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To investigate the effect of dexmedetomidine on 5-HT-induced constrictions of isolated human intrapulmonary arteries and explore the mechanisms.
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To determine whether a mixture for intravenous perfusion containing tramadol (5 mg/ml), ranitidine (1.5 mg/ml), ketorolac (1.5 mg/ml) and metoclopramide (0.5 mg/ml) in a 0.9% sodium chlorides solution is compatible and stable at room temperature during a 48-hour period.
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HH can be clearly differentiated by its clinical presentation as well as imaging and electrophysiological study results from other primary headaches such as migraine or cluster headache. The underlying pathophysiology is still enigmatic but a hypothalamic involvement seems to be likely.
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In the current study, vasorelaxant effect produced by the aqueous extract of Melissa officinalis L. ssp. officinalis (MOO) (Lamiaceae) and its possible mechanism in isolated rat aortic rings precontracted with phenylephrine were examined. In the first series of experiments, effect of MOO on the baseline and phenylephrine (10(-5)M) precontracted arteries was investigated, while in the second group of experiments, endothelium intact or endothelium denuded effect was determined. The agents used were N(omega)-nitro-L-arginine (L-NAME), an irreversible inhibitor of nitric oxide (NO) synthase, indomethacin (10 microM), a cyclooxygenase (COX) inhibitor, and glibenclamide (10 microM), an ATP-sensitive potassium channel blocker. The extract was found to exert a vasorelaxant effect and rosmarinic acid quantity, the characteristic compound of the plant, was analyzed by reversed-phase high-performance liquid chromatography (18.75%), and was further confirmed by LC-MS analysis giving a prominent [M(+1)] molecular ion peak at m/z 365. Total phenol amount in the extract was determined using Folin-Ciocalteau reagent (0.284 mg/mg extract). Vasorelaxant effect of the extract was entirely dependent on the presence of endothelium and was abolished by pretreatment with L-NAME, whereas pretreatment with indomethacin and glibenclamide reduced the relaxation to a minor extent. Rosmarinic acid was also tested in the same manner as the extract and was found to exert vasorelaxant effect. These results suggest that the aqueous extract of MOO vasodilates via nitric oxide pathway with the possible involvement of prostacycline and endothelium-derived hyperpolarizing factor (EDHF) pathways as well.
Experiments were designed to determine the mechanism of the relaxation induced by tamoxifen in porcine coronary arteries at the tissue, cellular and molecular levels.
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Two review authors independently evaluated methodological quality and extracted data. We sought additional information from study authors. Results are presented using risk ratio (RR; dichotomous data) and mean difference (MD; continuous data) with 95% confidence interval (CI). The number needed to treat for benefit (NNTB) and the number needed to treat for harm (NNTH) were calculated for statistically different categorical outcomes.
Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used to treat inflammatory diseases including rheumatoid arthritis and gout. The anti-inflammatory action of NSAIDs is due to the inhibition of prostaglandin synthesis by preventing cyclooxygenase (COX) activity of prostaglandin H synthase (PGS). However, administration of NSAIDs causes gastrointestinal mucosal lesions and a decrease of granulocytes as side effects. PGS catalyzes two distinct enzyme reactions: (1) bis-dioxygenation of arachidonic acid catalyzed by COX activity of PGS to form PGG(2); and (2) reduction of the hydroperoxide group in PGG(2) by PGS hydroperoxidase. Most NSAID are oxidized by peroxidases to produce NSAID radicals that damage biological components such as lipids and enzymes. Indomethacin, phenylbutazone, and piroxicam are more toxic under aerobic conditions than anaerobic conditions during the interaction with peroxidase. We discuss the contribution of peroxidases in the formation of gastrointestinal mucosal lesions induced by NSAIDs.
While SC-560 significantly delayed recovery from the effects of cutaneous barrier disruption, NS-398 had no such effect. SC-560 was significantly more effective than NS-398 in reducing skin PG levels at 6 and 24 h after cutaneous barrier disruption. SC-560 strongly inhibited biosynthesis of cutaneous PGD(2) to a greater extent than that of other PGs.
