Abstract

Ration disbalancing in highly‐productive cows, as well as the influence of toxic elements often leads to the development of steatosis, which almost always occurs latently. As a rule, the development of the first clinical signs is registered already with irreversible damage of hepatocytes, which causing death of animal. In 2018, 13 samples of liver biomaterial obtained from cows with steatosis of different severity of the disease were examined. Material for histological research were fixed in a 95% solution of ethanol for 24 hours. Further, according to the standard method, paraffin is embedded. Slices were made 5–7 microns thick. The resulting sections were stained with hematoxylin and eosin, Schiffod‐iodic acid by McManus to detect glycogen. Morphological study of histological preparations was carried out using a Carl Zeiss light‐optical microscope with a magnification of 50–400. Microphotos were taken using an Axio Scope A1 digital camera. In the analysis of histological samples, pathological changes in the liver were observed in the form of expressed centrolobular local and diffuse small‐droplet and large‐droplet fatty degeneration of hepatocytes (Fig. 1), as well as a decrease and absence of glycogen cells (Fig. 2, 4). The liver had a regular girder structure, it was full‐blooded. The sinusoids of the liver and Disse spaces were medium dilated (Fig. 3). Portal triad had a typical histological structure, in some cases were expanded, in the stroma of the tracts were found hepatic triad, represented by the interlobular artery, vein and bile duct. Thickening of the portal triad with poorly expressed mononuclear infiltration was also noted, with no significant inflammatory changes in the samples presented (Fig. 5). These changes may be toxic. In addition to the above dystrophic and functional changes, a dilation of Disse sinusoidal spaces was also noted (Fig. 3). Staining of Schiff‐iodic acid by MacManus showed the absence of glycogen in four samples. Using the same staining protocol showed positive staining effect of the reticular fibers of the interstitial tissue of the cow's kidney. The remaining samples, the amount of glycogen in the hepatocytes was significantly reduced. In animals whose liver samples showed a lack of glycogen clinical finding of liver dysfunction were expressed. As a result, in the acute form of cows' steatosis, the amount of glycogen in hepatocytes sharply decreases. This leads to irreversible consequences, and often fatal.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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