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Erythromycin stimulates stomach smooth muscle contraction via action on motilin receptors, but the effects of erythromycin on non-pregnant uterine smooth muscle are unknown. The purpose of this study was to assess the effect of erythromycin on non-pregnant uterine smooth muscle and to examine the possible mechanism of its action.
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The present study aimed to investigate the possible influence of several inhibitors and blockers on the vascular effect produced by the acute in vitro application of rosuvastatin to phenylephrine-precontracted aortic rings from rats with a semi-solid, cafeteria-style (CAF) diet. It also aimed to examine the effects of rosuvastatin on the expression of endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase, constitutive cyclooxygenase, and inducible cyclooxygenase in aortic rings from rats with a CAF diet. From comparisons of the effect on phenylephrine-precontracted aortic rings extracted from rats with two different diets (a standard and a CAF diet), it was found that 10(-9) -10(-5) -mol/L rosuvastatin produced lower concentration-dependent vasorelaxation on rings from the CAF diet group. The vasorelaxant effect was unaffected by the vehicle, but it was significantly attenuated by 10(-5) -mol/L N(G) -nitro-l-arginine methyl ester, 10(-2) -mol/L tetraethylammonium, 10(-3) -mol/L 4-aminopyridine, 10(-7) -mol/L apamin plus 10(-7) -mol/L charybdotoxin, 10(-5) -mol/L indomethacin, or 10(-5) -mol/L cycloheximide. Moreover, in aortic rings from rats with a CAF diet, rosuvastatin enhanced the expression of eNOS, inducible nitric oxide synthase, constitutive cyclooxygenase, and inducible cyclooxygenase. The acute in vitro application of rosuvastatin to phenylephrine-precontracted aortic rings from rats with a CAF diet had a vasorelaxant effect. Overall, the present results suggest that the stimulation of eNOS, the opening of Ca(2+) -activated and voltage-activated K(+) channels, the stimulation of prostaglandin synthesis and enhanced protein levels of eNOS, inducible nitric oxide synthase, constitutive cyclooxygenase, and inducible cyclooxygenase are involved in this relaxant effect.
The goal of this study was to determine the effect of angiotensin type 1 (AT(1)) receptor antagonism on vasodilator responses in isolated skeletal muscle resistance arteries. Normotensive Sprague-Dawley rats were fed normal rat chow with the AT(1) receptor antagonist losartan (1mg/ml) in the drinking water for 7 days and compared with untreated control rats. Changes in the diameter of isolated resistance arteries supplying the gracilis muscle were assessed with a video micrometer. Arteriolar responses to acetylcholine, iloprost, and sodium nitroprusside were unaffected by losartan administration, whereas dilation to reduced Po(2) was converted into a constriction. Hypoxia-induced constriction of vessels from losartan-treated rats was inhibited by endothelium removal or indomethacin (1 microM). Blockade of the PGH(2)-thromboxane A(2) receptor with SQ-29548 (10 microM), thromboxane synthase inhibition with dazoxiben (10 microM), or the addition of the superoxide dismutase mimetic 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (TEMPOL, 100 microM) converted hypoxic vasoconstriction to a dilation that was blocked by inhibiting nitric oxide synthase with N(omega)-nitro-l-arginine methyl ester (100 microM). These data suggest that AT(1) receptor activation has an important role in maintaining the vascular release of prostaglandins responsible for mediating hypoxic dilation in skeletal muscle microvessels.
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Low event rate, FPS not prospectively captured.
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The ED50 values for affinities of capsaicin, resiniferatoxin were obtained in nmol/kg b.w. range, whereas the values were in the nmol/kg to micromol/kg b.w. ranges for effects on the gastric basal, stimulated (bethanechol, pentagastrin, histamine) gastric secretion, and the gastric mucosal damage-produced by different ulcerogenic agents (ethanol, HCl, aspirin, indomethacin).