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Human aldo-keto reductases (AKRs) regulate nuclear receptors by controlling ligand availability. Enzymes implicated in regulating ligand occupancy and trans-activation of the nuclear receptors belong to the AKR1C family (AKR1C1-AKR1C3). Nuclear receptors regulated by AKR1C members include the steroid hormone receptors (androgen, estrogen, and progesterone receptors) and the orphan peroxisome proliferator-activated receptor (PPARgamma). In human myeloid leukemia (HL-60) cells, ligand access to PPARgamma is regulated by AKR1C3, which diverts PGD(2) metabolism away from J-series prostanoids (Desmond et al., 2003). Inhibition of AKR1C3 by indomethacin, a nonsteroidal anti-inflammatory drug (NSAID), caused PPARgamma-mediated terminal differentiation of the HL-60 cells. To discriminate between antineoplastic effects of NSAIDs that are mediated by either AKR1C or cyclooxygenase (COX) isozymes, selective inhibitors are required. We report a structural series of N-phenylanthranilic acid derivatives and steroid carboxylates that selectively inhibit recombinant AKR1C isoforms but do not inhibit recombinant COX-1 or COX-2. The inhibition constants, IC(50), K(I) values, and inhibition patterns were determined for the NSAID analogs and steroid carboxylates against AKR1C and COX isozymes. Lead compounds, 4-chloro-N-phenylanthranilic acid and 4-benzoyl-benzoic acid for the N-phenylanthranilic acid analogs and most steroid carboxylates, exhibited IC(50) values that had greater than 500-fold selectivity for AKR1C isozymes compared with COX-1 and COX-2. Crystallographic and molecular modeling studies showed that the carboxylic acid of the inhibitor ligand was tethered by the catalytic Tyr55-OH(2)(+) and explained why A-ring substituted N-phenylanthranilates inhibited only AKR1C enzymes. These compounds can be used to dissect the role of the AKR1C isozymes in neoplastic diseases and may have cancer chemopreventive roles independent of COX inhibition.
To investigate the effects of prostacyclin (PGI(2)) and nitric oxide (NO) in the development of hyperdynamic circulatory state on chronic portal hypertensive rats.
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We conducted oligonucleotide microarray experiments on the isolated mRNA from DA and ascending aorta from three study groups (premature fetus-97 ± 0 d, near-term fetus-136 ± 0.8 d, and newborn lamb-12 ± 0 h). We compared the alterations in mRNA expression in DA and aorta to identify genes specifically involved in DA maturation.
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Prostaglandin E(2) (PGE(2)) plays important roles in the bone resorption of inflammatory diseases such as rheumatoid arthritis and periodontitis via specific prostaglandin receptors (i.e., EP1-EP4). In this study, the authors examined whether Prevotella intermedia regulates PGE(2) production and EP expression in human periodontal ligament fibroblasts (hPDLs); they also explored the potential signaling pathways involved in PGE(2) production. P. intermedia induced PGE(2) production and cyclooxygenase-2 (COX-2) expression in a dose- and time-dependent manner. Indomethacin and NS-398 completely abrogated the P. intermedia-induced PGE(2) production without modulating COX-2 expression. Specific inhibitors of extracellular signal-regulated kinase, c-Jun N-terminal kinase, p38, phosphatidylinositol 3-kinase, and protein kinase C--but not c-AMP and protein kinase A--significantly attenuated the P. intermedia-induced COX-2 and PGE(2) expression. P. intermedia reduced EP1 expression in a concentration- and time-dependent manner. The results indicate that the COX-2-dependent induction of PGE(2) by P. intermedia in hPDLs is mediated by multiple signaling pathways.
