Beregovenko I. M., Zinenko D. Yu., Tverdokhlib I. V.

MORPHOLOGY

Scentific article

Background. The manifestations of acute pancreatitis in the clinic are three main levels: acinus lesion (tissue level), local changes in gland (organ level) and systemic symptoms (level of the body). Due to delayed clinical manifestations of the disease early morphological events acini during the so-called acinar phase of acute pancreatitis is not fully understood. Until now, there was a complex morphological studies of different models of pancreatitis considering pathological changes in the gland and the state of the microcirculation in the body. Objective. The purpose of research was definition of early microcirculation and hystosrtructure changes in a tissue of a pancreas in different models of an experimental sharp pancreatitis at rats. Methods. Used various variants of 2 models: 1) model with intraperitoneal application of L-arginin in dozes 3; 4 and 5 g/kg; 2) model with application of 50 mkl 1 %, 2,5 % and 5 % solutions of sodium taurocholat in a channel of a pancreas. Hystologic research and definition of an amylases level in the blood carried out in 1, 4, 8, 12, 24, 48 and 72 hours after an injection. Results. The lead researches on models with intraperitoneal application of L-arginin and intrachannel introduction of sodium taurocholat have revealed a similar orientation in development of a sharp pancreatitis on dynamics of an amylases level in the blood and on pathomorphological changes of the parenchyma, stroma and microcirculation in the gland. For model with introduction of sodium taurocholat in a channel of a pancreas are more characteristic gemorragycal displays alongside with inflammatory and necrotic changes which have an essential gradient from the head to a tail of the gland. Infiltration of lymphoid elements was particularly sensual in connective tissue structures surrounding pancreatic lobules. Perivascular edema and vascular wall damage observed in most part of arterioles and capillaries. Structure cancer less subject to changes in the group of animals that received L-arginine at a dose of 3 g/kg. After 48 hours postmortem changes were growing, and some improvement morphological picture we saw at the end of the 3rd day in animals treated with L-arginine in doses of 3 g/kg and 4 g/kg. In the group with the introduction of 4 g/kg single state of exocrine elements pancreas approaching the control group and with the application of 3 g/kg were significantly more. Most of acini in groups with the application of 4 g / kg and 5 g / kg showed abuse of tissue architecture and few maintain normal structure characteristic tubular shape in cross sections. Kept and leukocyte elements that were the result of infiltrative processes in the connective tissue layer around acini also appeared fibroblasts, indicating the beginning of fibrosis. Also in the wall of arteries showed signs of sclerosis. Violation of the total tissue structure was typical of exocrine component of the pancreas, while islets of Langerhans remained without significant microscopic changes. Conclusion. It is observed regenerative dynamics of amylase’s concentration in the blood condition, of microvessels and the general tissue structure of a pancreas of comparison with L-аrginin after application of sodium taurocholat.

pancreas, models of an acute pancreatitis, rat, microcirculation, histostructure

• 1. Диагностика нарушений микрогемодинамики при остром панкреатите / Ю.С. Винник, Д.В. Черданцев, А.А. Вахрунин [и др.] // Методология флоуметрии. – М. : Трансоник, 1997. – С. 93-106.
• 2. Колб В.Г. Справочник по клинической химии. – 2-е изд., перераб. и доп. / В.Г. Колб, В.С. Камышников. – Минск: Беларусь, 1982. – 366 с.
• 3. Лакин Г.Ф. Биометрия : [Учеб. пособие для биол. спец. вузов.- 4-е изд., перераб. и доп.] / Г.Ф. Лакин. – М. : Высшая школа, 1990. – 352 с.
• 4. Моделирование острого панкреатита / В.М. Буянов, И.В. Ступин, В.Н. Егиев [и др.] // Клин. хирургия. – 1989. – № 11. – С. 24-26.
• 5. A mouse model of acute biliary pancreatitis induced by retrograde pancreatic duct infusion of Na-taurocholate / J.M. Laukkarinen, G.J.D. Van Acker, E.R. Weiss [еt al.] // Gut. – 2007. – Vol. 56, № 6. – Р. 1590-1598.
• 6. Aho H.J. Experimental pancreatitis in the rat. Sodium taurocholate-induced acute haemorrhagic pancreatitis / H.J. Aho, S.M. Koskensalo, T.J. Nevalainen // Scand. J. Gastroenterol. – 1980. – Vol. 15, № 4. – P. 411-416.
• 7. Aho H.J. Experimental pancreatitis in the rat. Ultrastructure of sodium taurocholate-induced pancreatic lesions / H.J. Aho, T.J. Nevalainen // Scand. J. Gastroenterol. – 1980. – Vol. 15, № 4. – P. 417-424.
• 8. Arginine induced acute pancreatitis alters the actin cytoskeleton and increases heat shock protein expression in rat pancreatic acinar cells / M. Tashiro, C. Schafer, H. Yao [et al.] // Gut. – 2001. – Vol. 49. – P. 241-250.
• 9. Early activation of endoplasmic reticulum stress is associated with arginine-induced acute pancreatitis / C.H. Kubisch, M.D. Sans, T. Arumugam [et al.] // Am. J. Physiol. Gastrointest. Liver Physiol. – 2006. – Vol. 291. – P. 238-245.
• 10. Lampel M. Acute interstitial pancreatitis in the rat induced by excessive doses of a pancreatic secretagogue / M. Lampel, H.F. Kern // Virchows Arch. – 1997. – Vol. 373. – P. 97-117.
• 11. L-Arginine-induced experimental pancreatitis / P. Hegyi, Z. Jr. Rakonczay, R. Sari [et al.] // World J. Gastroenterol. – 2004. – Vol. 10. – P. 2003-2009.
• 12. Mizunuma T. Effects of injecting excess arginine on rat pancreas / T. Mizunuma, S. Kawamura, Y. Kishino // J. Nutr. – 1984. – Vol. 114. – P. 467-471.
• 13. New model of acute necrotizing pancreatitis induced by excessive doses of arginine in rats / S. Tani, H. Ito, Y. Okabayashi [et al.] // Dig. Dis. Sci. – 1990. – Vol. 35. – P. 367-374.
• 14. Relationship of plasma CCK to acinar cell regeneration in acute pancreatitis as studied by proliferating cell nuclear antigen / J. Sakagami, K. Kataoka, A. Ohta [et al.] // Dig. Dis. Sci. – 1996. – Vol. 41. – P. 1828-1837.
• 15. Steer M.L. Experimental acute pancreatitis: Studies of the early events that lead to cell injury / M.L. Steer, A.K. Saluja // York: Raven. – 1993. – P. 489-526.

«Bulletin of problems biology and medicine» Issue 2 part 1 (128), 2016 year, 331-335 pages, index UDK 616.361-007.272:616.37:616-005