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In LLC-PK1 cells exposed to CaOx, we observed increased cell permeability, no induction of ROS or lipid peroxidation, inability to produce lipopolysaccharide-induced ROS and increases in prostaglandin E2. Indomethacin used alone increased glycosaminoglycan synthesis but did not potentiate CaOx-induced effects. In MDCK cells exposed to oxalate we observed increased cell permeability, ROS production only at higher concentrations and inability to produce lipopolysaccharide-induced ROS. Indomethacin alone had no effect but increased oxalate-induced glycosaminoglycan synthesis.
To study the effect of topical ketorolac 0.4% (Acular LS), bromfenac 0.09% (Megabrom), and nepafenac 0.1% (Nevanac) on postoperative inflammation using laser flare photometry in patients having phacoemulsification with posterior chamber intraocular lens (PC IOL) implantation.
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1. The in vivo effects of the non-steroid anti-inflammatory drug (NSAID) amtolmetin guacyl, a pro-drug of the NSAID tolmetin, on lipid peroxidation, glutathione levels and activity of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase) in rat gastric mucosa, colon mucosa and liver, were compared with the effects of non-selective (indomethacin, diclofenac) and COX-2 selective (celecoxib) NSAIDs. 2. Indomethacin treatment led to an increase in lipid peroxidation, glutathione peroxidase and glucose-6-phosphate dehydrogenase activities and to a decrease in catalase activity and glutathione levels in gastric mucosa. In contrast, amtolmetin guacyl treatment was without effects in gastric and colon mucosa, or liver from control animals. Like amtolmetin guacyl, celecoxib had no effect on the lipid peroxidation, or on enzyme and non-enzyme antioxidant defence systems in gastric mucosa. 3. It is suggested that the lack of pro-oxidant effects in vivo associated with amtolmetin guacyl treatment contribute improved gastric tolerability.
In organ bath studies with arterial rings precontracted with phenylephrine (1 microM), before and after carotid artery occlusion, changes in isometric tension were recorded.
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A single IN ketorolac 31.5 mg dose was well tolerated and provided rapid and effective pain relief in oral surgery patients for a period up to 8 hours.
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Visfatin, also known as nicotiamide phosphoribosyltransferase or pre-B cell colony enhancing factor, is a pro-inflammatory cytokine whose serum level is increased in sepsis and cancer as well as in obesity. Here we report a pro-inflammatory role of visfatin in the brain, to mediate sickness responses including anorexia, hyperthermia and hypoactivity.
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In this paper, we describe a new process for the preparation of drug loaded nanocapsules using a membrane contactor which may be scaled up for industrial applications. Nanocapsules are prepared according to the nanoprecipitation method. The organic phase (solvent, polymer, oil, and drug) is pressed through the pores of an ultrafiltration membrane via the filtrate side. The aqueous phase (water and surfactant) circulates inside the membrane module, and sweeps away the nanocaspules forming at the pore outlets. Two model drugs are selected for the preparation of drug loaded nanocapsules: indomethacin and vitamin E. It is shown that indomethacin loaded nanocapsules with a mean diameter of 240 nm and vitamin E loaded nanocapsules with a mean diameter of 230 nm are obtained with a 150,000 daltons ultrafiltration membrane, a transmembrane pressure of 3 bar, and a crossflow rate of 1.7 m.s(- 1). High fluxes are also obtained (around 0.6 m3/h.m2), leading to the preparation of 1.8 10(- 3) m3 drug loaded nanocapsules in 8 min. The advantage of this membrane contactor compared to other processes for drug loaded nanocapsules preparation is shown to be its scale-up ability.
To describe an apparent association between the use of ketorolac 0.5% (Acular; Allergan) for cystoid macular edema (CME) prophylaxis and impaired corneal wound healing in patients undergoing extracapsular cataract extraction (ECCE) with intraocular lens (IOL) implantation.
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Nefopam group showed less nausea than Ketorolac group within 6 h after the operation. There were no significant differences in demographic data and other complications between both groups. At 48 h after operation, satisfaction and the infused PCA volumes of Nefopam group (34.0± 19.7 ml) showed no significant differences compared to Ketorolac group (30.7± 18.4 ml, P-value= 0.46).
