Type II alveolocytes are destroyed in suckling rabbits during adhesion of Vibrio cholerae, whereas in type I alveolocytes no ultrastruetural disorders are detected. The .number of lipid granules is increased in the lipofibroblast cytoplasm. Transendothelial micropinocytosis and endothelial edema and destruction are increased in pulmonary capillaries, and plasmatic impregnation of the stroma is observed. The development of experimental cholera is associated with progressive disorders of the regional circulation, degranulation of platelets and basophils, destruction of polymorphonuclear leukocytes and endotheliocytes, and a marked increase of vascular permeability.Key Words: cholera; lungs; ultrastructure An important role in the pathogenesis of cholera is played by cAMP, vegetative ganglia of the small intestine, and the effects of vasoaetive amines and other bioaetive substances (BAS) [2][3][4]10,11,14]. The development of cholera is associated with severe dehydration, metabolic, structural, and functional changes in various organs, and an increase of the histamine, serotonin, and prostaglandin E 2 (PGE2) levels in the blood [6,12,14].The pathogenetic significance of serotonin and PGE 2 in enteroeyte hypersecretion has been revealed. Blocking of serotonin receptors types I and II by ketanserine and the agent ICS 250-930, respectively [13][14][15], completely abolished the secretion induced by cholera exotoxin [13]; injection of indomethacin, an inhibitor of the cyclooxygenase route of arachidonic acid metabolism, reduced the secretory effect of the cholerogen, though to a lesser degree [14]. Special interest therefore attaches to the nonrespiratory functions of the lungs, namely the metabolism of certain BAS character- ized by pronounced vasomotor activity [8,9]. For example, a single passage of blood through the lung tissue inactivates up to 95% of serotonin and up to 90% of PGE~, PGE2, and PGE~ in the vascular bed [8]. Since the enzymatic systems involved in metabolism are concentrated mainly in the vascular endothelium of the lungs, damage to this may entrain quantitative changes in the blood levels of BAS and, hence, influence the course of cholera.Our aim, therefore, in this research was to perform an electron-microscopic examination of suckling rabbit lungs during adhesion of K cholerae and the development of clinical signs of cholera. MATERIALS AND METHODSExperiments were carded out with 26 suckling rabbits aged 10-12 days infected intragastrically [1]. One ml of 3% sodium bicarbonate solution was infused through a polyethylene tube to animals which had fasted for 24 h in order to neutralize the stomach contents, after which 1 ml of an 18-hour culture of the virulent E1-Tor 5879 strain, and then again 0.5 ml sodium bicarbonate were administered. According to the optic opacity start-

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Suckling mice aged 4-5 days were injected with Vibrio cholerae hemagglutinin/protease and ultrastructural changes in their small intestine were studied after 5 h. The preparation caused a statistically significant accumulation of fluid in the intestine, appearance of large gaps along cell-cell spaces in the villi and crypts, intense production and secretion of the mucus by goblet cells. The formation of interepithelial cavities was paralleled by vascular changes, supplemented by extravasal disorders caused by mast cell reaction. The role of enterochromaffin cells and lipofibroblasts, modulating the secretion in the intestine, is confirmed.

The development of experimental cholera in suckling rabbits is associated with typical cholerogenic syndrome: the presence of Vibrio cholerae in the blood, bile (in 60 and 70% cases, respectively), small and large intestine (in 100% cases). Simultaneously with enterocyte desquamation and increased permeability of the blood-enterocyte barrier, the vibrios are released into villous stroma and then into the microcirculatory bed. the zot toxin is involved in the mechanism of Vibrio cholerae invasion, the corresponding gene is present in the genome of the studied strain.

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