Oxidative stress as one of the pathogenetic mechanisms of hepatopulmonary syndrome in patients with liver cirrhosis

Abstract

Background. Hepatopulmonary syndrome is one of the most dangerous syntropies in case of liver cirrhosis. Consequently, it is important to determine the role of oxidative stress, acid-base balance and ventilation-perfusion disorders as factors of hepatopulmonary syndrome development in cirrhotic patients. Materials and methods. We included 44 cirrhotic patients with hepatopulmonary syndrome verified according to the patented Method for diagnosing degrees of hepatopulmonary syndrome severity in patients with liver cirrhosis. In addition to the traditional examinations, we determined the gas composition parameters in venous blood, acid-base balance parameters, catalase activity and malondialdehyde level in all the patients. The received material was processed on a personal computer using Excel 2010, Statistica 6.0, RStudio v. 1.1.442 and R Commander v. 2.4-4. Results. Analysis of blood gas parameters revealed the reliability of the difference for PCO2 (р = 0.03) depending on the class of liver cirrhosis severity. Also, with the liver cirrhosis severity increase, the malondialdehyde level increased, and catalase decreased. Moreover, significant inverse relationships between malondialdehyde content and PCO2 (p = 0.039), HCO3 (p = 0.039), TCO2 (p = 0.036), Beb (p = 0.049), BEecf (p = 0.043) were found resulting in hypocapnia and partially compensated metabolic acidosis. The found direct correlation between malondialdehyde level and AaDO2 (p = 0.044) indicates the arteriovenous pulmonary shunts, ventilation-perfusion disorders. The absence of catalase content changes can obviously be explained by the fact that its activity can be partially compensatory maintained. Conclusions. In patients with hepatopulmonary syndrome, the peroxidation activity enhances with an increase in the liver cirrhosis severity, resulting in the redox homeostasis imbalance, leading to the ventilation-perfusion disorders and partially compensated metabolic acidosis.

Keywords

• liver cirrhosis
• hepatopulmonary syndrome
• intrapulmonary vasodilatation
• oxidative stress
• metabolic acidosis