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Level III, therapeutic study. See Instructions for Authors for a complete description of levels of evidence.
Comparisons were made with respect to healing of the lesion without recurrence, time to radiological healing of the lesion, time to functional recovery, and complications related to treatment.
Previous studies have demonstrated that zymosan, a cell wall component of the yeast Saccharomyces cerevisiae, induces inflammation in experimental models. However, few studies have evaluated the potential of zymosan to induce sickness behavior, a central motivational state that allows an organism to cope with infection. To determine whether zymosan administration results in sickness behavior, mice were submitted to the forced swim (FST) and open field (OFT) tests 2, 6, and 24 h after treatment with zymosan (1, 10, or 100 mg/kg). Additionally, to evaluate the possible relationship between zymosan-induced sickness behavior and prostaglandin synthesis, mice were pretreated with the cyclooxygenase inhibitors indomethacin (10 mg/kg) and nimesulide (5 mg/kg) and the glucocorticoid drug dexamethasone (1 mg/kg). Zymosan induced time-dependent decreases in locomotor activity in the OFT, and an increase in immobility in the FST, and increased plasma levels of corticosterone at 2 h. Pretreatment with indomethacin, nimesulide, or dexamethasone blocked zymosan-induced behavioral changes in both the FST and OFT at 2 h post administration. These findings confirm previous observations that zymosan induces sickness behavior. Furthermore, our results provide new evidence that prostaglandin synthesis is necessary for this effect, as anti-inflammatory drugs that inhibit prostaglandin synthesis attenuated zymosan-induced behavioral changes.
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Municipal wastewaters contain a multitude of organic compounds derived from domestic and industrial sources including active components of pharmaceutical and personal care products and compounds used in agriculture, such as pesticides, or food processing such as artificial sweeteners often referred to as micropollutants. Some of these compounds or their degradation products may have detrimental effects on the environment, wildlife and humans. Acesuflame is one of the most popular artificial sweeteners to date used in foodstuffs. The main objectives of this descriptive study were to evaluate the presence of micropollutants in both the influent and effluent of a large-scale conventional biological wastewater treatment plant (WWTP) in South-East Queensland receiving wastewater from households, hospitals and various industries.
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Criteria for diagnosis of AERD as well as desensitization protocols for oral ASA challenge and combined intranasal ketorolac and oral ASA challenge, are detailed in this article based on literature review.
In the present study, we investigated the relation between the inflammatory mediators such as nitric oxide, prostaglandins, and cysteinyl-leukotrienes with mucin release and the sympathetic system in submandibular glands from rats with experimental periodontitis.
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Nonsteroidal anti-inflammatory drugs (NSAIDs) cause gastrointestinal erosions and ulcers. Apoptosis is one of the mechanisms. The role of survivin, an antiapoptosis protein, in NSAID-induced gastric injury is unknown. We examined the role of survivin in NSAID-induced gastric mucosal and gastric cell injury.
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This meta-analysis indicated that prophylactic rectal indomethacin is not suitable for all patients undergoing ERCP but it is safe and effective to prevent PEP in high-risk patients. In addition, rectal indomethacin administration before ERCP is superior to its administration after ERCP for the prevention of PEP.
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Psychological stress-induced hyperthermia is a fundamental autonomic response in mammals. However, the central circuitry underlying this stress response is poorly understood. Here, we sought to identify sympathetic premotor neurons that mediate a hyperthermic response to social defeat stress, a psychological stress model. Intruder rats that were defeated by a dominant resident conspecific exhibited a rapid increase in abdominal temperature by up to 2.0 °C. In these defeated rats, we found that expression of Fos, a marker of neuronal activation, was increased in the rostral medullary raphe region centered in the rostral raphe pallidus and adjacent raphe magnus nuclei. In this region, Fos expression was observed in a large population of neurons expressing vesicular glutamate transporter 3 (VGLUT3), which are known as sympathetic premotor neurons controlling non-shivering thermogenesis in brown adipose tissue (BAT) and thermoregulatory constriction of skin blood vessels, and also in a small population of tryptophan hydroxylase-positive serotonergic neurons. Intraperitoneal injection of diazepam, an anxiolytic agent, but not indomethacin, an antipyretic, significantly reduced both the stress-induced hyperthermia and Fos expression in these medullary raphe neuronal populations. Systemic blockade of β3 -adrenoreceptors, which are abundantly expressed in BAT, also attenuated the stress-induced hyperthermia. These results suggest that psychological stress signals activate VGLUT3-expressing medullary raphe sympathetic premotor neurons, which then drive hyperthermic effector responses including BAT thermogenesis through β(3) -adrenoreceptors.