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The antiulcerogenic effect of diffractaic acid (DA) isolated from Usnea longissima, a lichen species, on indomethacin (IND)-induced gastric lesions was investigated in rats. Administration of 25, 50, 100 and 200 mg/kg doses of DA and ranitidine (RAN) (50 mg/kg dose) reduced the gastric lesions by 43.5%, 52.9%, 91.4%, 96.7% and 72.7%, respectively. It is known that oxidative stress leads to tissue injury in organisms. Thus, in all treated groups of rats, the in vivo activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and the levels of reduced glutathione (GSH) and lipid peroxidation (LPO) were evaluated. IND caused oxidative stress, which resulted in LPO in tissues, by decreasing the levels of GPx, SOD and GSH as compared to healthy rats. In contrast to IND, the administration of DA and RAN showed a significant decrease in LPO level and an increase in tissue SOD, GPx and GSH levels. However, while CAT activity was significantly increased by the administration of IND, the administration of DA and RAN decreased CAT activity. The administration of IND also increased the myeloperoxidase (MPx) activity, which shows neutrophil infiltration into the gastric mucosal tissues. In contrast to IND, the administration of DA and RAN decreased MPx activity. The changes in activities of gastric mucosal nitric oxide synthases (NOS) throughout the development of gastric mucosal damage induced by IND were also studied. A decrease in constitutive NOS (cNOS) activity and an increase in inducible NOS (iNOS) activity were determined in gastric damaged tissues induced by IND. The administration of DA (100 mg/kg dose) and RAN reversed the activities of iNOS and cNOS. These results suggest that the gastroprotective effect of DA can be attributed to its enhancing effects on antioxidant defense systems as well as reducing effects of neutrophil infiltration.
Dodonaea viscosa Linn. (Sapindaceae) is used as a medicinal herb by the tribes of Shola forest regions of Western Ghats. It is used for headaches, backaches, stomach pain, piles and simple ulcers. The present study was performed to evaluate the gastroprotective effect and acute toxicity of this plant in various experimental models.
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patients with primary or recurrent inguinal hernia underwent Lichtenstein repair with a polypropylene mesh. All patients with a follow-up of at least three years were sent a detailed questionnaire and offered an outpatient visit. Kaplan-Meier estimates and Cox proportional hazard regressions were used to analyse the relationship between time to event variables and explanatory variables including anaesthesia type.
To evaluate the risk of post-tonsillectomy hemorrhage associated with perioperative ketorolac use.
Intravenous regional blocks (IVRBs) with ketorolac and lidocaine have been reported to be useful in the treatment of complex regional pain syndrome (CRPS). This is the first controlled prospective study of IVRB with lidocaine and ketorolac for treatment of pain and edema in CRPS of the lower extremity in adults.
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To assess the effect of indomethacin on the growth and invasion of Hep-2 cell line in human laryngeal cancer in vitro.
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Advancing age as well as diseases such as diabetes are characterized by both increased large artery stiffness and impaired peripheral artery function. It has been hypothesized that greater large artery stiffness causes peripheral artery dysfunction; however, a cause-and-effect relationship has not previously been established. We used elastin heterozygote mice (Eln(+/-) ) as a model of increased large artery stiffness without co-morbidities unrelated to the large artery properties. Aortic stiffness, measured by pulse wave velocity, was ∼35% greater in Eln(+/-) mice than in wild-type (Eln(+/+) ) mice (P = 0.04). Endothelium-dependent dilatation (EDD), assessed by the maximal dilatation to acetylcholine, was ∼40% lower in Eln(+/-) than Eln(+/+) mice in the middle cerebral artery (MCA, P < 0.001), but was similar between groups in the gastrocnemius feed arteries (GFA, P = 0.79). In the MCA, EDD did not differ between groups after incubation with the nitric oxide (NO) synthase inhibitor N(ω) -nitro-l-arginine methyl ester (P > 0.05), indicating that lower NO bioavailability contributed to the impaired EDD in Eln(+/-) mice. Superoxide production and content of the oxidative stress marker nitrotyrosine was higher in MCAs from Eln(+/-) compared with Eln(+/+) mice (P < 0.05). In the MCA, after incubation with the superoxide scavenger TEMPOL, maximal EDD improved by ∼65% in Eln(+/-) (P = 0.002), but was unchanged in Eln(+/+) mice (P = 0.17). These results indicate that greater large artery stiffness has a more profound effect on endothelial function in cerebral arteries compared with skeletal muscle feed arteries. Greater large artery stiffness can cause cerebral artery endothelial dysfunction by reducing NO bioavailability and increasing oxidative stress.
