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Hepatic injury induced by thioacetamide causes aortic endothelial dysfunction by a cyclooxygenase-dependent mechanism

M Nascimento1, R Piran1, R M Da Costa2

  • 1Institute of Health Science, Federal University of Mato Grosso, Sinop, MT, Brazil.

Life Sciences
|October 8, 2018
PubMed

Insights

Liver cirrhosis causes vascular hyporesponsiveness via cyclooxygenase (COX) activation, not nitric oxide (NO). This study in thioacetamide-induced liver injury reveals COX-2

Area of Science:

  • Cardiovascular Physiology
  • Hepatology
  • Pharmacology

Background:

  • Liver cirrhosis is linked to cardiovascular abnormalities like hyperdynamic circulation and cirrhotic cardiomyopathy.
  • Vascular dysregulations are key pathogenic mechanisms contributing to these cardiovascular changes.

Purpose of the Study:

  • To investigate if systemic vascular hyporesponsiveness in thioacetamide (TAA)-induced liver injury is mediated by nitric oxide (NO) or cyclooxygenase (COX) derivatives.
  • To elucidate the role of NO and COX pathways in vascular dysfunction associated with liver injury.

Main Methods:

  • Wistar rats were administered TAA for eight weeks to establish a liver injury model.
  • Aortic contractile responses to phenylephrine were assessed with and without endothelium, L-NAME, and indomethacin.
  • Protein expression of COX-2 and inducible nitric oxide synthase (iNOS) was analyzed.

Main Results:

  • TAA-induced liver injury reduced maximal contractile response to phenylephrine in rat aorta, dependent on the endothelium.
  • Impaired nitric oxide (NO) synthesis was observed, but NO pathways did not explain the reduced contractile response.
  • Cyclooxygenase (COX) inhibition with indomethacin normalized the contractile response, indicating a COX-dependent mechanism.
  • Increased protein expression of COX-2 and iNOS was found in the aorta of TAA-treated rats.
  • Systolic blood pressure was reduced in TAA-treated animals.

Conclusions:

  • Cyclooxygenase-2 (COX-2) activation significantly contributes to extra-hepatic vascular dysfunction in TAA-induced cirrhosis.
  • Inflammatory processes, evidenced by increased COX-2 and iNOS expression, are present in the aorta of rats with liver injury.

Keywords:
AortaCyclooxygenaseLiver injuryThioacetamideVascular reactivity

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