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Biomedical subjects

E Prigge

Publications and source records attributed to E Prigge.

17 recordsLinked to original sources
PubMed1978

Early signs of oral and inhalative cadmium uptake in rats.

Female wistar rats, 170--190 g, were exposed for 90 days to cadmium oxide aerosols containing 25 and 50 microgram Cd/m3 and for 63 days to 100 microgram Cd/m3. Simultaneously female wistar rats, 170--190 g, were fed 25, 50, and 100 ppm cadmium in drinking water for 90 days. After inhalation and ingestion of the metal, there were comparable kidney cadmium levels, but higher liver and blood levels after oral uptake. Coincident with the higher blood cadmium concentrations, proteinuria was observed only after oral administration. Likewise, there was a significant decrease of serum iron after ingestion and no lowering of the serum iron after inhalation of the metal. The inhalation led to a marked dose dependent weight increase of the lungs, which was followed by an impairment of gas exchange. Obviously, after inhalative cadmium uptake of 90 days pulmonary changes precede renal damage.

Administration, Oral↗
PubMed1977

Effects of lead inhalation exposures alone and in combination with carbon monoxide in nonpregnant and pregnant rats and fetuses. I. Distribution of lead in blood and liver.

Nonpregnant and pregnant rats were continuously exposed for 3 weeks to an aerosol containing 1, 3 and 10 mg lead/m3 air and to a combination of 3 mg Pb/m3 and 500 ppm carbon monoxide. At the two lower lead doses, fetal blood lead levels exceeded those of the mothers. Active transport mechanisms were discussed to be responsible for these differences. A decrease of the fetal blood lead level below the maternal level in the high exposure group was explained by an increasing storage capacity of the fetal livers with increasing lead doses. Lead concentrations of the maternal livers exceeded the nonpregnant values at all 3 doses, probably caused by a higher ventilation and altered pharmacokinetics of lead in pregnancy. Additional CO-inhalation lowered the storage capacity of the livers of the adult animals and raised the blood concentration. In the fetuses additional CO-inhalation raised liver lead concentrations.

Air Pollutants↗
PubMed1977

Effects of lead inhalation exposures alone and in combination with carbon monoxide in nonpregnant and pregnant rats and fetuses. II. Effects on delta-aminolevulinic acid dehydratase activity, hematocrit and body weight.

Pregnant and nonpregnant rats were exposed for 21 days to an aerosol containing 1, 3 and 10 mg lead/m3 air and to a combination of 3 mg Pb/m3 and 500 ppm carbon monoxide (CO). Pregnant and nonpregnant rats exposed to uncontaminated air served as controls. The activity of the fetal delta-aminolevulinic acid dehydratase (ALA-D) was less inhibited by lead than the maternal activity. Furthermore, the degree of inhibition was highly reduced in the fetuses by additional CO-inhalation, whereas in adult animals the depression of the ALA-D was accentuated by additional CO-inhalation in accordance with epidemiological data. Therefore, it is concluded that the mode of plumbic inhibition of the ALA-D activity differs in fetuses from that in adults. Furthermore, the adaptation to the inhibition of the ALA-D by de novo synthesis of this enzyme was less in fetuses than in adult rats. The high lead aerosol concentration reduced hematocrit and body weight of the fetuses, but it did not influence these parameters in adult rats, thus pointing to a higher lead-sensitivity of the fetal than the adult organism. A stronger inhibition of maternal ALA-D activity than of the activity of nonpregnant animals possibly indicates a higher susceptibility to lead in pregnancy.

Air Pollutants↗
PubMed1976

[Pharmacology of 2'-[2-hydroxy-3-(propylamino)-propoxy]-3-phenylpropiophenone (Propafenone, SA 79)-hydrochloride].

The pharmacologic actions of 2'-[2-hydroxy-3-(propylamino)-propoxy]-3-phenylpropiophenone (propafenone, SA 79) hydrochloride were investigated in animal experiments. The drug showed antiarrhythmic action in anesthetized dogs, cats and rabbits after i.v. (1 mg/kg) and oral (2-10 mg/kg) application. The model arrhythmias were induced by epinephrine infusion plus chloroform inhalation or by infusion of digoxin, calciumchloride or aconitine or by occlusion of the left coronary artery. Propafenon prolonged the refractory period in isolated atria of guinea pigs and elevated the electrical fluttering level of the ventricle in anesthetized guinea pigs or conscious rabbits. It showed local-anesthetic action on the cornea of the guinea pigs. In doses of 3-10 mg/kg i.v. it lowered blood pressure, inhibited contraction force of the heart ventricle and dilated coronary arteries. Heart rate was unchanged by anti-arrhythmic doses. With higher doses (more than 7 mg/kg i.v.) ECG was altered. The autonomic nervous system was unaffected but bronchial adrenergic beta-receptors appeared to be inhibited. The results show, that propafenon has a specific antiarrhythmic action on the heart. The doses to be used have no influences on other circulatory parameters. Propafenon acts after oral application too.

Administration, Oral↗