Indomethacin
Cyclooxygenase Inhibitors
Prostaglandins
Anti-Inflammatory Agents, Non-Steroidal
Dinoprostone
Prostaglandins E
Prostaglandin-Endoperoxide Synthases
Ductus Arteriosus, Patent
Cyclooxygenase 1
4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyrazol-3-amine
Stomach Ulcer
Ibuprofen
Gastric Mucosa
6-Ketoprostaglandin F1 alpha
Masoprocol
Meclofenamic Acid
Arachidonic Acid
Prostaglandins F
Dose-Response Relationship, Drug
Epoprostenol
Cyclooxygenase 2
Lipoxygenase Inhibitors
Bradykinin
16,16-Dimethylprostaglandin E2
Aspirin
Vasodilation
Cyclooxygenase 2 Inhibitors
Biological Factors
5,8,11,14-Eicosatetraynoic Acid
Nitric Oxide
NG-Nitroarginine Methyl Ester
Nitroarginine
Thromboxane B2
Rats, Wistar
Guinea Pigs
Thromboxane A2
Acetylcholine
Vasoconstriction
Prostaglandins E, Synthetic
Dinoprost
Rats, Inbred Strains
Muscle Contraction
Endothelium, Vascular
SRS-A
Rabbits
Histamine
Piroxicam
Drug Interactions
Pyrazoles
Rats, Sprague-Dawley
Thromboxanes
Edema
Muscle, Smooth
Phenylbutazone
Nitric Oxide Synthase
Quinacrine
Enzyme Inhibitors
Ketoprofen
Sodium Salicylate
Eicosanoids
Diclofenac
Mesenteric Arteries
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
Carrageenan
Trachea
Muscle Tonus
Dipyrone
Lipoxygenase
Flurbiprofen
Isoenzymes
Suppositories
Thromboxane-A Synthase
Mefenamic Acid
Tocolytic Agents
Charybdotoxin
Salicylates
Arterioles
p-Aminohippuric Acid
Prostaglandin Endoperoxides, Synthetic
Ulcer
Cimetidine
Flufenamic Acid
Dogs
Stimulation of renin release from rabbit renal cortex by arachidonic acid and prostaglandin endoperoxides. (1/4263)
The mechanism by which renal prostaglandins stimulate renin secretion in vivo is unknown. In this in vitro study we measured the effects of activation of the prostaglandin (PG) system on renin release from slices of rabbit renal cortex. The PG precursor arachidonic acid (C20:4), a natural PG endoperoxide (PGG2), two stable synthetic PG endoperoxide analogues (EPA I and II), PGE2, PGF2alpha, and two different PG synthesis inhibitors [indomethacin and 5,8,11,14-eicosatetraynoic acid (ETA)] were used to evaluate the possibility of a direct action of the cortical PG system on renin secretion. Renin release increased significantly with time after addition of C20:4, PGG2, EPA I, and EPA II to the incubation medium. Stimulation of renin release was se-related for C20:4 in concentrations of 0.6 to 4.5 X 10(-6) M, for EPA I in concentrations of 0.7 to 2.8 X 10(-6) M, and for EPA II in concentrations of 1.4 to 14.0 X 10(-6) M. Indomethacin (10(-4) M) and ETA (10(-4) M) significantly decreased basal renin release as well as the renin release stimulated by C20:4 and EPA I. PGE2(10(-12) to 10(-6) M) had no effect on renin release, whereas PGF2alpha (10(-12) to 10(-6) M) decreased renin release in a dose-dependent manner. These data raise the possibility of a direct action of the renal cortical PG system on renin secretion. The results further indicate that stimulation of renin release by C20:4 may depend more specifically on the action of PG endoperoxides than on the primary prostaglandins. (+info)Non-steroidal anti-inflammatory drug-induced apoptosis in gastric cancer cells is blocked by protein kinase C activation through inhibition of c-myc. (2/4263)
Apoptosis plays a major role in gastrointestinal epithelial cell turnover, ulcerogenesis and tumorigenesis. We have examined apoptosis induction by non-steroidal anti-inflammatory drugs (NSAIDs) in human gastric (AGS) cancer cells and the role of protein kinase C (PKC) and apoptosis-related oncogenes. After treatment with aspirin or indomethacin, cell growth was quantified by MTT assay, and apoptosis was determined by acridine orange staining, DNA fragmentation and flow cytometry. The mRNA and protein of p53, p21waf1/cip1 and c-myc was detected by Northern and Western blotting respectively. The influence of PKC on indomethacin-induced apoptosis was determined by co-incubation of 12-O-tetradecanoylphorbol 13-acetate (TPA). The role of c-myc was determined using its antisense oligonucleotides. The results showed that both aspirin and indomethacin inhibited cell growth and induced apoptosis of AGS cells in a dose- and time-dependent manner, without altering the cell cycle. Indomethacin increased c-myc mRNA and protein, whereas p53 and p21wafl/cip1 were unchanged. Down-regulation of c-myc by its antisense oligonucleotides reduced apoptosis induction by indomethacin. TPA could inhibit indomethacin-induced apoptosis and accumulate cells in G2/M. Overexpression of c-myc was inhibited by TPA and p21waf1/cip1 mRNA increased. In conclusion, NSAIDs induce apoptosis in gastric cancer cells which may be mediated by up-regulation of c-myc proto-oncogene. PKC activation can abrogate the effects of NSAIDs by decreasing c-myc expression. (+info)Anti-ulcer effects of 4'-(2-carboxyetyl) phenyl trans-4-aminomethyl cyclohexanecarboxylate hydrochloride (cetraxate) on various experimental gastric ulcers in rats. (3/4263)
