Histological changes of the liver and kidneys in experimental sepsis related with structural features of their microvasculature

Abstract

Pathogenic mechanisms of multiple-organ failure in sepsis are not completely clear. Studies of morphogenetic bases for sepsis performed on experimental models are promising. The aim of this study was to analyze histological changes in the liver and kidneys on a model of experimental sepsis and to identify a relationship of these changes and morphological features of the microvasculature. Material and methods. The study was performed on 27 mature C57Bl/6 male mice. A 24-h broth culture of the Pseudomonas aeruginosa 1840 strain isolated from burn disease wound fluid was injected intraperitoneally by 0.5 ml per animal at doses of 1 x 10⁶ CFU/ml in Group 1, 1.1 x 10⁵ CFU/ml in Group 2, 1 x 10⁴ CFU/ml in Group 3, and 1 x 10³ CFU/ml in Group 4. Control animals were injected with 0.5 ml of sterile isotonic sodium chloride solution. At the terminal stage of sepsis, mice were euthanized with ether vapour. Excised organs were fixed, dehydrated, and embedded into paraffin blocks. Serial sections were stained with haematoxylin and eosin and analyzed using a light microscope. Results. The nature of microscopic changes in the liver and kidneys from infected animals did not basically depend on the dose of causative agent, but severity of these changes was the highest in animals of Group 1. Changes in the liver were pronounced and evident as venous stasis, dilated and blood-filled sinusoids, destruction of hepatocytes, formation of fibrin clots, and leukocyte infiltration. These signs were consistent with inflammation, which resulted in destruction and transformation of hepatocyte laminas into amorphous eosinophilic masses. Histological changes in kidneys, where glomerular capillaries with arterial blood predominate in the microvasculature, were less pronounced and evident as decreased blood filling of glomerular capillaries, de struction of proximal tubules of the nephron, and blood filling of veins. Foci of leukocyte infiltration and venous clots were occasional and small. The observed changes were discussed from the perspective of morphological peculiarities of kidney microvasculature. Conclusion. Morphological features of hepatic sinusoidal capillaries and the capillary network of renal nephrons related with specificity of their function exert a certain influence on the mechanism and nature of histological changes in the liver and kidneys in sepsis.