In recent years there has been growing interest in advancing amorphous pharmaceuticals as an approach for achieving adequate solubility. Due to difficulties in the experimental measurement of solubility, a reliable estimate of the solubility enhancement ratio of an amorphous form of a drug relative to its crystalline counterpart would be highly useful. We have developed a rigorous thermodynamic approach to estimate enhancement in solubility that can be achieved by conversion of a crystalline form to the amorphous form. We rigorously treat the three factors that contribute to differences in solubility between amorphous and crystalline forms. First, we calculate the free energy difference between amorphous and crystalline forms from thermal properties measured by modulated differential scanning calorimetry (MDSC). Secondly, since an amorphous solute can absorb significant amounts of water, which reduces its activity and solubility, a correction is made using water sorption isotherm data and the Gibbs-Duhem equation. Next, a correction is made for differences in the degree of ionization due to differences in solubilities of the two forms. Utilizing this approach the theoretically estimated solubility enhancement ratio of 7.0 for indomethacin (amorphous/gamma-crystal) was found to be in close agreement with the experimentally determined ratio of 4.9.
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The onset of diabetes causes disruption of respiratory epithelial mediators. The present study investigates whether diabetes modifies the epithelium mediated bronchial responses in hyper-reactive airway smooth muscle (ASM) primarily through nitric oxide (NO), cyclooxygenase (COX), and epithelium derived hyperpolarizing factor (EpDHF) pathways.
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We collected data from 102 patients who had received elective colorectal resection. The patients were randomly allocated into 2 groups and received intravenous patient-controlled analgesia (IVPCA) morphine (M group) or IVPCA morphine plus ketorolac (M+K group). Time-scale morphine consumption (per 12 h), recovery of bowel functions (the first bowel movement and passage of flatus), pain scores, and opioid-related side effects were then recorded.
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Gastric ulcers were induced in rats by acetic acid. Four days later, animals were treated daily with equivalent acid-inhibiting doses of esomeprazole or famotidine, alone or in combination with indomethacin. At day 3 or 7 of treatment, ulcerated tissues were processed to assess: ulcer area; malondialdehyde; prostaglandin E(2); nuclear factor-kB; proliferating cell nuclear antigen and caspase-3 (Western blot).
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Male Wistar rats were treated with 2 mg/kg diet of folic acid for 21 days. Gastric ulceration was induced by indomethacin, scored, and assayed to determine the concentration of total protein, mucus, malondialdehyde (MDA), catalase (CAT) and superoxide dismutase (SOD) in homogenized samples. Normal saline and Ranitidine treated group served as negative and positive control, respectively. Basal and stimulated acid secretion was measured by continuous perfusion method.
The results of the pharmacological studies on MELP demonstrated potent and effective gastroprotection against ethanol, indomethacin and cold stress-induced acute ulcers and ulcer healing in acetic acid induced chronic ulcer. MELP had no significant effect on the intestinal motility and it is also independent of mucus production but rather have a mucolytic effect. In pylorus-ligated rats the extract showed anti-secretory activity by decreasing total gastric juice volume and gastric acidity while increasing the gastric pH. The gastroprotection against ethanol is partially attributed to effective attenuation in the decrease in NP-SH levels, inhibition of the increases in the pro-inflammatory cytokines, TNF-α and IL-17. Phytochemical analysis of MELP revealed the presence of pyrrogalic tannins, saponins, steroids, triterpenoids and simple phenols, with ellagic acid being the major components.
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Previous studies have reported that mouth breathing is associated with respiratory acidosis. Regarding to the reports that renal elimination of weak acids such as indomethacin is pH dependent, this study was carried out to evaluate the role of mouth breathing on plasma level of indomethacin and indomethacin-induced gastric damage in rabbits. Mouth breathing was induced by surgical ligation of nostrils under general anesthesia. One day after the operation, arterial blood samples were collected for acid-base balance analysis and indomethacin was administered intraperitoneally in a single dose of 40mg/kg. The animals were killed 4h after indomethacin administration and blood samples were collected for spectrofluorometric determination of indomethacin in plasma. The results showed that indomethacin induces more severe gastric damage in nose obstructed rabbits compared with sham and unoperated (UNOP) animals. Acid-base analysis revealed a respiratory acidosis in nose obstructed rabbits and indomethacin level of plasma was significantly higher in nose obstructed animals in comparison with control rabbits. The study shows that mouth breathing can increase the potentiation of indomethacin-induced gastric mucosal damage that may be due to higher level of indomethacin in plasma of nose obstructed animals.