Title | Increases in plasma and bone cephalosporin levels in experimental hyperlipidaemia | |
Authors | E. Tsivou, N. Kazanas, C. Karageorgiou and C. Tesseromatis
Department of Experimental Pharmacology, Medical School, University of Athens, Goudi 11527 Athens, Greece |
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Citation | Tsivou, E., Kazanas, N., Karageorgiou, C., Tesseromatis, C.: Increases in plasma and bone cephalosporin levels in experimental hyperlipidaemia, Epitheorese Klin. Farmakol. Farmakokinet. 16(2): 137-140 (2002) | |
Publication Date | Received for publication: 15 September 2001
Accepted for publication: 25 October 2001 |
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Full Text Language | English | |
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Keywords | Cephalosporins, mandible, serum, free fatty acids, lipids. | |
Other Terms | review article | |
Summary | Hyperlipidaemia affects mainly the western population and it is associated with the majority of morbidity and mortality. Furthermore, hyperlipidaemia can alter the pharmacodynamic and pharmacokinetic properties of drugs, since it leads to modification of plasma protein levels, interfering with the drug-protein binding. In this study we investigated the role of hyperlipidaemia on the level of a number of cephalosporins (cefazolin, cefalothin, cefapirin, cefaloridin, cefalexine) in plasma and mandible of Wistar rats. Two groups of animals (A control, B experimental), divided in 6 subgroups each (n=7) were used. Hyperlipidaemia was induced by feeding the animals for 4 weeks with a special diet and assessed by the increase, of total lipids, total cholesterol and free fatty acids as well as by the decrease of albumin in plasma of the hyperlipidaemic animals. The cephalosporins’ concentrations were detected by the Bennet method. The concentration of cephalosporins in serum and mandible was found to be higher in the experimental groups compared to the control The observed increases of all investigated cephalosporins in plasma may be attributed to the modified binding of cephalosporins to the serum proteins resulting from the decreased serum albumin levels and the displacement of the drugs from their albumin binding sites by FFAs. | |
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