Dicksonia sellowiana (Presl.) Hook is a native plant from the Central and South Americas that contain high levels of polyphenols, antioxidant compounds involved in protection against inflammation, cancer and cardiovascular risk. A phytomedicinal preparation obtained from aerial parts of D. sellowiana is currently under clinical evaluation in Brazil against asthma, and has been associated with several other beneficial effects. This study demonstrates that a hydroalcoholic extract obtained from D. sellowiana leaves (HEDS) fully relax, in a concentration-dependent manner, rat aortic rings precontracted with phenylephrine. Moreover, administration of HEDS (10, 20 and 40 mg/kg, i.v.) in anaesthetized rats resulted in a strong but reversible hypotension. Aortic relaxation induced by HEDS was abolished by endothelium removal, by incubation of the nitric oxide synthase inhibitor L-NAME, or the soluble guanylate cyclase inhibitor ODQ. In addition, this effect was partially inhibited by indomethacin (a cyclooxygenase inhibitor) and KT 5730 (a PKA inhibitor). The potassium channels blockade by either tetraethylammonium or charybdotoxin also resulted in a potent inhibition of HEDS-induced aortic relaxation, whereas apamine only slightly reduced it. In addition HEDS-induced relaxation was unchanged by 4-amynopiridine and glibenclamide. The selective muscarinic receptor antagonist atropine counteracted both aortic relaxation and blood pressure reduction generated by HEDS. Experiments using HPLC revealed the presence of high amounts of phenolic compounds in this extract. Taken together, our results reveal that the D. sellowiana possess substances with both in vivo and in vitro activities and that the vascular effect of HEDS involves activation of muscarinic receptors, stimulation of the nitric oxide pathway and opening of calcium-activated potassium channels.
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1. This study compares the role of endothelial factors in alpha-adrenoceptor contractile responses in mesenteric resistance (MRA) and superior (SMA) mesenteric arteries from ouabain-treated (8.0 microg day(-1), 5 weeks) and untreated rats. The role of the renin-angiotensin system was also evaluated. 2. Ouabain treatment increased systolic blood pressure. In addition, ouabain reduced the phenylephrine response in SMA but did not alter noradrenaline responses in MRA. 3. Endothelium removal or the nitric oxide synthase (NOS) inhibitor (l-NAME, 100 microm) increased the responses to alpha-adrenergic agonists in both vessels. After ouabain treatment, both endothelial modulation and the l-NAME effect were increased in SMA, while only the l-NAME effect was increased in MRA. Endothelial NOS expression remained unaltered after ouabain treatment. 4. Indomethacin (10 microm) similarly reduced the noradrenaline contraction in MRA from both groups; in contrast, in SMA, indomethacin only reduced phenylephrine-induced contractions in segments from untreated rats. Co-incubation of l-NAME and indomethacin leftward shifted the concentration-response curves for noradrenaline more in MRA from ouabain-treated rats; tetraethylammonium (2 mm) shifted the noradrenaline curves further leftward only in MRA from untreated rats. 5.Losartan treatment prevents the development of hypertension but not all vascular changes observed after ouabain treatment. 6. In conclusion, a rise in endothelial NO and impaired prostanoid participation might explain the reduction in phenylephrine-induced contraction in SMA after ouabain treatment. An increase in the modulatory effect of endothelial NO and impairment of endothelium-dependent hyperpolarizing factor effect might explain why the ouabain treatment had no effect on noradrenaline responses in MRA.