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Experimental acute peritonitis was induced by single and repeated injections of 1.5-3% fecal autosuspension in the abdominal c a t t y of white rats. The blood content of medium-weight molecular proteins, which increases 1.5-2-fold during the course of entry of toxic products into the blood over 1-3 days, was measured. Examination of the vascular system and parenchymatous elements of many organs helped reveal three morphogenetic mechanisms of their injury: hyperfunction of cells, followed by their depletion and death; the direct action of toxic products on membranous structures of cells due to severe impairment of the histohematic barrier at the level of the microcirculation; the destructive effect of hypoxia due to the development of the disseminated intravascular coagulation syndrome. Key Words: experimental peritonitis; endotoxicosis; visceral involvementOne of the principal contributors to the pathogenesis of acute peritonitis (AP) is endotoxicosis, including three components: the source of intoxication (bacterial toxins, products of abdominal organ tissue degradation, medium-weight molecular proreins, etc.), the circulation of toxins in the body, and their action on target organs, involving injury to highly specialized visceral structures. The release of lysosomal enzymes (hyperfermentemia) and of bioactive substances associated with it leads to a second wave of intoxication with the formation of a "vicious circle" [2,3] which aggravates the course of the disease. However, our knowledge of the morphogenetic mechanisms of involvement of the smallest biosystems in AP is inaccurate and incomplete. Special attention should be paid to the P a t h o a n a t o m y Department. M e d i c a l Institute, Izhevsk. {Presented b y D. S. Sarkisov, M e m b e r of t h e R u s s i a n Academy of Medical Sciences) adequacy of AP reproduction and experimental verification of the endogenous intoxication syndrome.The purpose of this research was to define the criteria for assessing endogenous intoxication in experimental animals and to identify the mechanisms of the injurious action of some endotoxins on the structural components of organs and tissues. MATERIALS AND METHODSExperiments were carried out with 120 outbred male white rats. AP was induced as described previously [9], with our modifications [4]. To induce AP, 1.5-2.0 ml of 3% fecal autosuspension were injected in the abdominal cavity (group 1). The "hypertoxicosis" state was attained either by a single injection of fecal suspension of an increased concentration, or by repeated injections thereof during 24 h (group 2). The animals were sacrificed under chloroform narcosis 3, 6, 12, and 24
Experimental acute peritonitis was induced by single and repeated injections of 1.5-3% fecal autosuspension in the abdominal c a t t y of white rats. The blood content of medium-weight molecular proteins, which increases 1.5-2-fold during the course of entry of toxic products into the blood over 1-3 days, was measured. Examination of the vascular system and parenchymatous elements of many organs helped reveal three morphogenetic mechanisms of their injury: hyperfunction of cells, followed by their depletion and death; the direct action of toxic products on membranous structures of cells due to severe impairment of the histohematic barrier at the level of the microcirculation; the destructive effect of hypoxia due to the development of the disseminated intravascular coagulation syndrome. Key Words: experimental peritonitis; endotoxicosis; visceral involvementOne of the principal contributors to the pathogenesis of acute peritonitis (AP) is endotoxicosis, including three components: the source of intoxication (bacterial toxins, products of abdominal organ tissue degradation, medium-weight molecular proreins, etc.), the circulation of toxins in the body, and their action on target organs, involving injury to highly specialized visceral structures. The release of lysosomal enzymes (hyperfermentemia) and of bioactive substances associated with it leads to a second wave of intoxication with the formation of a "vicious circle" [2,3] which aggravates the course of the disease. However, our knowledge of the morphogenetic mechanisms of involvement of the smallest biosystems in AP is inaccurate and incomplete. Special attention should be paid to the P a t h o a n a t o m y Department. M e d i c a l Institute, Izhevsk. {Presented b y D. S. Sarkisov, M e m b e r of t h e R u s s i a n Academy of Medical Sciences) adequacy of AP reproduction and experimental verification of the endogenous intoxication syndrome.The purpose of this research was to define the criteria for assessing endogenous intoxication in experimental animals and to identify the mechanisms of the injurious action of some endotoxins on the structural components of organs and tissues. MATERIALS AND METHODSExperiments were carried out with 120 outbred male white rats. AP was induced as described previously [9], with our modifications [4]. To induce AP, 1.5-2.0 ml of 3% fecal autosuspension were injected in the abdominal cavity (group 1). The "hypertoxicosis" state was attained either by a single injection of fecal suspension of an increased concentration, or by repeated injections thereof during 24 h (group 2). The animals were sacrificed under chloroform narcosis 3, 6, 12, and 24
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