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Biomedical subjects

H Altenkirch

Publications and source records attributed to H Altenkirch.

At least 37 records · Page 2Linked to original sources
PubMed1982

Ultrastructural alteration of the alveolar epithelium after exposure to organic solvents.

Adult rats were exposed to the solvents n-hexane and methylethylketone (MEK) in different concentrations. Lung tissue was examined systematically after various periods by electron microscopy. The direct toxic effect to pneumocytes could be demonstrated as definite regressive alterations, such as fatty degeneration and changes of lamellar bodies of type II pneumocytes as well as increased detachment of cells. Besides these findings, after chronic inhalation of solvents conspicuous aggregation of lamellar discharge material of type II pneumocytes can be seen, and probably, as a result of an irritated fat metabolism, large lysosome-like bodies with densely packed lipid material appear in type I pneumocytes. The most distinguished changes could be demonstrated after exposure to a mixture of n-hexane and MEK, while they were less obvious after n-hexane alone. The observation suggests a profound enzymatic irritation of metabolism.

Animals↗
PubMed1980

[Importance of predisposing factors and personality characteristics in cluster headache patients (author's transl)].

Predisposing factors and concomitant diseases were examined in cluster headache patients. A positive or negative correlation to a particular disease, e.g. gastrointestinal ulcerative disease, could not be showen. Factors indicating a genetic predisposition could also not be found. In the Freiburg Personality Inventory cluster and migraine patients had an essentially normal profile; however, both groups evidenced a tendency towards psychosomatic reactions.

Adolescent↗
PubMed1979

[Sniffing addiction: chronic solvent abuse with neurotoxic effects in children and juveniles (author's transl)].

25 cases of clinically severe toxic polyneuropathy were observed among young people in Berlin who were addicted to sniffing methylethylketone-containing solvents. The peripheral motor defects took 2 1/2 to 3 years to regress. In severe cases there were additional spastic signs. This form of neurotoxic effect can be reproduced in animals. It is due to a disorder of axonal transport which destroys peripheral and central axons.

Adolescent↗
PubMed1979

Therapy of cluster headache with histamine H1 and H2 receptor antagonists.

Treatment with the histamine H2 receptor antagonist, cimetidine, alone and/or in combination with the histamine H1 receptor antagonist, chlorpyramine, in 13 patients showed that cimetidine alone was ineffective. 7 of 9 patients taking the combination of H1 and H2 receptor antagonists responded well to the treatment; in 1 patient, medication was ineffective and in 1 patient, success was doubtful. In 3 patients with chronic cluster headache, the effect faded after 4 weeks. The results are discussed.

Cimetidine↗
PubMed1978

Experimental studies on hydrocarbon neuropathies induced by methyl-ethyl-ketone (MEK).

An outbreak of neuropathies among Berlin solvent sniffers was closely related to the denaturation by methyl-ethyl-ketone (MEK) of the mixture used. The solvent was composed of n-hexane, toluene and ethyl-acetate. Nervous system responses to chronic repeated exposure to 10,000 ppm pure n-hexane, 10,000 ppm MEK/n-hexane (ratio 1:9) and 6000 ppm pure MEK were investigated in rats. Motor neuropathy of the dying back type with giant swelling of axons in the peripheral and central nervous system developed in animals exposed to MEK/n-hexane and n-hexane. Severe potentiation of n-hexane neurotoxicity and shortened onset of morphological and clinical signs were demonstrated in animals exposed to MEK/n-hexane. MEK alone did not produce neuropathy under these conditions. The findings suggest that commercial solvent mixtures containing MEK/n-hexane should be avoided.

Administration, Intranasal↗
PubMed1977

Toxic polyneuropathies after sniffing a glue thinner.

In West Berlin in the autumn of 1975 through the following 5 months we observed 18 juvenile patients who had a toxic polyneuropathy and had sniffed a glue thinner. The neurological picture consisted of a symmetrical, progressive, ascending, mainly motor, polyneuropathy with pronounced muscle atrophy and characteristic vegetative alterations. The height of the disease was reached after 1 1/2-2 1/2 months and was characterized by tetraplegia in 7 patients. After 8 months all patients still had a motor deficit. Nerve biopsy showed paranodal axon swelling, dense masses of neurofilaments and secondary myelin retraction. The neurological and morphological data correspond to the "glue sniffer's neuropathy" and the n-hexane and MBK polyneuropathy after industrial exposure, as described in 10 cases to date. However, there was no MBK in the glue thinner. The polyneuropathies occurred in close time relation with the denaturation of the thinner with MEK (2-butanone). It is concluded from the data n-hexane and MBK have a common toxic mechanism with primary axonal changes and that there is an additional synergistic effect of MEK.

