PubMed Health⌕ Search

Biomedical subjects

R Gohlke

Publications and source records attributed to R Gohlke.

At least 19 recordsLinked to original sources
PubMed1985

[Soot lung as occupational disease].

Lung findings among 13 workers employed in a carbon black plant are presented. The concentrations of respirable dust at the work place exceeded the MAC for dust free of quartz. X-rays show disseminated small irregular and large shadows with slow progress. In two cases lung tissue was examinated histologically. Both accumulation of carbon black and development of collagen fibers were seen. According to x-rays and histological findings the lung disease can be estimated as a pneumoconiosis. Legal recognition of carbon black lung as an occupational disease can be achieved in a special procedure called "Sonderentscheidverfahren".

Aged↗
PubMed1983

[Enzyme activities in the blood serum from rats with chronic liver damage. part 3: Effect of thioacetamide].

Liver damage was produced in male Wistar rats aged 15 weeks by daily oral administration of 40 mg/kg thioacetamide over a period of 24 weeks. All of the animals were weighed once a week. Furthermore, the duration of hexobarbital anaesthesia and the activities of the enzymes ASAT, ALAT, GIDH, LDH, LAP and alkaline phosphatase in the serum were determined in 6 experimental and 4 control animals after 3 d and 1, 2 and 4 weeks, and then at intervals of 4 weeks. For the purpose of comparison the same investigations were performed (under identical experimental conditions) both in rats fed normally and rats starved for 24 h to which a single dose of thioacetamide was applied. The histological study of the livers revealed destruction of the lobule architecture and profuse bile-duct proliferations after 12 weeks. Cirrhosis was observed after 16 weeks. The activities of ASAT, ALAT, GIDH and LDH increased for a short time and then returned closely to normal. During the whole experimental period, the LAP and alkaline phosphatase activities remained in the pathological range, as well as the duration of hexobarbital anaesthesia. Enzyme diagnosis is not suitable for assessing the degree of severity of a liver damage produced by thioacetamide.

Acetamides↗
PubMed1980

The effect of simultaneous oral application of ethanol and styrene. [1. Acute and subacute experiments on rats].

Within the lethal dose range, 8.70 mmol/ml ethanol (EtOH, LD50 = 226 mmol/kg) and 6.86 mmol/ml styrene (ST, LD50 = 77.4 mmol/kg) had an additive effect in rats. A four-week pretreatment with 1/10 of the LD50 of the corresponding combination partner did not modify the lethal dose effect of the subsequently administered substance (EtOH or ST). Subchronical treatment with EtOH and ST had an additive effect, too but produced no cumulative effect in relation to lethality. Unlike EtOH, subchronical treatment with ST caused severe symptoms of illness, decrease in body weight and liver lesions. Histological examination at the combined application of EtOH plus ST showed no evidence of qualitatively or intensified effects. Subchronic administration of 1/10 of the LD50-ies of EtOH and ST produced in rats more pronounced histological liver changes than single application of the corresponding LD16-ies. Except for ATP'ase activity, histochemical reactions following EtOH or ST application showed minimal quantitative differences.

Adenosine Triphosphatases↗
PubMed1980

Combined action of hepatotoxic substances and increased environmental temperature on the liver of rats.

Male albino rats were orally treated in a single dose with 40 mg allyl alcohol/kg or 50 mg 4,4'-methylenedianilline/kg, or 100 mg 1,1,2,2-tetrachloroethane/kg, or 400 mg carbon tetrachloride/kg, or 800 mg chloroforme/kg, immediately after-wards exposed to increased temperature (35 degrees C, 50% RH, 4 h), and examined 20--22 hours later. Under these conditions, only carbon tetrachloride led to a more intensified changes manifesting themselves in changes of the serum enzymes LAP, ALAT, and GLDH, as well as in liver histology. The liver lesions, caused by the substances mentioned, reacted to an additional thermal strain in a comparable manner as the LD50-values determined under identical exposure conditions. The temperature-dependent enhancement of the carbon tetrachloride hepatotoxicity is ascribed to an intensification of liver peroxidation processes due to increased core temperature.

1-Propanol↗