The correctional modification of inflammatory response at the experimental acute pancreatitis

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DOI: 10.4236/abb.2012.324062    3,612 Downloads   6,642 Views  Citations

ABSTRACT

This study investigated the effects of the L-17 compound of the group of substituted 5R1, 6H2-1,3,4- thiadiazine-2-amines on the possibility of inflammatory reaction evolvement correction in experimental acute pancreatitis. The study was based upon recent clinical and experimental work which demonstrated the role of local and systemic inflammatory reactions in pancreatonecrosis. Pancreatonecrosis modeling in rats was performed in accordance with the author’s modification of ligation model of acute pancreatitis. The biochemical and hematological analysis were performed in all groups at day 1. For microscopic analysis, five histological slices of each animal were analyzed. The main group, consisting of 15 animals with the average body weight 223 g each, got intraperitoneal injection of L-17 compound, dozed 40 mg/kg in an hour after surgery of pancreatitis formation. Later on, a 40 mg/kg doze of L-17 compound was repeatedly injected as often as once every 24 hours. Already during the 1st day of the experiment, no leucopenia was observed and the signs of proliferative inflammation were detected. Later, at the background of L-17 compound introduction (5th day of the experiment) the necrosis area got surrounded by demarcation bank, and further on (by the 7th day) had been entirely replaced by granulation tissue. Thus, the application of L-17 compound in experimental acute pan-creatitis results in replacement of destructive purulent inflammation by exudative-proliferative one, prevents lympho- and monocytopenia development, minimizes amylase and pancreatic ferments level during the first day of development of the disease and cuts down the lethality rate as result of pancreatonecrosis complications twofold.

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Sarapultsev, A. , Chupakhin, O. , Rantsev, M. , Sarapultsev, P. , Danilova, I. , Medvedeva, S. and Sidorova, L. (2012) The correctional modification of inflammatory response at the experimental acute pancreatitis. Advances in Bioscience and Biotechnology, 3, 442-448. doi: 10.4236/abb.2012.324062.

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