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F S VOGEL

Publications and source records attributed to F S VOGEL.

31 records · Page 2Linked to original sources

Demyelinization induced in living rabbits by means of a lipolytic enzyme preparation.

Purified lipase, injected intracerebrally and intravasculariy in rabbits, gave rise to focal areas of demyelinization in the central nervous system in 10 of 13 animals so treated. In one instance the lesions became manifest within 48 hours and in another they persisted for 6 months; they were not infrequently accompanied by paresis and by tilting or tremor of the head. They were characterized by a focal loss of myelin and moderate gliosis with little or no neuronal destruction or inflammatory reaction, in these respects resembling the plaques of multiple sclerosis. The intracerebral injection of trypsin and chymotrypsin in control animals failed to produce the characteristic demyelinization, but by contrast caused focal areas of necrosis in which all the cerebral tissues were involved. Furthermore, demyelinization did not result when heat-inactivated pancreatic lipase was injected intracerebrally, and similarly negative results were obtained when an incubated mixture comprised of fatty connective tissue that had been acted upon by the pancreatic preparation and then heated to inactivate the lipase, was injected into the brains of rabbits. In supplementary experiments the pancreatic lipase preparation and fresh rabbit brain, incubated together in vitro, were found to form acid, presumably owing to the breakdown of brain lipids to fatty acids; trypsin and chymotrypsin mixed with brain in control experiments failed to form acid. When incubated with segments of the spinal cord of experimental animals, the lipolytic enzyme brought about a loss of stainable myelin in peripheral areas and in the spinal nerve roots; again trypsin and chymotrypsin had no such effect in control experiments. The findings as a whole show that an enzyme preparation with lipolytic activity has the ability to destroy myelin in living animals, and in vitro as well, and to produce lesions remarkably similar to those of multiple sclerosis. They have additional interest in light of the demonstration that a lipolytic enzyme is regularly present in the reactive histiocytes of guinea pigs with experimental encephalomyelitis (5).

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A lipolytic enzyme in reactive histiocytes of guinea pigs with experimental encephalomyelitis.

A lipolytic enzyme has been demonstrated by means of a cytochemical technique and by direct chemical assay in granulomatous tissues of guinea pigs with encephalomyelitis and demyelinization resulting from the injection of an emulsion comprised of brain tissue and adjuvants, including Mycobacterium butyricum. Combined histologic and cytochemical studies showed that the lipolytic enzyme was present in the cytoplasm of a large proportion of the reactive histiocytes in the granulomatous tissue around the site of injection in the diseased animals, and that the enzyme-containing histiocytes were even more numerous in the inflamed regional lymph nodes. In control experiments, when emulsions lacking either brain tissue or M. butyricum were injected in previously normal guinea pigs, the experimental condition did not develop; under these circumstances the lipolytic enzyme was found in only a small proportion of the cells of the granulomatous tissue around the injection sites, and it was almost negligible in the regional lymph nodes of these animals. It was absent from the cells of the lymph nodes of normal animals, and from the cells of talcum and aluminum hydroxide granulomas produced experimentally in guinea pigs. The lipolytic enzyme may be a factor in the pathogenesis of the experimental encephalomyelitis and demyelinization.

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