Analysis of histochemical changes in neutrophils during experimental hypoxic hepatitis

This study examined changes in the cytochemical status of neutrophils following experimental modeling of hypoxic hepatitis in rats. The experiment was conducted on 40 white rats divided into two groups: Group I (control, intact animals) and Group II (experimental), which included subgroups examined 5 days (subgroup A), 10 days (subgroup B), and 15 days (subgroup C) after induction of hypoxic hepatitis. The severity of liver injury was assessed by measuring the activity of hepatic enzymes alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyltransferase (GGT). To evaluate changes in neutrophils, blood smears were prepared from samples collected before and after modeling hypoxic hepatitis at the specified time points. The cytochemical content of succinate dehydrogenase (SDH), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, myeloperoxidase (MPO), acid phosphatase (AP), alkaline phosphatase (ALP), glycogen (GL), and phospholipids (PL) in neutrophils was determined using standard cytochemical methods. The results demonstrated that hypoxic hepatitis was accompanied by a significant progressive increase in ALT, AST, and GGT activity within 15 days following the development of systemic hypoperfusion and hepatic hypoxia. These changes correlated with alterations in the cytochemical parameters of circulating neutrophils, including a gradual increase in the activity of mitochondrial (SDH, NADPH oxidase) and lysosomal (AP, ALP) enzymes, as well as elevated levels of glycogen and phospholipids. These findings indicate enhanced intracellular metabolism of neutrophils in rats with hypoxic hepatitis and, consequently, activation of their functional state. Alterations in neutrophil cytochemical parameters in hypoxic hepatitis are associated with a parallel increase in liver enzyme activity and may serve as additional informative criteria for the diagnosis of ischemic liver injury under conditions of severe systemic hypoperfusion and hepatic ischemia.