Anti-ulcer effects of cetraxate, a new compound possessing anti-plasmin, anti-casein and anti-trypsin actions were investigated by using experimental gastric ulcer models in rats. Cetraxate, 300 mg/kg p.o. showed significant inhibitory effects of 65.3%, 70.0%, 30.2%, and 67.1% against aucte types of ulcers producing by aspirin, phenylbutazone, indomethacin, and pyloric ligature (Shay's ulcer), respectively. These effects were greater than those obtained by gefarnate and aluminum sucrose sulfate may be mainly attributed to the protecting action of this drug on gastric mucosa. Ctraxate further revealed remarkable inhibitory effects on chronic types of ulcers produced by acetic acid, clamping, and clamping-cortisone. In acetic acid ulcer in particular, cetraxate was found to have a dose-dependent inhibitory effect at doses over 50 mg/kg. Of test drugs including L-glutamine and methylmethionine sulfonium chloride, cetraxate showed the most remarkable inhibitory effect on beta-glucuronidase activity in ulcer tissue of these three types of ulcers. These findings suggest that cetraxate may prevent the connective tissue in the ulcer location from decomposition due to lysosomal enzymes such as beta-glucuronidase, thereby accelerating the recovery from ulcer. (+info)Raf-1 is activated by the p38 mitogen-activated protein kinase inhibitor, SB203580. (4/4263)
SB203580 (4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imi dazole) is widely used as a specific inhibitor of p38 mitogen-activated protein kinase (MAPK). Here, we report that SB203580 activates the serine/threonine kinase Raf-1 in quiescent smooth muscle cells in a dose-dependent fashion. The concentrations of SB203580 required lie above those necessary to inhibit p38 MAPK and we were unable to detect basal levels of active p38 MAPK. SB203580 does not directly activate Raf-1 in vitro, and fails to activate Ras, MEK, and ERK in intact cells. In vitro, however, SB203580-stimulated Raf-1 activates MEK1 in a coupled assay. We conclude that activation of Raf-1 by SB203580 is not mediated by an inhibition of p38 MAPK, is Ras-independent, and is uncoupled from MEK/ERK signaling. (+info)The cyclo-oxygenase-dependent regulation of rabbit vein contraction: evidence for a prostaglandin E2-mediated relaxation. (5/4263)
1. Arachidonic acid (0.01-1 microM) induced relaxation of precontracted rings of rabbit saphenous vein, which was counteracted by contraction at concentrations higher than 1 microM. Concentrations higher than 1 microM were required to induce dose-dependent contraction of vena cava and thoracic aorta from the same animals. 2. Pretreatment with a TP receptor antagonist (GR32191B or SQ29548, 3 microM) potentiated the relaxant effect in the saphenous vein, revealed a vasorelaxant component in the vena cava response and did not affect the response of the aorta. 3. Removal of the endothelium from the venous rings, caused a 10 fold rightward shift in the concentration-relaxation curves to arachidonic acid. Whether or not the endothelium was present, the arachidonic acid-induced relaxations were prevented by indomethacin (10 microM) pretreatment. 4. In the saphenous vein, PGE2 was respectively a 50 and 100 fold more potent relaxant prostaglandin than PGI2 and PGD2. Pretreatment with the EP4 receptor antagonist, AH23848B, shifted the concentration-relaxation curves of this tissue to arachidonic acid in a dose-dependent manner. 5. In the presence of 1 microM arachidonic acid, venous rings produced 8-10 fold more PGE2 than did aorta whereas 6keto-PGF1alpha and TXB2 productions remained comparable. 6. Intact rings of saphenous vein relaxed in response to A23187. Pretreatment with L-NAME (100 microM) or indomethacin (10 microM) reduced this response by 50% whereas concomitant pretreatment totally suppressed it. After endothelium removal, the remaining relaxing response to A23187 was prevented by indomethacin but not affected by L-NAME. 7. We conclude that stimulation of the cyclo-oxygenase pathway by arachidonic acid induced endothelium-dependent, PGE2/EP4 mediated relaxation of the rabbit saphenous vein. This process might participate in the A23187-induced relaxation of the saphenous vein and account for a relaxing component in the response of the vena cava to arachidonic acid. It was not observed in thoracic aorta because of the lack of a vasodilatory receptor and/or the poorer ability of this tissue than veins to produce PGE2. (+info)Nitric oxide limits the eicosanoid-dependent bronchoconstriction and hypotension induced by endothelin-1 in the guinea-pig. (6/4263)
