Germine Mono‐ and Diacetate in Myasthenia Gravis*

Flacke, Werner; Blume, Robert P.; Scott, William R.; Foldes, Francis F.; Osserman, Kermit E.

doi:10.1111/j.1749-6632.1971.tb30762.x

Cited by 6 publications

(1 citation statement)

References 10 publications

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“…Subsequently, it has been demonstrated that a semisynthetic veratrum alkaloid, germine-3.16-diacetate (GDA) has a similar effect (Flacke, 1963). First, this compound (Flaclee et al, 1966) and, later, the more active germine-3-monoacetate (GMA) (Flacke et al, 1971) were used for the treatment of myasthenia gravis. Both GDA (Flaclee et al, 1968) and GMA (Katz, R. L., personal communication) were also employed for the improvement of muscle function in partially curarized patients at the end of anaesthesia.…”

Section: Introductionmentioning

confidence: 99%

The effects of protoveratrine and germines on the release of acetylcholine from the auerbach plexus of the guinea-pig ileum

Vízi

Foldes

Theunissen

1975

J. Neural Transmission

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The effect of protoveratrine A and germine-3-acetate (GMA) on the release mechanism of acetylcholine from the nerve terminals of the Auerbach plexus in the longitudinal muscle layer of the guinea-pig ileum was studied. Protoveratrine A, GMA and germine potentiated neuroeffector transmission in Auerbach's plexus in the longitudinal muscle preparation provided the neurons were stimulated at low frequencies (less than 10 Hz). Protoveratrine A and GMA enhanced the release of acetylcholine from the nerve terminals during the resting period and at low frequency of stimulation (less than 10 Hz). At continous stimulation with high frequency they were ineffective (greater than 10 Hz). When trains of 20 stimuli, with a pulse interval of 0.1 s (10 Hz) were repeatedly applied with intervals of 0.1 to 20 s between trains, the effect of GMA to increase ACh release depended on the length of the train interval; the longer the resting period between trains the higher was the output of ACh. This fact indicates that the release of ACh increased primarily during the resting periods following single stimuli or trains. The effect of GMA on ACh release proved to be highly temperature-dependent: in the presence of GMA Q10 increasing from 3.25 to 4.92. A high Ca concentration, removal of Mg or lowering of the Na concentration abolished the effect of GMA to enhance ACh release.

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Section: Introductionmentioning

confidence: 99%

The effects of protoveratrine and germines on the release of acetylcholine from the auerbach plexus of the guinea-pig ileum

Vízi

Foldes

Theunissen

1975

J. Neural Transmission

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Myasthenia gravis: Review of diagnosis and management

Patten

1978

Muscle and Nerve

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Although the cause of myasthenia gravis is still unknown, its pathogenesis appears clear: immunologic attack on synaptic receptors in muscle causes receptor deficiency, decreased miniature endplate potentials, and decrements in the compound action potentials evoked from muscles on repetitive stimulation of peripheral nerves. In addition to the involvement of skeletal muscle, some MG patients may manifest subtle alterations of the function of heart, lung, smooth muscle, and CNS, indicating that this is truly a systemic disorder. Modern therapy involves adjusting treatment to the needs of individual patients. Anticholinesterases, calcium, ephedrine, potassium, and germine partially correct the defect in neuromuscular transmission; prednisone, ACTH, cytotoxic drugs, antilymphocyte serums, gamma globulin, thoracic duct drainage, plasmapheresis, and thymectomy partially modify the abnormalities of the immune system.

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Neurochemistry of Cholinergic Terminals

MacIntosh¹,

Collier²

1976

Neuromuscular Junction

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Germine Mono‐ and Diacetate in Myasthenia Gravis*

Cited by 6 publications

References 10 publications

The effects of protoveratrine and germines on the release of acetylcholine from the auerbach plexus of the guinea-pig ileum

The effects of protoveratrine and germines on the release of acetylcholine from the auerbach plexus of the guinea-pig ileum

Myasthenia gravis: Review of diagnosis and management

Neurochemistry of Cholinergic Terminals

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