Introduction. The pathogenesis of hepatopulmonary syndrome (HPS) has not been clarified, but since the basis of HPS development is the dilation of inner lung capillaries, researchers suggest that HPS is caused by the prolonged action of biologically active compounds on the blood vessels of pulmonary circuit and a syndrome of systemic inflammatory response has also been implicated in its development.
The objective of the study was to evaluate the indices of endogenous intoxication and inflammation in blood serum and lung tissue of animals with different models of hepatopulmonary syndrome.
Material and methods. The first experimental model of HPS was made by imposing a double ligature on common bile duct and its further dissection with a scalpel. The animals of second experimental group were fed with a mixture of maize flour, lard, cholesterol, and alcohol plus subcutaneously injection with carbon tetrachloride oil solution for 8 weeks. Determination of the middle mass molecules contents, TNF-α and CRP was carried out in blood serum and lung tissue.
Results. The modelling of HPS resulted in a statistically significant increase in endogenous intoxication, manifested by an increase in the content of MMM and inflammation indices in blood serum and supernatant of lung tissue homogenate. An increasing of middle mass molecules was more significant for a pool of МMМ2.
Conclusions. Comparing the indices of endogenous intoxication and inflammation in blood serum and lung tissue in both models of hepatopulmonary syndrome, we have found the synchronous development of destructive processes on systemic and local levels with predominance in lungs.
Keywords: endogenous intoxication, rats, hepatopulmonary syndrome.
Abbreviations: HPS – hepatopulmonary syndrome; MMM – middle mass molecules; TNF-α – tumor necrosis factor-α; CRP – C-reactive protein.Full text sources https://doi.org/10.31688/ABMU.2019.54.1.05 How to Cite Email to Author
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I. Horbachevsky Ternopil State Medical University, Ternopil, Ukraine
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