Motrin
Ibuprofen overdose: the first two years of over-the-counter sales.

Perry SJ, Streete PJ, Volans GN.

Experience during 14 years of prescription only use indicates that the non-steroidal anti-inflammatory drug (NSAID) ibuprofen is of low toxicity in acute overdose. In August 1983 ibuprofen was licensed for over-the-counter (OTC) use in the UK and it was recognised that this change could have an impact upon the epidemiology of analgesic overdose in this country. The London centre of the National Poisons Information Service (NPIS) began a new prospective survey of ibuprofen overdose at the time of OTC release. The first 2 years of this survey detected a marked increase in enquiries concerning ibuprofen overdose but there was no evidence to contradict the former claims of low toxicity. The importance of continued monitoring is stressed.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3557476&dopt=Abstract ibuprofen Motrin



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Ibuprofen can increase serum lithium level in lithium-treated patients.

Ragheb M.

The interaction between lithium and ibuprofen was studied in nine male patients admitted to the geropsychiatric ward of a veterans administration medical center. The patients, diagnosed as having bipolar affective disorder or schizoaffective disorder, who had been kept on a steady-state lithium level, received lithium for 3 days, then lithium and ibuprofen (1800 mg/day) for 6 days, and then lithium for 5 days. Ibuprofen increased the serum lithium level and decreased the lithium clearance with marked interindividual variations. These findings indicate that lithium dosage may need to be reduced in some patients following initiation of ibuprofen therapy. There was no significant correlation between changes in lithium serum level and creatinine clearance. The possibility that a tubular renal prostaglandin system may affect lithium excretion needs further investigation.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3558329&dopt=Abstract ibuprofen Motrin



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Ibuprofen as an antagonist of inhibitors of fibrinolysis in wound fluid.

Ehrlich HP, MacGarvey U, McGrane WL, White ME.

Fibrin plate assay revealed that rat serum and wound fluid harvested from seven day subcutaneously implanted wound chambers prevented fibrinolysis. Samples of wound fluid from one to four hour burns displayed greater inhibiting activity than unburned or 24 hour old burns. Ibuprofen, a non-steroid anti-inflammatory drug, reversed the blocking of fibrinolysis in wound fluid, but it had no action on rat serum. The activity of ibuprofen appears unrelated to the synthesis of prostanoids. Fractionation of wound fluid and serum by column chromatography showed differences in elutions of inhibitors of fibrinolysis. Serum fractions having molecular weights greater than 60,000 prevented fibrinolysis and they were unaffected by the addition of ibuprofen. Fractionations of wound fluid produced a number of inhibitors, some of which had molecular weights of approximately 40,000. This inhibitor(s) was not detected in serum and was reversed by adding ibuprofen. Wound fluid has a fibrinolytic inhibitor which differs from that in the circulatory system, and which may be critical to the vascular changes of burn trauma.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3563975&dopt=Abstract ibuprofen Motrin



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Topical ibuprofen decreases early postburn edema.

Demling RH, Lalonde C.

Longwood Area Trauma Center at Brigham and Women's Hospital, Boston, Mass. 02115.

We determined the effect of topically applied ibuprofen on formation of second-degree burn edema and prostanoid production, a possible causative factor. Six adult sheep were given second-degree burns on both flanks with water at 80 degrees C while they were under general anesthesia. Lymph (QL), draining the flank areas, was used to monitor edema formation and prostanoid production. A 5% ibuprofen cream was applied at 2 and 5 hours after the burn and full-thickness biopsy specimens of burned hide were obtained at 8 hours for determination of water content. The QL increased sixfold in nontreated and 2.5 times in treated burn tissue. The lymph/plasma (L/P) protein ratio increased from 0.4 to 0.58 in both sides. Lymph TxB2 was increased from baseline of 200 pg/ml to 500 +/- 100 and 310 +/- 90 pg/ml in untreated and treated sides, respectively. Lymph 6-keto-PGF1 alpha increased from a baseline of 50 +/- 10 to 150 +/- 40 and 90 +/- 80 pg/ml in untreated and treated sides. The difference between PG content of lymph in treated and untreated sides was significant. Plasma prostanoids, except for a transient early rise, remained at preburn baseline. Lymph ibuprofen content on the treated side rose to 1.9 +/- 0.8 mcg/ml with no detectable plasma level. Water content of hide increased from a control value of 74 +/- 2% to 84 +/- 2% in untreated burn, while the value in the treated side was 76 +/- 4%, a significant difference between the two sides. We conclude that topically applied ibuprofen decreases both local edema and prostanoid production in burn tissue without altering systemic production.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3672325&dopt=Abstract ibuprofen Motrin



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Effects of ibuprofen on the hypoxemia of established ethchlorvynol-induced unilateral acute lung injury in anesthetized dogs.

Sprague RS, Stephenson AH, Dahms TE, Asner NG, Lonigro AJ.

Medical Service, Veterans Administration Medical Center, St. Louis.

