Experimental Acute Pancreatitis-Induced Lung Injury—Prevented with “Cytoflavin®”

Abstract

Severe acute pancreatitis represents about 20% of all pancreatitis diagnosis and it has a high mortality rate when associated with a lung dysfunction. The aim of this research was to investigate the use of a wild spectrum metabolic drug (Cytoflavin®) for the treatment of acute lung injury in experimental pancreatitis. A L-arginine-induced acute pancreatitis (groups II and III) was simulated experimentally in a rat population. A combined metabolic drug was used as treatment. We determined the levels of amylase, medium molecules (MM 254 and 280), malonic aldehyde (MA), diene conjugates (DC), interleukin-8 (IL-8), interleukin-10 (IL-10), and tumor necrosis factor-α (TNF-α) in the blood and we performed a histologic examination of the lungs and pancreas of the rat population. The activation of lipid peroxidation peaks at 24-48 h from the onset of the disease. The level of malonic aldehyde in groups II and III was higher (39.09% and 30.99%, respectively) than that in the control group I (p < 0.02; p < 0.01), the diene conjugates level was higher by 43.66% and 42.03% respectively (p < 0.01). With medical correction after 72 h (group III), the level of malonic aldehyde and diene conjugates decreased by 17.0% and 30.5% when compared with group II (no medical correction) (p < 0.05). The level of medium molecules peaked after 72 h of the disease induction (p < 0.001). A correlation was established between the level of endogenous intoxication with the membrane-destructive processes in the lung tissue 48 h after modeling of acute experimental pancreatitis. The use of the proposed medicament correction reduces the manifestations of endogenous intoxication.