Virodhamine, unlike WIN 55,212-2, relaxed 5-HT-precontracted vessels concentration dependently. The effect of virodhamine was reduced by endothelium denudation, two antagonists of the endothelial cannabinoid receptor, cannabidiol and O-1918, and a high concentration of the CB(1) receptor antagonist rimonabant (5 muM), but only slightly attenuated by the NOS inhibitor L-NAME and not affected by a lower concentration of rimonabant (100 nM) or by the CB(2) and vanilloid receptor antagonists SR 144528 and capsazepine, respectively. The COX inhibitor indomethacin and the fatty acid amide hydrolase inhibitor URB597 and combined administration of selective blockers of small (apamin) and intermediate and large (charybdotoxin) conductance Ca(2+)-activated K(+) channels attenuated virodhamine-induced relaxation. The vasorelaxant potency of virodhamine was lower in KCl- than in 5-HT-precontracted preparations.
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The present study was designed to establish whether penile dorsal arteries isolated from rabbits fed a high cholesterol diet show an enhanced contractile and/or impaired vasodilator response to histamine, and to characterize the histamine receptor subtype involved through in vitro isometric techniques. New Zealand White rabbits were fed a normal diet or a 1% cholesterol diet for 16 weeks. Arteries from cholesterol-fed rabbits retained the ability to relax in response to acetylcholine, whereas histamine and noradrenaline induced a greater contraction response compared to that observed in controls. In both groups, histamine-induced contraction was unaffected by the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME), its precursor L-arginine or the cyclooxygenase inhibitor indomethacin. Treatment of arterial rings in the control and hypercholesterolemia groups with the H1 receptor antagonist, mepyramine, unmasked a vasodilation response to histamine. This was followed by contraction at higher concentrations showing a leftward displacement of the histamine curve compared to controls. The histamine receptor that induced contraction in preparations from the hypercholesterolemic animals was of the H1 subtype, whereas the receptor involved in histamine-induced relaxation was H2. The affinity of histamine receptor agonists was comparable to their effects in control animals, and receptor antagonists showed the same potency in both groups. Our findings indicate a preserved endothelial function and enhanced contraction in response to histamine in penile dorsal arteries, probably due to a change in the sensitivity of the contractile machinery of smooth muscle but not a mechanism mediated by a receptor.
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The effect of three concentrations of safranal on histamine (H(1)) receptors was tested on two groups of tracheal chains incubated with: 1) indomethacin, and 2) indomethacin, propranolol and atropine (n = 6). The EC(50) (effective concentration of histamine causing 50% of maximum response) obtained in the presence of chlorpheniramine and all concentrations of safranal in both groups were significantly greater than those of saline (p < 0.05 to p < 0.001). The EC(50) obtained in the presence of all concentrations of safranal and maximum response of its two higher concentrations (1.25 and 2.5 μg/mL) in group 2 were greater than in group 1 (p < 0.05 to p < 0.001).
Neonatal piglets were fed a liquid milk replacer and on day 3 of age infected or not with 10(8) C. parvum oocysts and the milk replacer supplemented with L-arginine or L-alanine. Milk consumption, body weight, fecal consistency, and oocyst excretion were recorded daily. On day 3 postinfection, piglets were euthanized and serum concentration of NO metabolites and histological severity of villous atrophy and epithelial infection were quantified. Sheets of ileal mucosa were mounted in Ussing chambers for measurement of barrier function (transepithelial resistance and permeability) and short-circuit current (an indirect measurement of Cl secretion in this tissue).
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Establishment, growth, and total burden of endometriotic lesions.
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Indomethacin chitosan nanoparticles (NPs) were developed by ionotropic gelation and optimized by concentrations of chitosan and tripolyphosphate (TPP) and stirring time by 3-factor 3-level Box-Behnken experimental design. Optimal concentration of chitosan (A) and TPP (B) were found 0.6mg/mL and 0.4mg/mL with 120min stirring time (C), with applied constraints of minimizing particle size (R1) and maximizing encapsulation efficiency (R2) and drug release (R3). Based on obtained 3D response surface plots, factors A, B and C were found to give synergistic effect on R1, while factor A has a negative impact on R2 and R3. Interaction of AB was negative on R1 and R2 but positive on R3. The factor AC was having synergistic effect on R1 and on R3, while the same combination had a negative effect on R2. The interaction BC was positive on the all responses. NPs were found in the size range of 321-675nm with zeta potentials (+25 to +32mV) after 6 months storage. Encapsulation, drug release, and content were in the range of 56-79%, 48-73% and 98-99%, respectively. In vitro drug release data were fitted in different kinetic models and pattern of drug release followed Higuchi-matrix type.
