Follicle and systemic hormone interrelationships during induction of luteinized unruptured follicles with a prostaglandin inhibitor in mares

Background—Diagnosis of drug induced liver injury is usually based on a temporal relation between drug intake and clinical picture as well as on the exclusion of alternative causes. More precise diagnosis has been attempted by using in vitro specific T cell reactivity to drugs but the test has never reached general acceptability because of frequent negative results which could be explained, in part, by prostaglandin producing suppressor cells (PPSC).Aim—To analyse the diagnostic value of a modified test where lymphocyte responses to drugs are detected in the presence of a prostaglandin inhibitor.Patients—Ninety five patients with a clinical diagnosis of drug induced liver injury, 106 healthy controls, 35 individuals with recent exposure to the same drugs without adverse effects, and 15 patients with liver disease unrelated to drugs.Methods—Peripheral blood mononuclear cells (PBMC) were cultured in the presence of drugs alone and in the presence of drugs and a prostaglandin inhibitor. Responses were assessed by3H-thymidine incorporation in lymphocytes. Results were expressed as counts per minute and as stimulation indexes (SI).Results—When PBMC were stimulated with drugs alone, lymphocyte sensitisation to drugs (SI>2) was detected in 26% of the cases. This was noticeably increased (56%) when a prostaglandin inhibitor was added to the cultures. No reactivity was found in controls. In patients with possible sensitivity to several drugs, lymphocyte reactivity was detected to only one drug. The severity of the lesions, as assessed by aminotransferase concentrations and disease duration, was lower in patients with evidence of PPSC.Conclusions—This new approach is useful for the diagnosis of drug induced liver injury, particularly in patients exposed to more than one drug; furthermore, the presence of putative PPSC is associated with less severe forms of drug induced hepatitis.

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Ophthalmoplegic Migraine: Amelioration by Flufenamic acid, a Prostaglandin inhibitor

Ophthalmologica ◽

10.1159/000308647 ◽

1977 ◽

Vol 175 (3) ◽

pp. 148-152 ◽

Cited By ~ 8

Author(s):

J.M. Rabey ◽

Y. Vardi ◽

D. Van Dyck ◽

M. Streijler

Keyword(s):

Flufenamic Acid ◽

Ophthalmoplegic Migraine ◽

Prostaglandin Inhibitor

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Diflunisal, a New-Acting Analgesic and Prostaglandin Inhibitor: Effect of Concomitant Acetylsalicylic Acid Therapy on Ototoxicity and on Disposition of Both Drugs

Journal of International Medical Research ◽

10.1177/030006057900700110 ◽

1979 ◽

Vol 7 (1) ◽

pp. 61-68 ◽

Cited By ~ 7

Author(s):

P Schulz ◽

C V Perrier ◽

F Ferber-Perret ◽

W J A VandenHeuvel ◽

S L Steelman

Keyword(s):

Single Dose ◽

Urinary Excretion ◽

Acetylsalicylic Acid ◽

Blood Levels ◽

Concomitant Therapy ◽

Significant Drop ◽

Acid Therapy ◽

Prostaglandin Inhibitor ◽

Clinically Significant ◽

Higher Doses

Intermittent and concomitant acetylsalicylic acid (ASA) therapy was superimposed onto a 21-day regimen with diflunisal 250 mg b.i.d. Low doses of ASA (600 mg single dose or 300 mg q.i.d.) did not influence significantly diflunisal blood levels whereas a 600 mg q.i.d. dosing caused a small significant drop, especially at trough level. This drop is not expected to be clinically significant. No ototoxicity could be demonstrated with any treatment of diflunisal though four of fourteen subjects reported mild tinnitus during concomitant therapy at the higher doses of ASA. Diflunisal at 375 mg b.i.d. failed to alter the metabolism of a single dose of labelled ASA (600 mg) as judged by plasma levels, urinary excretion and plasma binding. Daily urinary excretion of prostaglandins E1 and E2 major metabolite was decreased by about 70% by diflunisal.

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Indomethacin does not influence natural cell-mediated cytotoxic response to endurance exercise

Journal of Applied Physiology ◽

10.1152/jappl.1999.87.6.2237 ◽

1999 ◽

Vol 87 (6) ◽

pp. 2237-2243 ◽

Cited By ~ 14

Author(s):

W. A. Braun ◽

M. G. Flynn ◽

D. E. Jacks ◽

T. McLoughlin ◽

J. Sowash ◽

...

Keyword(s):

Whole Blood ◽

High Intensity ◽

Nk Cell ◽

Cell Activity ◽

Peripheral Blood Mononuclear ◽

Cytotoxic Response ◽

Assay Procedure ◽

Before And After ◽

Prostaglandin Inhibitor ◽

Natural Cell

Natural cell-mediated cytotoxicity (NCMC) has been shown to be attenuated during recovery from high-intensity or prolonged exercise. Two theories have been proposed to explain the transient suppression of NCMC: prostaglandin-induced inhibition of natural killer (NK) cell activity or a numerical redistribution of NK cells. This study was designed to examine the effects of oral indomethacin (a prostaglandin inhibitor) on NCMC before and after 1 h of high-intensity running (85% maximal oxygen uptake). A secondary purpose was to compare whole blood and isolated peripheral blood mononuclear cell assay procedures for assessing NCMC. Ten male distance runners completed two trials that were preceded by either 48 h of indomethacin (Indo; 150 mg/day) or no treatment (control). NK (CD3−/CD16+/CD56+) cell concentrations were significantly elevated postexercise but were not affected by Indo. NCMC was significantly suppressed at 1.5 h of recovery relative to preexercise only with the whole blood assay procedure. Indo was not found to influence NCMC, leukocyte, or lymphocyte subset concentrations. Mean cytotoxic response was significantly greater with the whole blood method.

