaline synthesis (tyrosine hydroxylase [TH], dopamine-β-hydroxylase [DBH]) are crucial for cardiac autonomic control.
- Atrial natriuretic peptide (ANP) is also implicated in cardiac function during liver disease.
Purpose of the Study:
- To investigate the effects of experimentally induced hepatic dysfunction on the cardiac expression of proANP, ChAT, TH, and DBH.
- To assess the relationship between liver injury models and alterations in intracardiac neurotransmitter synthesis pathways.
Main Methods:
- Hepatic dysfunction was induced in rats using thioacetamide (TAA) or bile duct ligation (BDL).
- Biochemical markers of hepatic injury and lipid peroxidation in the liver and heart were measured.
- Gene expression levels of proANP, ChAT, TH, and DBH in the heart were analyzed.
Main Results:
- Elevated plasma liver enzymes confirmed hepatic injury in both models.
- Cardiac lipid peroxidation increased in the BDL group but not in the TAA group.
- In BDL rats, left atrial expression of TH and DBH was significantly reduced, while ChAT expression remained unchanged compared to controls.
Conclusions:
- Experimental liver injury induced by bile duct ligation leads to an imbalance in intracardiac innervation.
- Reduced expression of TH and DBH suggests impaired noradrenergic neurotransmission in the heart during hepatic dysfunction.
- These neurochemical changes may contribute to the impaired nervous control of the heart observed in liver disease.
Abstract:
Liver cirrhosis is associated with impairment of cardiovascular function including alterations of the heart innervation, humoral and nervous dysregulation, changes in systemic circulation and electrophysiological abnormalities. Choline acetyltransferase (ChAT), enzyme forming acetylcholine, tyrosine hydroxylase (TH), and dopamine-β-hydroxylase (DBH), enzymes participating in noradrenaline synthesis, are responsible for the production of classical neurotransmitters, and atrial natriuretic peptide (ANP) is produced by cardiomyocytes. The aim of this study was to evaluate the influence of experimentally induced hepatic dysfunction on the expression of proANP, ChAT, TH, and DBH in the heart. Hepatic dysfunction was induced by application of thioacetamide (TAA) or by ligation of bile duct. Biochemical parameters of hepatic injury and levels of peroxidation in the liver and heart were measured. Liver enzymes measured in the plasma were significantly elevated. Cardiac level of peroxidation was increased in operated but not TAA group animals. In the left atrium of operated rats, the expression of TH and DBH was lower, while expression of ChAT remained unchanged. In TAA group, no significant differences in the expression of the genes compared to controls were observed. Liver injury induced by ligation leads to an imbalance in the intracardiac innervation, which might impair nervous control of the heart.