1. This study attempts to investigate if endogenous nitric oxide (NO) can modulate the eicosanoid-releasing properties of intravenously administered endothelin-1 (ET-1) in the pulmonary and circulatory systems in the guinea-pig. 2. The nitric oxide synthase blocker N(omega)-nitro-L-arginine methyl ester (L-NAME; 300 microM; 30 min infusion) potentiated, in an L-arginine sensitive fashion, the release of thromboxane A2 (TxA2) stimulated by ET-1, the selective ET(B) receptor agonist IRL 1620 (Suc-[Glu9,Ala11,15]-ET-1(8-21)) or bradykinin (BK) (5, 50 and 50 nM, respectively, 3 min infusion) in guinea-pig isolated and perfused lungs. 3. In anaesthetized and ventilated guinea-pigs intravenous injection of ET-1 (0.1-1.0 nmol kg(-1)), IRL 1620 (0.2-1.6 nmol kg(-1)), BK (1.0-10.0 nmol kg(-1)) or U 46619 (0.2-5.7 nmol kg(-1)) each induced dose-dependent increases in pulmonary insufflation pressure (PIP). Pretreatment with L-NAME (5 mg kg(-1)) did not change basal PIP, but increased, in L-arginine sensitive manner, the magnitude of the PIP increases (in both amplitude and duration) triggered by each of the peptides (at 0.25, 0.4 and 1.0 nmol kg(-1), respectively), without modifying bronchoconstriction caused by U 46619 (0.57 nmol kg(-1)). 4. The increases in PIP induced by ET-1, IRL 1620 (0.25 and 0.4 nmol kg(-1), respectively) or U 46619 (0.57 nmol kg(-1)) were accompanied by rapid and transient increases of mean arterial blood pressure (MAP). Pretreatment with L-NAME (5 mg kg(-1); i.v. raised basal MAP persistently and, under this condition, subsequent administration of ET-1 or IRL 1620, but not of U-46619, induced hypotensive responses which were prevented by pretreatment with the cyclo-oxygenase inhibitor indomethacin. 5. Thus, endogenous NO appears to modulate ET-1-induced bronchoconstriction and pressor effects in the guinea-pig by limiting the peptide's ability to induce, possibly via ET(B) receptors, the release of TxA2 in the lungs and of vasodilatory prostanoids in the systemic circulation. Furthermore, it would seem that these eicosanoid-dependent actions of ET-1 in the pulmonary system and on systemic arterial resistance in this species are physiologically dissociated. (+info)Role of iNOS in the vasodilator responses induced by L-arginine in the middle cerebral artery from normotensive and hypertensive rats. (7/4263)
1. The substrate of nitric oxide synthase (NOS), L-arginine (L-Arg, 0.01 microM - 1 mM), induced endothelium-independent relaxations in segments of middle cerebral arteries (MCAs) from normotensive Wistar-Kyoto (WKY) and hypertensive rats (SHR) precontracted with prostaglandin F2alpha (PGF2alpha). These relaxations were higher in SHR than WKY arteries. 2. L-N(G)-nitroarginine methyl ester (L-NAME) and 2-amine-5,6-dihydro-6-methyl-4H-1,3-tiazine (AMT), unspecific and inducible NOS (iNOS) inhibitors, respectively, reduced those relaxations, specially in SHR. 3. Four- and seven-hours incubation with dexamethasone reduced the relaxations in MCAs from WKY and SHR, respectively. 4. Polymyxin B and calphostin C, protein kinase C (PKC) inhibitors, reduced the L-Arg-induced relaxation. 5. Lipopolysaccharide (LPS, 7 h incubation) unaltered and inhibited these relaxations in WKY and SHR segments, respectively. LPS antagonized the effect polymyxin B in WKY and potentiated L-Arg-induced relaxations in SHR in the presence of polymyxin B. 6. The contraction induced by PGF2alpha was greater in SHR than WKY arteries. This contraction was potentiated by dexamethasone and polymyxin B although the effect of polymyxin B was higher in SHR segments. LPS reduced that contraction and antagonized dexamethasone- and polymyxin B-induced potentiation, these effects being greater in arteries from SHR. 7. These results suggest that in MCAs: (1) the induction of iNOS participates in the L-Arg relaxation and modulates the contraction to PGF2alpha; (2) that induction is partially mediated by a PKC-dependent mechanism; and (3) the involvement of iNOS in such responses is greater in the hypertensive strain. (+info)Effects of tumour necrosis factor-alpha on left ventricular function in the rat isolated perfused heart: possible mechanisms for a decline in cardiac function. (8/4263)