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Topical Indometacin, a prostaglandin inhibitor, in acute anterior uveitis. A controlled clinical trial of non-steroid versus steroid anti-inflammatory treatment

Acta Ophthalmologica ◽

10.1111/j.1755-3768.1991.tb02703.x ◽

2009 ◽

Vol 69 (2) ◽

pp. 145-148 ◽

Cited By ~ 18

Author(s):

B. B. Sand ◽

E. Krogh

Keyword(s):

Clinical Trial ◽

Anterior Uveitis ◽

Controlled Clinical Trial ◽

Acute Anterior Uveitis ◽

Prostaglandin Inhibitor ◽

Anti Inflammatory

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Inhibition of Platelet Reactivity by Endothelial Cells

10.1055/s-0039-1682695 ◽

1977 ◽

Author(s):

L.A. Harker ◽

N. Joy ◽

R.T. Wall ◽

L. Quadracci ◽

G. Striker

Keyword(s):

Endothelial Cells ◽

Cultured Cells ◽

Light Transmission ◽

Platelet Reactivity ◽

Umbilical Vein ◽

Inhibitory Effect ◽

Serotonin Release ◽

Prostaglandin Inhibitor ◽

Cell Synthesis ◽

Induced Aggregation

The process of endothelial thromboresistance has been studied by measuring platelet reactivity to cultured human endothelial cells (EC), vascular smooth muscle cells (SMC), and fibroblasts (FB). Human C-serotonin labeled platelets in a concentration of 300,000 cells/ul and washed cultured cells (brought into monocellular suspension by EDTA buffer) were reacted in stirred plasma suspensions at 37°C while assessing light transmission, C-serotonin release and electron microscopy. SMC from adult arteries and veins induced aggregation and release (A-R) in a dose response fashion with maximal C-serotonin release of 62% ± 7 by 106 SMC/ml, whereas comparable reactivity was induced by 3 × 106 /ml umbilical vein SMC and 5 × 10 FB/ml. Trypsinization at 0.05% solution for 2 minutes destroyed the capacity of SMC and FB to induce A-R.EC failed to induce aggregation and release in concentrations as high as 10 × 106 cells/ml. Moreover, the addition of EC to suspensions of SMC or FB in ratios as low as 1:5 prevented platelet A-R. The inhibitory effect of EC was not destroyed by trypsinization. Platelet A-R induced by ADP, epinephrine or collagen were similarly impaired by the addition of EC (106 cells/ml) while control studies using comparable numbers of SMC and FB produced no change. EC grown in the presence of indomethacin failed to inhibit platelet reactivity. ADP, epinephrine and collagen induced A-R were also significantly reduced by supernatant media from EC cultures. Supernatant media from SMC and FB failed to affect A-R. These results indicate that the lack of platelet reactivity to endothelial cells is mediated through endothelial cell synthesis of a soluble platelet prostaglandin inhibitor, probably prostacyclin.

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Effects of prostaglandin E2 and prostaglandin inhibitors on adrenal regeneration hypertension.

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1977.232.2.e95 ◽

1977 ◽

Vol 232 (2) ◽

pp. E95

Author(s):

D J Paulson ◽

W J Eversole

Keyword(s):

Blood Pressure ◽

Prostaglandin E2 ◽

Mean Blood Pressure ◽

Female Rats ◽

Heart Weight ◽

Progressive Reduction ◽

Blood Pressures ◽

Prostaglandin Inhibitor ◽

Prostaglandin Inhibitors

The effects of prostaglandin E2 (PGE2) and a prostaglandin inhibitor, indomethacin, on the development of adrenal regeneration hypertension (ARH) were investigated. Weanling female rats underwent right adrenonephrectomy and left adrenal enucleation. PGE2 was injected subcutaneously daily in dosages of 0, 20, 40 and 80 mug/day. Indomethacin, 1 mg/kg, was administered twice daily by gavage. Blood pressures were determined by a tail and cuff plethysmographic method at 3, 5, and 7 wk after surgery. Increases in dosage of PGE2 produced a progressive reduction in mean blood pressures, heart, and kidney weights. Indomethacin produced significant increases in mean blood pressure, heart, kidney, and adrenal weights. The effects of aspirin and indomethacin on the blood pressures of rats with right adrenalectomy, left adrenal enucleation, and intact kidneys were studied. Administration of asprin twice daily (25 or 50 mg/kg) produced a fall in blood pressure, body and heart weight. Administration of 1 mg/kg twice daily of indomethacin resulted in a significant increase in blood pressure at 3 wk, and 0.1 or 1 mg/kg caused significant increases at 5 wk. The heart, kidney, and adrenal weights also showed increases with indomethacin administration. This study suggests that a deficiency of renal PGE2 may be involved in the etiology of ARH.

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