Nonsteroidal anti-inflammatory agents, given prior to induction of unilateral acute lung injury with ethchlorvynol (ECV) in anesthetized dogs, prevent the decreases in systemic oxygen tension (PaO2) which are observed when ECV is given alone. We investigated whether ibuprofen, administered after acute lung injury, would result in improvement in arterial oxygenation. In animals not receiving ibuprofen after unilateral acute lung injury with ECV, PaO2 decreased and venous admixture increased significantly from control values at all experimental time-periods. In those animals receiving ibuprofen, significant decreases in venous admixture were noted. The decrease in PaO2 after ECV administration was significantly less than that observed in animals that did not receive ibuprofen after acute lung injury (p less than 0.05). Ibuprofen had no effect on extravascular lung water. These results demonstrate that in an ECV model of acute lung injury the administration of ibuprofen, after the acute lung injury, results in significant decreases in venous admixture.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3677816&dopt=Abstract ibuprofen Motrin



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The influence of excipients on the diffusion of ibuprofen and paracetamol in gastric mucus.

Shaw LR, Irwin WJ, Grattan TJ, Conway BR.

Medicines Research Unit, School of Life and Health Sciences, Aston University, Aston Triangle, Birmingham B4 7ET, UK.

The aim of this study was to examine the diffusion of commonly administered analgesics, ibuprofen and paracetamol, through gastric mucus. As ibuprofen and paracetamol are often formulated with alkalising excipients, or are commonly co-administered with antacids that have been demonstrated to alter their absorption, diffusion was also studied in the presence of a range of soluble and insoluble antacids or buffering agents. The effect of pH, which has been demonstrated to modify the properties of mucus, was also studied. Mucus was a significant barrier to diffusion for both drugs, compared to an unstirred aqueous layer with diffusion rates significantly lower in the presence of a mucus barrier for both drugs; ibuprofen diffusion also demonstrated a significant increase in the lag time. Paracetamol diffusion was not significantly affected by addition of any antacid, whereas ibuprofen rates were affected and the diffusion lag time for ibuprofen was significantly reduced in all cases. Isolated increases in pH increased the rate and reduced the lag time for ibuprofen diffusion. It was shown that mucus acts as a passive barrier in the case of paracetamol diffusion, and an interactive barrier to ibuprofen diffusion. Changes in mucus viscosity at different pH values may be responsible for the observed changes in ibuprofen diffusion rate.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15664140&dopt=Abstract ibuprofen Motrin



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Hemodynamic evaluation of ibuprofen in canine hypovolemic shock.

Beamer KC, Daly T, Vargish T.

Department of Surgery, West Virginia University School of Medicine, Morgantown 26506.

This study was done to evaluate the role of ibuprofen, a cyclooxygenase inhibitor, in a standard model of hypovolemic shock. Fifteen dogs were subjected to fixed mean arterial blood pressure (MABP) shock (40-45 mmHg) for 45 min and then treated with physiologic saline (NS), low-dose ibuprofen (6.25 mg/kg), and high-dose ibuprofen (12.5 mg/kg) by IV bolus and continuous IV infusion. After 60 min of treatment, the shed blood was returned. Survival was monitored for 72 h. Both dose levels resulted in a significant increase in MABP and total peripheral resistance over NS during the infusion period but heart rate, cardiac output, and left ventricular contractility were similar for all groups. Survival at 72 h was also similar for the three groups. Ibuprofen treatment, while increasing MABP and total peripheral vascular resistance did not seem to alter cardiac function or improve survival when compared to NS in this model of hypovolemic shock.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3690813&dopt=Abstract ibuprofen Motrin



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Ibuprofen and apigenin induce apoptosis and cell cycle arrest in activated microglia.

Elsisi NS, Darling-Reed S, Lee EY, Oriaku ET, Soliman KF.

College of Pharmacy and Pharmaceutical Sciences, Florida A&M University, Tallahaeess, FL 32307, USA.

In case of injury or disease, microglia are recruited to the site of the pathology and become activated as evidenced by morphological changes and expression of pro-inflammatory cytokines. Evidence suggests that microglia proliferate by cell division to create gliosis at the site of pathological conditions such as the amyloid plaques in Alzheimer's disease and the substantia nigra of Parkinson's disease patients. The hyperactivation of microglia contributes to neurotoxicity. In the present study we tested the hypothesis that anti-inflammatory compounds modulate the progression of cell cycle and induce apoptosis of the activated cells. We investigated the effects of ibuprofen (non-steroidal anti-inflammatory drug) and apigenin (a flavonoid with anti-inflammatory and anti-proliferative properties) on the cell cycle of the murine microglial cell line BV-2. The findings indicate that apigenin-induced cell cycle arrest preferentially in the G2/M phase and ibuprofen caused S phase arrest. The binding of annexin V-FITC to the membranes of cells which indicates the apoptotic process were examined, whereas the DNA was stained with propidium iodide. Both apigenin and ibuprofen induced apoptosis significantly in early and late stages. The induction of apoptosis by ibuprofen and apigenin was confirmed using TUNEL assay, revealing that 25 microM apigenin and 250 microM ibuprofen significantly increased apoptosis in BV-2 cells. The results from the present study suggest that anti-inflammatory compounds might inhibit microglial proliferation by modulating the cell cycle progression and apoptosis.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15670648&dopt=Abstract ibuprofen Motrin