Adolescent↗
PubMed1976

[Toxic polyneuropathy after sniffing contact glue thinner (author's transl)].

Four men aged 16 to 19 years who had sniffed contact glue ("Pattex") thinner almost daily for 3 to 7 years developed a pronounced polyneuropathy. They had to be admitted nearly at the same time. A uniform neurological syndrome similar to Landry's paralysis with progressive ascending symmetrical pareses had developed. Motor deficiencies and atrophies affected the lower extremities more frequently and more severely. Only minimal sensory disturbances were found. The disease shows remarkable similarity to the "glue-sniffing neuropathy" described in the US and Japan which is attributed to n-hexane.

Adolescent↗
PubMedDate not supplied

Neurotoxicity of organic solvent mixtures: embryotoxicity and fetotoxicity.

The toxicity of organic solvents at different concentrations was examined to determine their effect on pregnant rats and their offspring. A very serious effect which inhalational exposure to n-hexane, methyl-ethyl-ketone and a mixture of the two organic solvents produced in pregnant rats was a concentration-dependent increase of intrauterine mortality. In cases of only prenatal exposure, the persistence of reduced body growth was an important result obtained at all concentrations we investigated (first solvent experiment, 500 ppm; second solvent experiment, 800 ppm; and third solvent experiment, 1000 to 1500 ppm; 23 hr day). In these cases, a delay in the maturation of cerebellar cortex was also observed. In cases of pre- and postnatal solvent exposure, the effects of malnutrition were added to the solvent-induced retardation. This resulted in an extreme delay in tissue maturation accompanied by a retarded cell maturation. The solvents examined had no teratogenic effect in pregnant rodents and their offspring. Neurotoxicity was restricted to the known structures of the adult animals, whose axons were damaged. They did, however, show a concentration-dependent embryotoxic and fetotoxic effect.

Administration, Inhalation↗
PubMedDate not supplied

Effects of lipoic acid in hexacarbon-induced neuropathy.

The effects of lipoic acid on hexacarbon neurotoxicity in rats were investigated. Rats were exposed by inhalation to n-hexane for 24 hours/day, 7 days/week, up to a total period of 9 weeks. Eight animals were exposed to 700 ppm n-hexane only, and eight animals were exposed to 700 ppm n-hexane and additionally received 100 mumol/kg lipoic acid PO daily. Clinical status of the animals was evaluated by examination of general condition, motor performance tests and neurophysiological measurements of caudal nerve motor conduction velocity. Results showed that animals exposed to 700 ppm n-hexane developed severe motor neuropathy leading to paralysis by the 6th week. Motor distal latencies of these animals were severely prolonged. In contrast, in animals treated with lipoic acid the onset of motor neuropathy was delayed for approximately 3 weeks as could be demonstrated by motor performance tests and measurements of motor distal latencies.

Action Potentials↗
PubMedDate not supplied

Potentiation of hexacarbon-neurotoxicity by methyl-ethyl-ketone (MEK) and other substances: clinical and experimental aspects.

Hexacarbon-containing solvents can induce specific functional and morphological disorders in the peripheral and central nervous system. The neurological manifestations consist in polyneuropathy syndromes and neuromyelopathies. Such clinical pictures have been observed both after exposure at industrial work and after abuse of hexacarbon-containing solvents as narcotics. An outbreak of neuropathies among solvent-sniffers after denaturation of the hexacarbon-containing solvent with methyl-ethyl-ketone led to the assumption that the neurotoxic properties of n-hexane can be considerably potentiated with methyl-ethyl-ketone. Experimental studies on laboratory rats have shown that solvent mixtures with n-hexane and methyl-ethyl-ketone bring about an earlier onset of clinical-neurological deficits and hexacarbon-specific morphological changes than exposure to n-hexane alone. First results of a combined exposure to lead and n-hexane solvents also indicate an intensified effect of the combined neurotoxins.

Animals↗