Calcium content of serum and myocardium in vitamin D-induced cardionecrosis.

The dynamics of calcium content alterations in serum and heart muscle in relation to vitamin D-induced cardionecrosis was the aim of the experiment performed on female Wistar rats killed at different times after one or two intraoral doses of 100,000 IU of vitamin D. Calcium concentration in the serum showed great individual variability, although the mean value was significantly elevated after 22 h following one dose and after 2 h following two doses of vitamin D. In the heart muscle the mean calcium content increased 72 h after one dose and 24 h after two doses of 100,000 IU of calciol, but in individual rats the increase of Ca concentration was observed as early as 30 h after one dose, in some it was normal even after 144 h of two doses and varied between individual rats 20-30-fold. The degree of cardionecrosis showed great variability among rats treated with the same dose of calciol and at the same phase of the experiment. Cardionecrosis was always preceded by great accumulation of calcium in the heart muscle and its extent was in direct correlation to the amount of calcium in the tissue, regardless of the dose of calciol and phase of the experiment.

The fate of 14C-carbendazim in rat.

The disappearance of 14C-carbendazim in rat (i.v. 12 mg/kg) followed the kinetics of a two-compartment open-system model. Half-lives of the alpha-phase were 0.1 h (blood), 0.16 h (liver), 0.25 h (kidney), and of the beta-phase: 2.15 h, 6.15 h, respectively. Two metabolites: methyl 5-hydroxy-2-benzimidazolecarbamate (5-HBC) and 2-aminobenzimidazole (2-AB) were formed very rapidly. Their peak concentrations in liver and kidney were 15 min after i.v. injection. Unchanged carbendazim was found in highest concentrations in blood. 5-HBC prevails in organs. 2-AB was present only in minor amounts. The extent of bioavailability in orally administered 14C-carbendazim (12 mg/kg) was about 85%. The disposition of radioactivity in subcellular fractions was not uniform, its highest concentration was in cytosol, the lowest in microsomes. The elimination of 14C-carbendazim in urine is biphasic. Half-lives of the alpha-phase were 1.4 h (i.v.) and 2.5 h (oral), and of the beta-phase 11.2 h and 12.1 h, respectively. Irrespective of the route of administration, 95% of the radioactivity in urine was composed of 5-HBC. The concentration of unchanged carbendazim in blood and of 5-HBC in urine may be of diagnostic value in acute poisoning with carbendazim.