Effect of induced hepatic dysfunction on the innervation of the rat heart

      Alteration of the heart innervation, humoral and nervous dysregulation, changes in systemic circulation and electrophysiological abnormalities are the factors involved in cardiovascular complications of cirrhosis. Tyrosine hydroxylase (TH) is enzyme participating in synthesis of a principal sympathetic neurotransmitter noradrenalin (NA). Neuropeptide Y (NPY) is a cotransmitter of NA and is localized in the heart ganglia. The aim of this investigation was to study the influence of experimentally induced hepatic dysfunction on the intracardiac nervous systems. Hepatic dysfunction was induced by application of thioacetamide (TAA) for 12 weeks or by ligation of biliary duct. Controls received an equivalent injection of saline. Biochemical parameters of hepatic injury and levels of peroxidation in the liver, heart and kidneys were measured. Relative expressions of mRNAs for TH and NPY were expressed as a ratio of target gene Cq value to Cq value of reference gene. In the left atrium of operated rats, the expression of TH of animals was lower, while expression of NPY remained unchanged. The expression of TH and NPY in TAA group remained unchanged. Liver enzymes measured in plasma were significantly elevated. Level of peroxidation was increased in the liver of the TAA group, while operated animals showed reduction. Glutathione concentration in the plasma was significantly increased in both groups. Liver injury induced by ligation leads to imbalance in the intracardiac nervous innervation, while chronic administration of TAA does not alter expression of tested mediators in the heart. Support: CZ.1.05/2.1.00/03.0076 from European Regional Development Fund and Charles University Research Fund (P36).
      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'


      Subscribe to Autonomic Neuroscience: Basic and Clinical
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect