Deleterious effects of local corticosteroid injections on the Achilles tendon

Purpose: The purpose of this study is to examine the pathologic changes in the Achilles tendon and its paratenon after intratendinous corticosteroid injections at different intervals and to reveal the effects of this drug on healthy tendon, and also to search the effects of these injections comparing to that of compression with a clamp on the Achilles tendons of the rats. Material and Method: Fifty-two Achilles tendons of twenty-six male Vistar rats were included in the study to search the effects of intratendinous Betamethasone injections comparing that of compression with a clamp. Betamethasone injections were applied to the left tendons in different intervals, while the right tendons served for compression with Mosquito clamps in varied durations. At the end of 30 days, all tendons were excised and examined histopathologically according to a semiquantitative scoring system. Results: Histopathologic evaluation showed some degree of degeneration in both groups. Statistical analysis showed no significant difference among two groups, but in macroscopic evaluation, the tendons in Betamethasone group demonstrated enlargement and strong adhesiveness to the subcutaneous tissue. Discussion: It is concluded that intratendinous Betamethasone injections are as harmful as compression of it with a clamp and it can be used as a degeneration performing model in further studies. Enlargement of the tendon mass and strong adhesiveness to the subcutaneous tissue can be due to injection of the Betamethasone partly outside of tendon

Effects of MK-886, a leukotriene biosynthesis inhibitor, in a rabbit model of endotoxic shock

WOS: 000074468700011PubMed ID: 9696411Leukotrienes are one of the biological mediators that play a role in endotoxic shock. In this study, we investigated the effects of a leukotriene biosynthesis inhibitor, MK-886, in a rabbit model of endotoxic shock. Lipopolysaccharide (Escherichia coli serotype 055:B5) infusion (1 mg kg(-1) h(-1)) to rabbits caused a biphasic decline in arterial blood pressure and decreased the vasoresponsiveness to phenylephrine, potassium chloride, sodium nitroprusside and acetylcholine in abdominal aortic rings. Oral administration of MK-886 (3-(1-(4-chlorobenzyl)-3-t-butyl-thio-5-isopropylindol-2-yl(-2,2-dimethylpropanoic acid) (5 mg/kg) 3 h prior to lipopolysaccharide infusion significantly inhibited the decline in arterial blood pressure and enhanced the responsiveness to phenylephrine and acetylcholine, whereas the changes in sodium nitroprusside and potassium chloride responses were not significant. However, the pD(2) (-log EC50) values for sodium nitroprusside in this group were higher than those of the group that received lipopolysaccharide alone. Neither the administration of the vehicle alone to endotoxemic rabbits, nor MK-886 administration to control animals, caused significant changes. These data suggest that MK-886 attenuates the hypotension and partially reverses the impaired vascular responsiveness observed in endotoxic shock. (C) 1998 Elsevier Science B.V. All rights reserved

Effect of a 5-lipoxygenase inhibitor on blood pressure and vascular responses in a rabbit model of endotoxic shock

WOS: 00007520770103

Contradictory effects of chlorpromazine on endothelial cells in a rat model of endotoxic shock in association with its actions on serum TNF-alpha levels and antioxidant enzyme activities

WOS: 000184402600001PubMed ID: 12860438We examined the effects of the phenothiazine derivative, chlorpromazine on thoracic aortic endothelial cell histology (14 h after LPS challenge) in a model of endotoxic shock in rats. Since excessive formation of tumor necrosis factor-alpha (TNF-alpha) and oxygen-derived free radicals contribute to endothelial injury in endotoxemia, we also evaluated the effect of the drug on the activities of antioxidant enzymes superoxide dismutase (SOD) and catalase in liver tissue in this model and tried to find out whether this possible effect was associated with a change in serum TNF-alpha levels (measured 90 min after chlorpromazine administration). Endotoxemia was induced by a single i.p. injection of lipopolysaccharide (LPS) (5 mg kg(-1) in 1.5 ml of saline; LPS from Escherichia coli serotype 055:135, L-2880, Sigma Chemical Company). Electron microscopic evaluation of the aortas revealed that chlorpromazine (administered 30 min prior to LPS challenge), in smaller doses (3 mg kg(-1)) ameliorated the endothelial cell injury caused by LPS, whereas it caused deterioration of endothelial cell morphology in higher doses (10 and 25 mg kg(-1)). Chlorpromazine administration caused a significant reduction in serum TNF-alpha levels, which was correlated well with an increase in SOD activity in all drug doses (3, 10 and 25 mg kg(-1)). Catalase activity was increased only in the 25 mg kg(-1) chlorpromazine group. (C) 2003 Elsevier Science Ltd. All rights reserved

Effect of vitamin E on vascular responses of thoracic aorta in rat experimental arthritis

WOS: 000073508200026PubMed ID: 95952941. Vascular contractile and relaxant responses were evaluated in isolated aortic rings of adjuvant induced arthritic rats in comparison with control rats, and the effect of an antioxidant treatment on the development of the arthritis was investigated by vitamin E administration (100 mg/kg/day, IM, for 26 days). 2. Arthritis was induced by an intradermal injection of Freund's complete adjuvant into rat paw. Vascular responses, arthritic lesions and serum copper levels were evaluated after 26 days from adjuvant inoculation. 3. Serum copper levels were significantly lower in arthritic rats than in the control. 4. The contractile response of aortic rings to phenylephrine (PE), but not to KCl, was increased in preparations from arthritic rats, which could be explained by an enhancement of intracellular calcium contents. 5. Acetylcholine (Ach)-mediated endothelium-dependent and sodium nitroprusside (SNP)-mediated endothelium-independent relaxations were not changed significantly in vascular preparations from arthritic rats. 6. In arthritic rats, vitamin E treatment improved arthritic lesions with an increase in copper levels. Despite this ameliorating effect, vitamin E treatment caused an increase in contractile response to PE and a decrease in the relaxant response to Ach and SNP in arthritic rats. 7. These data show that vitamin E provides ameliorating effects in improving systemic signs of experimental arthritis, but it fails to restore abnormalities in vascular function, indicating that adjuvant-induced alterations in vascular function may include mechanisms other than oxygen-free radical formation. (C) 1998 Elsevier Science Inc