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Nablyudaemyj v poslednie desyatiletiya rost chisla sluchaev tuberkuleznogo peritonita obuslovlen limfogematogennym rasprostraneniem mikobakterij tuberkuleza (MBT) iz legkih i drugih ekstrapul'monal'nyh istochnikov. Do sih por ostaetsya neyasnym, pochemu pri generalizacii tuberkuleznoj infekcii v vospalitel'nyj process vovlekayutsya te ili inye organy i anatomicheskie oblasti. Pochemu v odnih sluchayah razvivaetsya tuberkulez bryushiny, a v drugih tuberkulez pochek? Cel'yu raboty bylo izuchit' patogenez tuberkuleznogo peritonita s pomoshch'yu sozdaniya vosproizvodimoj biologicheskoj modeli. Tuberkuleznyj peritonit modelirovali na 18 krolikah (10 osobej — eksperimental'naya gruppa, 8 — kontrol'naya) putem vnutribryushinnoj inokulyacii vzvesi MBT. Krolikam eksperimental'noj gruppy pered zarazheniem vvodili ingibitor TNF — i zheleza (III) gidroksid saharoznyj kompleks s cel'yu podavleniya aktivnosti peritoneal'nyh makrofagov i osnovnyh citokinov; v kontrol'noj gruppe vvedenie immunosupressivnyh preparatov ne proizvodili. Pri autopsii zhivotnyh kontrol'noj gruppy v 37,5% sluchaev vyyavleny izmeneniya, harakternye dlya tuberkuleza legkih, porazheniya drugih organov i sistem ne otmecheno. Naprotiv, u krolikov eksperimental'noj gruppy v bryushnoj polosti vyyavleny priznaki tuberkuleznogo peritonita. Po rezul'tatam provedennoj raboty, anatomicheskaya oblast', gde razvivaetsya vtorichnyj ochag vnelegochnoj tuberkuleznoj infekcii, vo mnogom zavisit ot mestnoj immunnoj zashchity. Tak, dlya bryushiny takim neobhodimym i dostatochnym usloviem razvitiya tuberkuleznogo peritonita yavlyayutsya umen'shenie pula peritoneal'nyh makrofagov i snizhenie citokinovoj produkcii.

Osobennosti patogeneticheskih mekhanizmov tuberkuleznogo peritonita v eksperimente