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The authors made an analysis of results of examination of 41 patients with ischemic heart disease treated by the standard medicamentous therapy and when using different methods of photohemotherapy against its background. It was established that medicamentous therapy during 2 weeks failed to result in a substantial improvement of rheological properties of blood, while its combination with photohemotherapy could give a considerable positive effect coinciding with clinical improvement of the patient's state. Shorter terms are required to correct hemorheological indices when autotransfusions of photomodified blood are used.

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A Baikal seal (Phoca sibirica) was experimentally infected with Baikal seal morbillivirus (BSMV) isolated from Baikal seals during an epizootic in 1987-1988. The seal was infected with BSMV with an infectious titer of 10(7.0) TCD50/ml, and daily observations of the animal clinical condition were made. The virus-specific antibodies in the seal serum were determined by ELISA and virus neutralization test. The clinical picture showed a mild infection. The ELISA-active antibodies were detected 10 days postinfection and reached the maximum in 20 days. Virus-neutralizing antibodies were detected in 16 days after infection, reached the maximum titer of 1:640 in 20 days and remained at this level for 39 days (the observation period). These data indicate that BSMV can induce a disease in the natural host with production of virus-neutralizing antibodies. The results of this work and the earlier reports show that the epizootic in Baikal seals was induced by BSMV.

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A morbillivirus was isolated from the organs of a seal (Phoca sibirica) which had died during 1987-1988 epizootic in Baikal. This Baikal seal morbillivirus (BSM) was adapted to Vero cell cultures in which it induced a cytopathic effect developing to complete destruction of the monolayer. Typing of BSM was done by indirect immunofluorescence test and enzyme immunoassay using antibodies to distemper and measles viruses. A method for virus concentration and purification was developed. According to electron microscopic examinations, the virus virions were spherical particles of heterogeneous sizes over 100 nm in diameter. The clinical picture of seal infection, pathological anatomy and histopathology are described. A possible role of BSM in the epizootics of Baikal seals is discussed.

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In guinea pigs and noninbred white mice, infected subcutaneously with anthrax which resulted in their death, characteristic generalized infection with the hematogenic contamination of their organs and the signs of intoxication and shock could be observed. In inbred white rats (Fisher 344) the invasion and dissemination of B. anthracis are relatively slightly pronounced, the phenomena of intoxication and shock being clearly prevalent.

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The pathomorphological picture of experimental B. anthracis infection in white rats (strain Fisher-344) essentially corresponds to experimental anthracic intoxication with very moderately pronounced morphological manifestation of B. anthracis invasion. This indicates that specific anthracic intoxication is an essential component of the pathological process in B. anthracis infection.

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Anthrax toxin introduced subcutaneously into white rats Fisher-344 caused specific intoxication accompanied by characteristic pathomorphological changes and, when studied by the immunoperoxidase method in histological sections, could be detected in the blood stream (in plasma) and in the cytoplasm of macrophages (in the lungs and the spleen). The content of the preparation introduced into the animals in the blood stream is directly related to its toxicity, being probably indicative of the relative functional failure of the macrophagal system.

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In experimental anthrax intoxication, a highly important stage of its pathogenesis consists in microcirculatory disturbances with the phenomena of blood sludge, accompanied by the increased permeability of blood vessels not only for plasma, but also for red blood cells. These disturbances result in perivascular hemorrhages, hemorrhagic infiltrations, edema and cavitary transudates. Pulmonary edema and, as a consequence, the accumulation of fluid in pulmonary alveoli and the respiratory tract are of particular importance and, probably, can be considered the basic cause of the ensuing acute and fatal asphyxia. Such vascular and pulmonary insufficiency is accompanied by a decrease in the content of macroergic compounds (and in particular ATP), the characteristic deformation of red blood cells and disturbances in their oxygen transport function, which is linked with the decreased content of 2,3-diphosphoglycerate.

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