1. The cardiac depressant actions of TNF were investigated in the isolated perfused rat heart under constant flow (10 ml min(-1)) and constant pressure (70 mmHg) conditions, using a recirculating (50 ml) mode of perfusion. 2. Under constant flow conditions TNF (20 ng ml(-1)) caused an early (< 25 min) decrease in left ventricular developed pressure (LVDP), which was maintained for 90 min (LVDP after 90 min: control vs TNF; 110 +/- 4 vs 82 +/- 10 mmHg, P < 0.01). 3. The depression in cardiac function seen with TNF under constant flow conditions, was blocked by the ceramidase inhibitor N-oleoylethanolamine (NOE), 1 microM, (LVDP after 90 min: TNF vs TNF with NOE; 82 +/- 10 vs 11 +/- 5 mmHg, P < 0.05). 4. In hearts perfused at constant pressure, TNF caused a decrease in coronary flow rate (change in flow 20 min after TNF: control vs TNF; -3.0 +/- 0.9 vs -8.7 +/- 1.2 ml min(-1), P < 0.01). This was paralleled by a negative inotropic effect (change in LVDP 20 min after TNF: control vs TNF; -17 +/- 7 vs -46 +/- 6 mmHg, P < 0.01). The decline in function was more rapid and more severe than that seen under conditions of constant flow. 5. These data indicate that cardiac function can be disrupted by TNF on two levels, firstly via a direct, ceramidase dependant negative inotropic effect, and secondly via an indirect coronary vasoconstriction. (+info)Patent ductus arteriosus (PDA) is a condition in which the DA fails to close after birth. This can result in excessive blood flow to the lungs and put extra strain on the heart. PDA is relatively common, occurring in about 1 in every 2000 live births.
Symptoms of PDA may include:
* Fast breathing (tachypnea)
* Shortness of breath (dyspnea)
* Fatigue
* Sweating during feedings
* Frequent respiratory infections
If left untreated, PDA can lead to long-term complications such as:
* Increased risk of respiratory infections
* Heart failure
* Developmental delays
* Cognitive impairments
Treatment for PDA may include:
* Medications to reduce blood pressure in the lungs and improve oxygenation
* Surgery to close the ductus arteriosus, either through a catheter or open-heart surgery
In some cases, PDA may be treated with medication alone. However, if the condition is not treated promptly, surgical intervention may be necessary to prevent long-term complications.
Stomach ulcers are caused by an imbalance between the acid and mucus in the stomach, which can lead to inflammation and damage to the stomach lining. Factors that can contribute to the development of a stomach ulcer include:
* Infection with the bacterium Helicobacter pylori (H. pylori)
* Overuse of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen
* Excessive alcohol consumption
* Smoking
* Stress
* Zollinger-Ellison syndrome, a rare condition that causes the stomach to produce too much acid.
Symptoms of a stomach ulcer may include:
* Pain in the upper abdomen, often described as a burning or gnawing sensation
* Nausea and vomiting
* Bloating and gas
* Abdominal tenderness
* Loss of appetite
* Weight loss
Treatment for stomach ulcers typically involves antibiotics to kill H. pylori, if present, and acid-suppressing medications to reduce the amount of acid in the stomach. In severe cases, surgery may be necessary. Lifestyle changes, such as avoiding NSAIDs, alcohol, and smoking, can also help manage symptoms and prevent recurrence.
Preventive measures for stomach ulcers include:
* Avoiding NSAIDs and other irritating substances
* Using acid-suppressing medications as needed
* Maintaining a healthy diet and lifestyle
* Managing stress
* Avoiding excessive alcohol consumption
It is important to seek medical attention if symptoms persist or worsen over time, as stomach ulcers can lead to complications such as bleeding, perforation, and obstruction. Early diagnosis and treatment can help prevent these complications and improve outcomes.
There are several types of edema, including:
1. Pitting edema: This type of edema occurs when the fluid accumulates in the tissues and leaves a pit or depression when it is pressed. It is commonly seen in the skin of the lower legs and feet.
2. Non-pitting edema: This type of edema does not leave a pit or depression when pressed. It is often seen in the face, hands, and arms.
3. Cytedema: This type of edema is caused by an accumulation of fluid in the tissues of the limbs, particularly in the hands and feet.
4. Edema nervorum: This type of edema affects the nerves and can cause pain, numbness, and tingling in the affected area.
5. Lymphedema: This is a condition where the lymphatic system is unable to properly drain fluid from the body, leading to swelling in the arms or legs.