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The colon cancer cell line Caco-2, exhibiting a small intestinal phenotype starting as a crypt cell and differentiating to a villous phenotype, and RIE, a rat intestinal epithelial cell line, were employed. Indomethacin was added to differentiated the Caco-2 and RIE monolayer, and cell death was quantified by MTT assay and LDH release in the cell culture supernatant. Indomethacin-induced cell death was also qualified by fluorescent probes under the fluorescent microscope. As a functional study, the permeability of the Caco-2 monolayer was assessed by measuring transepithelial electrical resistance (TEER) and the flux of FITC-conjugated dextran across the monolayer. Indomethacin-induced reactive oxygen species production in Caco-2 and RIE was evaluated by redoxsensitive fluorogenic probes using a fluorometer. In some experiments, antioxidants were used to clarify the role of reactive oxygen species on indomethacin-induced Caco-2 cell death.
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Recent studies have suggested that passive or active immunization with anti-amyloid beta peptide (Abeta) antibodies may enhance microglial clearance of Abeta deposits from the brain. However, in a human clinical trial, several patients developed secondary inflammatory responses in brain that were sufficient to halt the study.
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Fifty-four New Zealand white rabbits received ketorolac (250 μg/0.05 mL) in one eye by a single intracameral injection (group A, n = 18), single intravitreal injection (group B, n = 18), and single suprachoroidal injection (group C, n = 18). Drug concentrations in the vitreous, retina-choroid (RC), and plasma were determined by the methods of high-performance liquid chromatography at 0.5, 1, 2, 4, 8, and 24 hours after injection. The concentrations in the opposite eyes were also investigated.
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Three hundred and ninety one VLBW infants were admitted; 310 survived to discharge. Ninety five were diagnosed with a PDA during their hospitalisations; 21 had a PDA at discharge (10 received indomethacin, 11 were never treated). Among these, mean gestational age was 28 weeks, mean birth weight was 998 g, and median duration of hospitalisation was 73 days. Two infants were discharged on oxygen, two on diuretics, and two on both. None had congestive heart failure, and none died during infancy. Spontaneous closure occurred in 18 of 21 infants at a median PMA of 48 weeks (range 34-76; interquartile range 46-56). Two infants had coil occlusion at 11 months of age. One patient had a PDA at 14 months of age.
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Twelve previously untreated patients with various head and neck cancers were treated by peritumoral injection of a combination of cytokines (Multikine), in addition to zinc sulfate, indomethacin, and a single dose of cyclophosphamide, which were administered systemically. Response was evaluated clinically and histopathologically. T-lymphocyte determinants were studied by fluorescence-activated cell sorter analysis (against controls).
The HE was obtained by exhaustive extraction in Soxhlet apparatus. The chemical characterization of HE was performed by Electrospray Fourier transform ion cyclotron mass spectrometry (ESI FT-ICR MS) analysis. Mice were used for the evaluation of the gastroprotective activity. HE was analyzed in the HCl/ethanol, hypothermic restraint stress ulcer and acetic acid. In the investigation of the gastroprotective mechanisms of HE, were performed the amount of adhered gastric mucus, participation of the α2-adrenoceptor, nitric oxide (NO) and prostaglandins (PGs) using the HCl/ethanol-induced gastric mucosa lesion model.
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60 consecutive patients undergoing non-cemented THA were randomized into two groups in a double-blind and controlled study. During surgery, all patients received standardized pain treatment with LIA. Postoperatively, they were treated either with a solution of Ropivacain, Ketorolac, and Adrenaline (LINFA group) or placebo (placebo group) administered through a catheter to the hip 10 and 22 h after surgery. Pain score, opioid consumption, and length of stay (LOS) were evaluated.
