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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Pharmaceutical research 2 (1985), S. 124-130 
    ISSN: 1573-904X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Cefotaxime (CTX) was injected either intravenously or intramuscularly in dogs, and its pharmacokinetics in plasma and urine were determined with the use of HPLC assay. Cephalothin (CET) was administered in a similar manner as a reference agent. While both CTX and CET rapidly disappeared from plasma after intravenous injection, the half-life of CET was approximately 2.5 times shorter than that of CTX. Both drugs were deacetylated, and desacetyl-CTX and desacetyl-CET appeared in plasma. Both drugs were rapidly excreted into urine either in unchanged or deacetylated form, the sum of which accounted for 77 % and 63 % of the CTX and CET dose, respectively. The ratio of the amount of unchanged drug over that of deacetylated drug in the urine was 1:1 for CTX and 1:2 for CET. When CTX and CET were intramuscularly injected, the plasma levels of CTX and CET reached a maximum 30 min and 15 min after injection, respectively, followed by a rapid decline. The pattern of urinary CTX excretion was similar after i.m. and i.v. injections. In contrast, the amount of desacetyl-CET in the urine was larger after i.m. than i.v. injections. CTX metabolites other than desacetyl-CTX (M2 and M3) that were also assayed by HPLC accounted for only 2–4 % of the dose of CTX in the urine, but were below detectable levels in this plasma.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of bone and mineral metabolism 17 (1999), S. 211-216 
    ISSN: 1435-5604
    Keywords: Key words: rat ; DXA ; bone mineral content ; hypoxia ; chronic respiratory failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract: Time-dependent changes of bone mass in ambulant chronic respiratory failure patients 60 or more years of age were compared between those on home oxygen therapy (HOT) and those still free of HOT (non-HOT). HOT (n = 31) showed initial PaO2 of slightly greater than 60 Torr and non-HOT (n = 32) had PaO2 moderately greater than 60 Torr (64.4 Torr vs 75.1 Torr). PaCO2 in HOT was significantly higher than that of non-HOT (44.8 Torr vs 40.0 Torr). There was no difference in pulmonary function test results. The whole bone mineral density (BMD) as adjusted by age and sex was significantly lower in the HOT group than that in the non-HOT. At endpoints of the follow-up period over 2 years or more, daily bone losses in the whole BMD, whole bone mineral content, and lumber BMD were significantly more accelerated in HOT compared with non-HOT. When the Wistar rats were pair-fed and their locomotion was limited, the animal group placed for 4 weeks under hypoxic air showed a reduction in BMD as compared with the control. We suggest that hypoxemia contributes to bone mass loss.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1435-5604
    Keywords: diabetes mellitus ; mouse ; areal bone mineral density ; bone phosphatase activities ; DXA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To investigate the mechanisms of osteopenia in diabetes mellitus induced experimentally in mice, we measured the bone mineral content, expressed as the bone mineral density per surface area (areal BMD), by dual energy X-ray absorptiometry; and we assessed the alkaline (ALP) and acid phosphatase (ACP) activities of the calvarial tissues, which are assumed to represent the functional activities of osteoblasts and osteoclasts, respectively. We found that at 8 weeks after the onset of streptozotocin-induced diabetes mellitus the areal BMD values of the total body, femurs, calvariae, and lumbar vertebrae in the diabetic group were smaller than those in the control group. As compared with the control group, the ALP/ACP activity ratio of the calvariae in the diabetic group had a tendency to be reduced at 4 weeks of diabetes when the calvarial ABMD was not different between the two groups; it was definitely reduced at 8 weeks. These results suggest that an imbalance of osteoblast and osteoclast activity might be one of the mechanisms of osteopenia in the diabetic mouse.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of bone and mineral metabolism 18 (2000), S. 22-26 
    ISSN: 1435-5604
    Keywords: Key words: DA rat, stress, calcitonin, calcium, sympathetic nerve system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract: Calcitonin, one of the calcium-regulating hormones, is known to have diverse biological effects including those on the gastrointestinal tract. In this organ, the hormone is reported to inhibit gastric acid secretion, gastric motility, and gastrin secretion and to stimulate release of somatostatin, thereby exerting antiulcer and antilesion effects on stress-induced as well as other types of experimental gastric ulcers or lesions. This fact prompted us to examine changes in serum calcitonin concentration during the development of stress-induced gastric lesions in rats. DA rats were constrained in a stress cage after a 24-h fast and then immersed in 24°C water to the level of the xiphoid process for 2 or 5 h. Serum calcitonin concentrations in stressed rats were significantly lower than those in control rats. To investigate the mechanism of the decline in serum calcitonin level under stress in these rats, we conducted a time-course study of serum calcitonin concentration and ionized calcium level during water-immersion stress, lasting 2 h, and during 4 h following release from the stress. Water immersion caused a remarkable decrease in serum calcitonin concentration as early as at 30 min. After release from stress, serum calcitonin concentration gradually recovered. The ionized calcium level in the blood did not change significantly throughout the experimental period. Furthermore, to examine if the sympathetic nerve system was involved in the stress-induced change of serum calcitonin concentration, α- and β-receptor antagonists were administered intraperitoneally before stress exposure. Administration of α-receptor antagonist at a low dose that did not have any effect on serum calcitonin concentration in a preliminary study, restored the decline of serum calcitonin level, whereas β-receptor antagonist did not. These results suggest that stress-provoked decrease of serum calcitonin concentration may be mediated not by a change of ionized calcium level but by alteration of sympathetic nerve activity (particularly via the α-receptor).
    Type of Medium: Electronic Resource
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