Edema can be diagnosed through physical examination, medical history, and diagnostic tests such as imaging studies and blood tests. Treatment options for edema depend on the underlying cause, but may include medications, lifestyle changes, and compression garments. In some cases, surgery or other interventions may be necessary to remove excess fluid or tissue.
Heterotopic ossification can cause a range of symptoms depending on its location and severity, including pain, stiffness, limited mobility, and difficulty moving the affected limb or joint. Treatment options for heterotopic ossification include medications to reduce inflammation and pain, physical therapy to maintain range of motion, and in severe cases, surgical removal of the abnormal bone growth.
In medical imaging, heterotopic ossification is often diagnosed using X-rays or other imaging techniques such as CT or MRI scans. These tests can help identify the presence of bone growth in an abnormal location and determine the extent of the condition.
Overall, heterotopic ossification is a relatively rare condition that can have a significant impact on a person's quality of life if left untreated. Prompt medical attention and appropriate treatment can help manage symptoms and prevent long-term complications.
There are many different types of stomach diseases, some of which include:
1. Gastritis: This is inflammation of the stomach lining, which can be caused by infection, autoimmune disorders, or excessive alcohol consumption.
2. Peptic ulcer: This is a sore on the lining of the stomach or duodenum (the first part of the small intestine). Peptic ulcers are often caused by infection with the bacterium Helicobacter pylori, but they can also be caused by excessive acid production.
3. Gastroesophageal reflux disease (GERD): This is a condition in which stomach acid flows back up into the esophagus, causing symptoms such as heartburn and difficulty swallowing.
4. Stomach cancer: This is a type of cancer that affects the stomach lining, and it can be caused by a variety of factors including age, diet, and family history.
5. Inflammatory bowel disease (IBD): This is a chronic condition that causes inflammation in the digestive tract, including the stomach. Crohn's disease and ulcerative colitis are examples of IBD.
6. Gastrointestinal motility disorders: These are conditions that affect the muscles and nerves of the digestive system, causing problems with movement and contraction of the stomach and intestines.
7. Stomach polyps: These are growths on the lining of the stomach that can be benign or cancerous.
8. Hiatal hernia: This is a condition in which part of the stomach bulges up into the chest through a hole in the diaphragm, which can cause symptoms such as heartburn and difficulty swallowing.
9. Gastroesophageal reflux disease (GERD): This is a chronic form of acid reflux that can cause symptoms such as heartburn and difficulty swallowing.
10. Zollinger-Ellison syndrome: This is a rare condition that causes the stomach to produce too much acid, leading to symptoms such as heartburn, nausea, and vomiting.
These are just some of the many possible causes of stomach pain. It's important to see a doctor if you experience persistent or severe stomach pain, especially if it is accompanied by other symptoms such as fever, bleeding, or difficulty swallowing. Your doctor can perform tests and examinations to determine the cause of your stomach pain and recommend appropriate treatment.
There are several types of ulcers, including:
1. Peptic ulcer: A type of ulcer that occurs in the lining of the stomach or duodenum (the first part of the small intestine). Peptic ulcers are caused by excess acid production and are often associated with stress, spicy foods, and certain medications.
2. Stomal ulcer: A type of ulcer that occurs in the stoma (the opening) of a surgically created ostomy (a procedure that creates an artificial opening in the abdominal wall).
3. Pressure ulcer: A type of ulcer that occurs as a result of prolonged pressure on the skin, often seen in people who are bedridden or have mobility issues.
4. Venous ulcer: A type of ulcer that occurs on the legs and is caused by poor blood flow and increased pressure in the veins.
5. Diabetic foot ulcer: A type of ulcer that occurs on the feet of people with diabetes, often as a result of nerve damage (neuropathy) and poor blood flow.
The symptoms of an ulcer can vary depending on its location and severity, but may include:
* Pain or discomfort in the affected area
* Redness and swelling around the ulcer
* Discharge or pus from the ulcer
* Fever or chills
* Difficulty healing
Treatment for an ulcer will depend on its cause and severity, but may include:
* Antibiotics to treat any underlying infections
* Medications to reduce acid production or protect the stomach lining
* Wound care and dressing changes to promote healing
* Surgery to close the ulcer or remove any dead tissue
* Changes to diet and lifestyle to manage underlying conditions such as diabetes or high blood pressure.
Here are some examples of jejunal diseases:
1. Crohn's disease: This is a chronic inflammatory bowel disease that can affect any part of the gastrointestinal tract, including the jejunum. It causes inflammation and damage to the lining of the intestine, leading to symptoms such as diarrhea, abdominal pain, and fatigue.
2. Ulcerative colitis: This is a chronic condition that causes inflammation and sores in the lining of the colon and rectum, but can also affect the jejunum. Symptoms include diarrhea, abdominal pain, and bloody stools.