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The study was carried out at the College of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia, over the period 1999 to 2000. Male wistar rats were randomly divided into 12-16 rats in each group. Edema was induced by subplantar injection of 0.1 ml of carrageenan (10 mg/ml) and the resulting edema volume was measured by plethysmograph, 3 hours after the injections. Saline of 0.9% (0.1 ml/100 g) was administered to the first group serving as control. The second and third groups received variable concentration of allopurinol (12.5, 25, 50 mg/kg) and tenoxicam (0.0625, 0.125, 0.25 mg/kg) 30 minutes before carrageenan injection. The fourth group received a combination of tenoxicam and allopurinol. Similar procedures were carried out with respect to diclofenac at 1.25, 2.5, 5.0 mg/kg and indomethacin at 0.25, 0.5, 1.0 mg/kg. The activities of the drugs were expressed as percentage inhibition of edema.
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Ketorolac was administered to nine female and three male shorthair domestic cats as an I/V bolus of 0.5 mg/kg after intubation, and 20 minutes prior to ovariectomy or orchiectomy. Intra-operative cardiorespiratory variables were monitored and blood samples were collected over 24 hours. Concentrations of ketorolac in serum were determined by high-performance liquid chromatography to establish pharmacokinetic parameters.
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We have shown that indomethacin has the potential to activate Ca2+/ calmodulin-dependent protein kinase II (CaMKII), regardless of cyclooxygenase (COX) inhibition. To understand the underlying mechanism, the present study investigated the effect of indomethacin on protein phosphatases such as protein phosphatase 1 (PP1), protein phosphatase 2A (PP2A), and protein tyrosine phosphatase 1B (PTP1B).
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We present a patient, a sixty-seven-year-old woman, who had refractory accumulation of synovial fluid in the knee joints with pustulotic arthro-osteitis for more than 10 years. Fifty ml of synovial fluid from her right knee contained 6,480 pg/ml of interleukin-8 (IL-8) and 15,000/mm3 of neutorophils. At first, she was treated with 400 mg/day of indomethacin farnesil (a prodrug that is converted to indomethacin after intestinal absorption) for 24 weeks. Although, the volume of synovial fluid in her right knee had decreased to 35 ml at the 16th week, it increased to 50 ml at the 24th week again. She was treated with Kampo medicine, Keishikajutsubuto (Guizhi-shu-fu-tang). In the present case, Keishikajutsubuto showed more therapeutic effect to pustulotic arthro-osteitis to reduce volume of synovial fluid to almost 0 ml, IL-8 concentration to 673 pg/ml and number of neutrophils to 660/mm3. Our data showed that Keishikajutsubuto might be suitable for this patient to regulate synovial fluid volume, reduce IL-8 concentration in synovial fluid, and block neutrophils migration to synovial fluid compared to indomethacin therapy.
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IMT-treated animals presented better renal function with less acute tubular necrosis and reduced ROS and MPO production. Moreover, the treatment was associated with lower expression of TNF-alpha, PGE(2), PGES, and t-bet and upregulation of HO-1 and IL-10. This profile was mirrored in serum, where inhibition of COXs significantly decreased interferon (IFN)-gamma, TNF-alpha, and IL-12 p70 and upregulated IL-10.
Seventeen preterm infants and 13 term infants had MRIs performed. There was no significant difference in weight and length at the time of MRI (p = 0.76 and 0.11, respectively). There was no significant difference in total renal volume or total kidney volume to weight ratio between the preterm and term neonates (p = 0.83 and 0.6, respectively).
Our results highlight to the existence of a complex interaction between pulmonary allergy and gastric juice in the airways. The involvement of the non-adrenergic non-cholinergic system, NO, prostanoids and mast cells are directly related to this interaction. We suggest that the reduced contractile response observed in vitro may represent a protector mechanism of the airways. Despite its presence in the human body it can not be observed due to the predominant effects of excitatory the non-adrenergic non-cholinergic system.
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The death of chondrocytes by apoptosis is characteristic of degenerative joint diseases, such as osteoarthritis (OA). Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) have been shown to play an important role in the development of OA. In this study we analyzed the effects of TNF-alpha and IL-1beta on cell death in normal human chondrocytes.
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An English-language literature review was conducted using the PubMed database in November 2007. In compiling evidence on current management trends of ICP and FHF, the paired keywords: fulminant hepatic failure and either mannitol, hypertonic saline, hyperventilation, bioartificial liver, hypothermia, indomethacin, thiopental, or propofol were used. In compiling evidence on ICP monitoring in FHF, the terms "intracranial pressure monitoring" and "liver failure" were used. Excluded references were either pertinent to animal research or irrelevant to ICP monitoring and ICH management in the setting of FHF.