Effects of vertebral fusion on levels of pro-inflammatory and catabolic mediators in a rabbit model of intervertebral disc degeneration

Objective: The aim of this study was to explore the alterations in levels of pro-inflammatory and catabolic mediators following vertebral fusion in a rabbit model of intervertebral disc degeneration

The Addition of Exercise to High-Intensity Laser Therapy Improves Treatment Effectiveness on Pain and Muscle Strength in Patients with Subacromial Pain Syndrome: A Randomized Trial

Objective To assess the efficacy of adding exercise to high-intensity laser therapy (HILT) in improving treatment effectiveness for clinical outcomes in patients with subacromial pain syndrome.Methods Thirty patients with subacromial pain syndrome were randomly assigned to the HILT-only group (n=15) or HILT & Exercise group (n=15). The primary outcome was shoulder function and disability. Secondary outcomes were pain, range of motion, proprioception (joint position sense), and muscle strength.Results Shoulder function and disability, pain, range of motion, joint position sense, and some muscle strength improved in both groups (p0.05). Time-group showed significant effects for activity pain and strength in favor of the HILT & Exercise group. Middle trapezius, lower trapezius, and supraspinatus strength increased after HILT plus exercise (p<0.05), activity pain, upper trapezius, serratus anterior, and subscapularis strength improved more compared to HILT (p<0.05).Conclusions We found no clinically important differences between HILT and HILT-plus exercise in shoulder function and disability, rest pain, mobility, and proprioception, in patients with subacromial pain syndrome. The addition of exercise to HILT was superior to HILT for improving activity pain and muscle strength

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 homocysteine on nitric oxide production in coronary microvascular endothelial cells

WOS: 000247729400005PubMed ID: 17578710Hyperhomocysteinemia is widely recognized as an independent risk factor for coronary artery vascular disease, although the underlying mechanisms are not well understood. This study aims to investigate the effect of homocysteine on nitric oxide ( NO) production in coronary microvascular endothelial cells (CMECs) and putative mechanisms mediating this effect. CMECs were isolated on Langendorff system by collagenase perfusion of hearts from male rats and cultured. The effect of homocysteine (0.01 to 1 mM) on basal and stimulated NO production was evaluated by measuring nitrite in the culture media after incubation with or without N-G-nitro-L-arginine methyl ester (L-NAME) ( 1 mM), superoxide dismutase (100 U/mL), or catalase ( 1000 U/mL) for 24 h. Total nitrite was measured using Griess reaction after reduction of nitrate to nitrite with nitrate reductase. Homocysteine did not affect basal nitrite accumulation; however, it significantly increased the nitrite accumulation induced by the calcium ionophore A23187 or interleukin-1 beta only at 1 mM. This effect of homocysteine was significantly inhibited by L-NAME, superoxide dismutase, and catalase. In conclusion, homocysteine increases NO release from stimulated CMECs without affecting basal NO production, which is probably accompanied by increased production of reactive oxygen species. It can be postulated that endothelial cells generate NO in order to minimize the damage caused by homocysteine

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