PubMed Health⌕ Search

Biomedical subjects

G Krinke

Publications and source records attributed to G Krinke.

36 records · Page 2Linked to original sources
PubMed1981

Radicular myelinopathy in aging rats.

Naturally occurring degenerative lesions of nerve fibers in the spinal cord, spinal roots and peripheral nerves in nine male rats 877 days old were swollen myelin sheaths, forming "myelin bubbles." The myelin swellings were distributed throughout the spinal tracts and the peripheral nerves, but most frequently in the lumbar ventral spinal roots. Although most axons surrounded by swollen myelin were intact, some were constricted and degenerated, while others showed signs of remyelination.

Aging↗
PubMed1981

Pyridoxine megavitaminosis produces degeneration of peripheral sensory neurons (sensory neuronopathy) in the dog.

Pyridoxine, a water-soluble vitamin, produces a sensory neuronopathy when administered in high doses to dogs. Beagles who received a daily oral dose of 300 mg/kg of pyridoxol hydrochloride developed a swaying gait within 9 days. They eventually became unable to walk, but were not weak. Animals were sacrificed at intervals up to 78 days. Morphological examination revealed widespread neuronal degeneration in the dorsal root ganglia and the Gasserian ganglia. Cytoplasmic changes were first observed after 8 days and consisted of small, electronlucent vacuoles that subsequently coalesced leading to death of the cells. Degeneration of sensory nerve fibers in peripheral nerves, dorsal columns of the spinal cord and the descending spinal tract of the trigeminal nerve was apparent. The pathogenesis of these changes is unclear, but may, in part, reflect the selective permeability of blood vessels in the peripheral ganglia. It is apparent that the peripheral neuropathy previously attributed to pyridoxine actually represents a toxic, peripheral sensory neuronopathy.

Animals↗
PubMed1979

Clioquinol and 2,5-hexanedione induce different types of distal axonopathy in the dog.

The central distal axonopathy induced in dogs by the administration of high doses of clioquinol is contrasted with the central-peripheral distal axonopathy precipitated by intoxication with 2,5-hexanedione. Mature, pure-bred Beagle dogs received a daily oral dose of 400 mg/kg of clioquinol for up to 7 months, or 1 ml per animal (approximately corresponding to 110 mg/kg) of 2,5-hexanedione for up to 5 months. Intoxicated and control animal were killed and perfused at monthly intervals, so that the spatial-temporal development of the lesion could be followed and correlated with clinical symptoms. During the treatment, dogs intoxicated with 2,5-hexanedione developed symptoms of peripheral neuropathy consisting of flaccid weakness, muscle atrophy, hind-limb foot-drop and areflexia. By contrast, the dogs surviving clioquinol intoxication exhibited a stiff-legged gait, hyperreflexia but no muscle atrophy. Light and electron microscope examination of central and peripheral nervous tissue from dogs intoxicated with 2,5-hexanedione revealed giant axonal swelling and distal axonal degeneration. By contrast, dogs receiving clioquinol showed a distal axonal degeneration confined to the optic tract and the long spinal cord tracts, without any visible involvement of peripheral nerves.

Animals↗
PubMed1979

Differential susceptibility of peripheral nerves of the hen to triorthocresyl phosphate and to trauma.

The nerve fibres of largest diameter and of greatest length are considered to be the most vulnerable to triorthocresyl phosphate (TOCP). In this study, the differential vulnerability of the particular sciatic nerve branches was determined in the course of TOCP neuropathy and of Wallerian degeneration. The branch innervating the lateral gastrocnemius muscle, made up predominantly of large-diameter fibres, proved most susceptible to TOCP. By contrast, after proximal sciatic-nerve transection, degeneration commenced in the lateral nerve of the third digit, containing long nerve fibres of small diameter.

Animals↗
PubMed1978

Sensory denervation of the plantar lumbrical muscle spindles in pyridoxine neuropathy.

Male albino rats treated with excessive amounts of pyridoxine developed an impairment of neuromuscular function. The equatorial region of the plantar lumbrical intrafusal muscle fibres was studied in the electron microscope and the calibre of the nerve fibres was determined in semi-thin sections of the posterior tibial nerves. Degeneration of the primary sensory endings coincided with the onset of ataxia, and in more advanced stages of the neuropathy as well as after a 2-month treatment-free period the equatorial region was denervated. There was a corresponding decrease in the number of large nerve fibres. It is considered essential that primary sensory endings of lumbrical muscle spindles should be included in studies of distally accentuated sensory neuropathies.

Animals↗
PubMed1977

A study of long-term effects of guanethidine on peripheral noradrenergic neurones of the rat.

In long-term experiments in rats the effects of guanethidine sulphate on peripheral adrenergic neurons in the heart, the vas deferens, the superior cervical ganglion and the ganglion innervating the vas deferens were studied in relation to the dosage and route of administration of the drug by biochemical, histofluorimetric and electron-microscopic methods. When administered daily in very high doses, i.e. 180 mg/kg orally or 25 mg/kg intraperitoneally, for several weeks guanethidine was found to induce toxic effects which appeared to be a result of mitochondrial changes in the ganglion cells. These changes were not directly related to the decrease in catecholamine content and the capacity of the neurones to retain exogeneous transmitter. The short neurones innervating the vas deferens appeared to be the structures most sensitive to guanethidine. As in the other tissues, however, the changes in these structures proved reversible to a considerable extent upon cessation of high-dose treatment. The structural changes induced in the animal by toxic doses of guanethidine are considered to have no bearing upon the pharmacological action of the drug under practical conditions.

Administration, Oral↗
PubMed1975

Herpes genitalis in guinea-pigs. II. Morphological studies in female guinea-pigs infected with Herpesvirus hominis type 2.

Gross and microscopial morphological changes developing in female guinea-pigs after vaginal infection with HVH 2/Angelotti were studied. In the mucosa of the external genital tract there were inflammatory changes with formation of intra-epithelial vesicles, erosions and ulcerations. In the late stages of the infection signs of inflammatory dysplasia were also observed. The infection spread into the nervous system and produced characteristic inflammatory changes. The inflammation began as a bilateral posterior myelitis and ascended in the course of infection through the upper spinal-cord towards the brain-stem. The morphological changes were preceded by increased virus replication in the respective tissues and were correlated in time with clinical symptoms. The morphological changes seen at the site of inoculation in the external genital tract of the guinea-pig bore a certain resemblance to those seen in some cases of human infection with the same type of virus.

Animals↗
PubMedDate not supplied

Prolonged exposure to trimethylphosphate induces sensory motor neuropathy in the dog.

Five beagle dogs were treated daily with 1 ml of trimethylphosphate (TMP) for 1 to 4 months. Neurotoxicity was evaluated by observation of behaviour, neurologic examination, neurophysiologic tests and by neuropathology. Neurotoxicity was first detected at the neurologic examination following four weeks of treatment: the most predictive indicators of neuropathy were the impairment of hopping, of tactile placing and the atactic gait. Electrophysiologic tests indicated a prolonged latency of neuromuscular impulse transmission after week nine, followed by a decrease of maximum conduction velocity of sensory fibers. At this time peripheral nerve fibers had abnormalities including paranodal and internodal swelling, paranodal demyelination and distal fragmentation. An additional dog treated with daily doses of 2 ml developed a severe distally accentuated degeneration of long spinal tracts and peripheral nerve fibers, manifested by impairment of sensory and central motor impulse conduction. Organophosphate neuropathy can thus be assessed in the dog by functional and morphological changes after prolonged exposure, in particular at doses causing severe morbidity.

Animals↗