3. Jejunoileal bypass surgery: This is a type of bariatric surgery that involves rerouting the small intestine to reduce the amount of food that can be absorbed. While it can lead to weight loss, it can also cause nutrient deficiencies and other complications.
4. Jejunal tumors: These are growths that can occur in the jejunum, which can be benign or malignant. Symptoms include abdominal pain, bloating, and obstruction of the intestine.
5. Jejunal strictures: These are narrowing of the jejunum that can cause obstruction of food passage and lead to symptoms such as abdominal pain, nausea, and vomiting.
6. Jejunal inflammatory fibrosis: This is a condition where the jejunum becomes inflamed and scarred, leading to thickening of the intestinal walls and narrowing of the intestine. Symptoms include abdominal pain, diarrhea, and malabsorption.
7. Jejunal enteropathy: This is a condition where the jejunum becomes damaged, leading to symptoms such as diarrhea, abdominal pain, and weight loss. It can be caused by a variety of factors, including infection, inflammation, and autoimmune disorders.
8. Jejunal ulcers: These are open sores that can occur in the lining of the jejunum, often as a result of infection or inflammation. Symptoms include abdominal pain, nausea, and vomiting.
9. Jejunal ischemia: This is a condition where the blood supply to the jejunum is reduced, leading to damage to the intestinal tissue. Symptoms include abdominal pain, diarrhea, and rectal bleeding.
10. Jejunal cancer: This is a rare type of cancer that can occur in the jejunum. Symptoms include abdominal pain, weight loss, and rectal bleeding.
These are just a few examples of the many different conditions that can affect the jejunum. If you suspect that you or someone you know may have a condition affecting the jejunum, it is important to seek medical attention as soon as possible for proper diagnosis and treatment.
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Patent ductus art3
- Although intravenous indomethacin and ibuprofen are widely used for closure of patent ductus arteriosus in premature infants, these formulations are unavailable in the Islamic Republic of Iran. (who.int)
- Intravenous indometacin is administered to close a hemodynamically significant patent ductus arteriosus, as indicated by clinical evidence, in premature infants. (rcsb.org)
- A177871,L6778] Intravenous indometacin is indicated to induce closure of a hemodynamically significant patent ductus arteriosus in premature infants weighing between 500 and 1750 g when after 48 hours usual medical management (e.g., fluid restriction, diuretics, digitalis, respiratory support, etc.) is ineffective. (rcsb.org)
NSAIDs6
- Limit use of NSAIDs, including indomethacin capsules, between about 20 to 30 weeks in pregnancy due to the risk of oligohydramnios/fetal renal dysfunction. (nih.gov)
- anti-inflammatory drugs (NSAIDs) such as ibuprofen or indomethacin when symptoms begin. (nih.gov)
- A177871] Since then, indometacin has been extensively studied in clinical trials as one of the most potent NSAIDs in blocking prostaglandin synthesis and was among the first NSAIDs to be used in the symptomatic treatment of migraine and for headaches that eventually became known as "indomethacin-responsive" headache disorders. (rcsb.org)
- Indomethacin belongs to a class of non-steroidal anti-inflammatory drugs (NSAIDs). (buycialisonliney.com)
- To test the hypothesis that non-steroidal anti-inflammatory drugs (NSAIDs) accelerate the progression of osteoarthritis by reducing synthesis of vasodilator prostaglandins, thereby diminishing joint perfusion, 105 osteoarthritis patients awaiting hip arthroplasty were treated prospectively with a strong or weak prostaglandin synthesis inhibitor, indomethacin or azapropazone, respectively. (nih.gov)
- Some people may not be able to tolerate long-term use of indomethacin and may have to rely on less effective NSAIDs. (nih.gov)
Nonsteroidal anti1
- Indomethacin is a type of nonsteroidal anti-inflammatory drug. (medlineplus.gov)
Prostaglandin2
- A177871] The pharmacological effect of indometacin is not fully understood, however, it is thought to be mediated through potent and nonselective inhibition of the enzyme cyclooxygenase (COX), which is the main enzyme responsible for catalyzes the rate-limiting step in prostaglandin and thromboxane biosynthesis via the arachidonic acid (AA) pathway. (rcsb.org)
- Therefore, we examined the involvement of prostaglandin in experimentally induced ARDS by using prostaglandin synthesis inhibitor, indomethacin. (who.int)
Prostaglandins3
- Relationships between the concentrations of prostaglandins and the nonsteroidal antiinflammatory drugs indomethacin, diclofenac, and ibuprofen. (nih.gov)
- Indomethacin inhibits the production of prostaglandins and relieve the pain and inflammation. (dd-database.org)
- The patients receiving azapropazone, who had higher concentrations of synovial vasodilator prostaglandins, took longer than the indomethacin group to reach the arthroplasty end-point. (nih.gov)
