Modifications of clonidine binding to rabbit liver protein under the influence of non-steroid-anti-inflammatory drugs in vitro.

This study was designed to investigate the binding of clonidine to liver protein as well as the possible interactions with non-steroid anti-inflammatory drugs (NSAIDs) during the binding process in the rabbit. The binding of clonidine to slices (S) and homogenized slices (H) was estimated by a radioisotopic method following incubation with a mixture of cold and 3H-labelled clonidine in Ringer solution at 37 degrees C for 360 min. The binding of clonidine was assessed in the absence and presence of the following NSAIDs: flurbiprofen, ketoprofen, ibuprofen and acetylsalicylic acid. The results showed that the percentage of clonidine binding did not differ between intact and homogenized slices. The addition of all NSAIDs but ibuprofen, significantly decreased the protein binding of clonidine both in intact and homogenized liver slices. This finding could be attributed to the different affinity of ibuprofen for liver protein compared to the remaining NSAID's which may arise from a number of chemical properties including its dual Pka values.

Changes in serum levels of quinolones in rats under the influence of experimental trauma.

Administration of antibiotics is considered an important factor during, or after, operational procedures in the maxillofacial area, in order to avoid post-surgical complications. In the present study, the levels of quinolones in serum and tissues such as the parotid gland, the tongue and the bone of the jaws were estimated during traumatic injury in the oral cavity. For this purpose, two groups (A and B) of Wistar rats, consisting of 35 animals each were used. Group A (control) and group B (experimental) were divided in five subgroups (A1, A2, A3, A4, A5, and B1, B2, B3, B4, B5). In the experimental group, model traumatic injury was performed through the whole lenght of the cheek. Subjects received orally ciprofloxacin, pefloxacin, norfloxacin, ofloxacin and cinoxacin. The concentration of quinolones in serum and in most of the tissues was significantly higher in the experimental groups than in controls. In addition, the FFA levels and the weight of adrenals (as indicators of stress) were higher in the trauma groups. Stress seemed to affect many pathophysiological mechanisms which are responsible for the alterations observed.

How harmless is FFA enhancement?

Standard heparin as well as low molecular weight heparin (LMWH) increase lipid levels in serum. It has been reported that a diet rich in long chain saturated fatty acids can enhance the susceptibility to experimental thrombosis. The mechanism by which serum fatty acids may provoke thrombosis is not clear. It is possible that the fatty acids change the properties of the cell membrane and thereby modify the response of platelets to aggregating agents. Heparin and its LMW fractions, by mobilising lipoprotein lipase that hydrolyses serum triglycerides (TG), cause the serum TG to increase, a well known "clearing effect' of heparin in turbid lipemic plasma. This effect may have no significance when it lasts for a short time; however, a long-lasting heparin effect on TG serum levels may have important consequences. The purpose of this study was to examine the time span of the action of heparin and its fractions and to investigate variations in the concentration of digoxin, which is a compound with narrow therapeutic width. The investigated substances after 2 days administration, provoked serum concentration increases of free fatty acids (FFA), TG and HDL-C. Seven days after stopping drug administration, FFA and HDL-C levels remained high, while triglycerides declined. Serum total cholesterol remained unchanged throughout. Digoxin levels increased non-significantly after heparin administration and during swimming stress, while a lipid diet caused a serum digoxin concentration increase.

Cold swimming stress: effects on serum lipids, lipoproteins and LCAT activity in male and female rats.

Effects of consistent cold swimming stress on lipid and lipoprotein metabolism parameters were studied using male and female rats over a period of 60 and 20 days respectively. At the end of treatment serum total cholesterol, high density lipoproteins (HDL-C) and lecithin:cholesterol acetyltransferase (LCAT) activity declined in both male and female rats. TC/HDL-C ratio declined in 20 days in females, while in males it did not change. Free fatty acids increased, while triglycerides remained unchanged in both sexes. %Lipoprotein distribution in male animals did not show any phenotype alteration except in the group of 40 days where %VLDL declined and %LDL-C increased. Body weights did not change, except in males in 60 days. Consistent cold swimming stress by lowering HDL-C and LCAT activity seems to influence lipoprotein metabolism.