THE ROLE OF NITROGEN (II) OXIDE IN THE MECHANISMS OF THE EXPERIMENTAL HEPATOPULMONARY SYNDROME DEVELOPMENT
DOI:
https://doi.org/10.11603/mcch.2410-681X.2022.i4.13576Keywords:
liver, cirrhosis, tetrachloromethane, lungs, hepatopulmonary syndrome, nitrogen (II) oxideAbstract
Introduction. Liver cirrhosis is often accompanied by complications of the pulmonary system, which significantly reduces the life expectancy of such patients. Pulmonary complications of liver cirrhosis include hydrothorax, portopulmonary hypertension, and hepatopulmonary syndrome (HPS), the prevalence of which varies from 5 to 30 %. Nitrogen (II) oxide (NO) is involved in most metabolic processes occurring in the liver. Despite a large number of studies, today there are no clear ideas about the effect of NO and its metabolites on the biochemical mechanisms of the hepatopulmonary syndrome development.
The aim of the study – to investigate changes in the content of nitrogen (II) oxide metabolites in the blood serum and bronchoalveolar lavage of rats with simulated HPS and substantiate the role of NO in the mechanisms of lung damage in experimental HPS.
Research Methods. The experiments were carried out on 56 outbred male rats weighing 180–220 g. The first experimental model of HPS was created by applying a double ligature to the common biliary duct and then cutting it with a scalpel. The second experimental model of HPS was created by 8-week intragastric administration of an oily solution of carbon tetrachloride. Blood serum and bronchoalveolar lavage (BAL) were subjects for investigation. The content of NO metabolites was quantified by determining their sum, including nitrite ions previously present in the sample (NO2–) and nitrate ions reduced to nitrite (NO3–).
Results and Discussion. The total content of NO metabolites in the blood serum of rats on the 31st day after ligation of the common bile duct significantly increased by 3.9 times (p1<0.001) compared with the control group No. 1. In rats with carbon tetrachloride-induced cirrhosis, the total content of NO metabolites in blood serum increased by 3.1 times (p1<0.001). Changes in NO production occurred unidirectionally in the direction of deepening oxidative stress both in blood serum and in BAL.
Conclusions. When modeling HPS, nitroxidergic processes are activated due to a possible increase in the content of NO metabolites in the blood serum and BAL. When comparing the absolute values of the content of NO metabolites in the blood serum and BAL, a synchronous development of nitroxidergic processes at the systemic and local levels was revealed with a predominance of nitrogen (II) oxide synthesis in the lungs.
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