Osteoarthritis3
- and moderate to severe osteoarthritis is indomethacin capsules 25 mg two or three times a day. (nih.gov)
- A177871] Most commonly used in rheumatoid arthritis, ankylosing spondylitis, osteoarthritis, acute shoulder pains, and acute gouty arthritis, indometacin is currently available as oral capsules as well as other methods of administration, including rectal and intravenous formulations. (rcsb.org)
- Oral indometacin is indicated for symptomatic management of moderate to severe rheumatoid arthritis including acute flares of chronic disease, moderate to severe ankylosing spondylitis, moderate to severe osteoarthritis, acute painful shoulder (bursitis and/or tendinitis) and acute gouty arthritis. (rcsb.org)
Prescription17
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Preterm infants1
- In this study of the therapeutic effects of oral treatments, 20 preterm infants were randomized to oral ibuprofen (1 × 10 mg/kg, then 2 × 5 mg/kg at 24-hour intervals) or oral indomethacin (3 × 0.2 mg/kg at 24-hour intervals). (who.int)
Intravenous1
- The trial was divided into two groups (n=64) using a randomised number table group A will be given 100 mg of indomethacin suppository rectally and group B will be given 8 mg of intravenous lornoxicam. (bvsalud.org)
Infants3
- March 4 issue),* very early treatment with indomethacin was shown to prevent the development of a hemodynamically important shunt through the ductus arteriosus among newborn infants weighing less than 1000 g at birth. (elsevierpure.com)
- One of the important benefits to the indomethacin-treated infants but not to those receiving a placebo was a statistically significant shorter time needed to regain birth weight. (elsevierpure.com)
- Three of the 12 infants who received placebo had necrotizing enterocolitis, but none of the 10 infants given indomethacin had this problem. (elsevierpure.com)
Arthritis6
- The dosage for acute gouty arthritis is indomethacin capsules 50 mg three times a day. (nih.gov)
- Indomethacin is a potent nonsteroidal antiinflammatory drug (NSAID) typically used for chronic inflammatory arthritis. (nih.gov)
- Sudden death of a child with juvenile chronic arthritis, probably due to indomethacin. (nih.gov)
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Occurs2
- Indomethacin overdose occurs when someone takes more than the normal or recommended amount of this medicine. (medlineplus.gov)
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Inflammation3
- On the eye, indomethacin is used to treat inflammation of the front section of the eye after surgery. (dd-database.org)
- L10553] Ophthalmic indometacin has been studied and used in the symptomatic treatment of postoperative ocular inflammation and pain and/or complications after cataract surgery. (rcsb.org)
- Value of indomethacin suppository for preoperative analgesia and anti-inflammation in laparoscopic appendectomy: a protocol of prospective, double-blinded, single-centre, randomised controlled trial in China. (bvsalud.org)
Decreases1
- We have developed a valid predictive model for predicting SIVH as well as shown that exposure to indomethacin decreases the incidence of SIVH overall. (elsevier.com)
Capsules5
- These highlights do not include all the information needed to use INDOMETHACIN CAPSULES safely and effectively. (nih.gov)
- See full prescribing information for INDOMETHACIN CAPSULES. (nih.gov)
- Avoid use of indomethacin capsules in patients with severe heart failure unless benefits are expected to outweigh risk of worsening heart failure. (nih.gov)
- Indomethacin capsules are contraindicated in patients with aspirin-sensitive asthma. (nih.gov)
- Discontinue indomethacin capsules at first appearance of skin rash or other signs of hypersensitivity. (nih.gov)
Celecoxib3
- In fact, gout patients treated with Celecoxib have the same treatment response as Indomethacin. (nbmeanswers.com)
- Indomethacin is typically the DOC, better than celecoxib. (nbmeanswers.com)
- Higher doses of celecoxib are needed to reach similar pain relief in acute gout compared to indomethacin. (nbmeanswers.com)
Lymphocyte1
- In addition, indomethacin and atorvastatin ameliorated abnormal cytokine secretion, lymphocyte subset disorder, and hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-gonadal (HPG) axis imbalances in APP/PS1 mice. (nih.gov)
Diclofenac1
- Diclofenac es metabolizado por el hígado y excretado por vía biliar y renal, principalmente como metabolitos en forma de glucuronatos o sulfatos. (artistrydance.hu)
Abstract1
- abstract = "Prophylactic indomethacin may decrease Severe Intraventricular Hemorrhage (SIVH). (elsevier.com)
Drugs4
- Two other human proteins-PGES-2 and SIGMAR1-were of particular interest because they are targets of existing drugs, including the anti-inflammatory indomethacin for PGES-2 and antipsychotics like haloperidol for SIGMAR1. (nih.gov)
- Nonsteroidal anti-inflammatory drugs (including indomethacin) may rarely increase the risk for a heart attack or stroke. (healthwarehouse.com)
- Read also the information about the drug group non-steroidal anti-inflammatory drugs, to which belongs the active ingredient indomethacin. (dd-database.org)
- Indomethacin works like the other nonsteroidal anti-inflammatory drugs from subgroup of acetic acid compounds. (dd-database.org)
Symptoms2
- Below are symptoms of an indomethacin overdose in different parts of the body. (medlineplus.gov)
- Indomethacin provides rapid relief from symptoms. (nih.gov)
Acute2
- jaypat Indomethacin is typically the first choice NSAID for acute gout flares. (nbmeanswers.com)
- IMSEAR at SEARO: Indomethacin Exacerbates Oleic Acid-Induced Acute Respiratory Distress Syndrome in Adult Rats. (who.int)
Methotrexate2
- The simultaneous ingestion of indomethacin and digoxin, lithium, methotrexate, or phenytoin increases the concentration of those substances in the blood. (dd-database.org)
- 6. Enhancement of etoposide and methotrexate sensitivity by indomethacin in vitro. (nih.gov)
Headache disorders2
- Indomethacin-responsive headaches are a heterogeneous group of primary headache disorders distinguished by their swift and often absolute response to indomethacin. (ouchuk.org)
- Case reports of other primary headache disorders that also respond to indomethacin, such as cluster headache, nummular headache, and ophthalmoplegic migraine, have been described. (ouchuk.org)
Typically1
- For example, flare up are at of involvement potential to typically develop may require are how Do I Buy Indomethacin by a. (totoscleaning.com)
Subset1
- Traditionally, indomethacin-responsive headaches include a subset of trigeminal autonomic cephalalgias (paroxysmal hemicrania and hemicrania continua), Valsalva-induced headaches (cough headache, exercise headache, and sex headache), primary stabbing headache, and hypnic headache. (ouchuk.org)
Headaches2
- Indomethacin-responsive headaches. (ouchuk.org)
- These "novel" indomethacin-responsive headaches beg the question of what headache characteristics are required to qualify a headache as an indomethacin-responsive headache. (ouchuk.org)
Pharmacist1
- Read the Medication Guide provided by your pharmacist before you start using indomethacin and each time you get a refill. (healthwarehouse.com)
Treatment4
- How well someone does depends on how much indomethacin was swallowed and how quickly treatment is received. (medlineplus.gov)
- They found that COVID-19 patients taking indomethacin were less likely than those taking an anti-inflammatory that doesn't target PGES-2 to require treatment at a hospital. (nih.gov)
- Treatment with indomethacin and atorvastatin ameliorated impairments in spatial learning and memory, and the active avoidance response in APP/PS1 mice. (nih.gov)
- The headache must also be completely responsive to treatment with the non-steroidal anti-inflammatory drug (NSAID) indomethacin. (nih.gov)
Differential1
- These headache syndromes differ in extent of response to indomethacin, clinical features, and differential diagnoses. (ouchuk.org)
Significantly2
- More analysis shows that the volume as well as the surface area of the micelle expand significantly in the presence of indomethacin, and are fairly the same in the presence of ibuprofen. (aps.org)
- Pulmonary water content in indomethacin pretreated animals was also significantly greater than control group. (who.int)
Patients1
- Application of the model to patients receiving indomethacin suggests a benefit at the highest risk levels. (elsevier.com)
Joint3
- Indomethacin is used mostly for pain due to joint diseases. (dd-database.org)
- The joint are 2 get your erosive and activity, but soon the that how Do I Buy Indomethacin rowing, when (includes eggs and dairy) diets for x 16. (totoscleaning.com)
- In the indomethacin group the affected hips lost joint space more rapidly than did the contralateral hips, a difference not seen in the azapropazone group. (nih.gov)
Severe pain1
- The pain, which covers indomethacin here, range from mild to moderately severe pain or of strong to very severe pain. (dd-database.org)
Closure1
- Complete ductal closure was seen in 7/10 of the indomethacin and 8/10 of the ibuprofen group. (who.int)
Depends1
- Indometacin niereninsuffizienz, owned by state where it depends what one such investigation, that align to determine whether the late 1980s. (humboldtgreenjobs.com)
Drug4
- Known hypersensitivity to indomethacin or any components of the drug product. (nih.gov)
- Indomethacin has been associated with rare cases of idiosyncratic drug induced liver disease. (nih.gov)
- Indometacin, or indomethacin, is a non-steroidal anti-inflammatory drug (NSAID) with anti-inflammatory, analgesic, and antipyretic properties. (rcsb.org)
- The non-steroidal anti-inflammatory drug indomethacin suppository has antipyretic and analgesic effects. (bvsalud.org)