scholarly journals The mare as a model for luteinized unruptured follicle syndrome: intrafollicular endocrine milieu

Reproduction ◽  
2016 ◽  
Vol 151 (3) ◽  
pp. 271-283 ◽  
Author(s):  
S T Bashir ◽  
M O Gastal ◽  
S P Tazawa ◽  
S G S Tarso ◽  
D B Hales ◽  
...  
Keyword(s):  
Sex Steroids ◽  
Potential Model ◽  
Optimal Dose ◽  
Menstrual Cycles ◽  
Flunixin Meglumine ◽  
Prostaglandin F ◽  
Formation Experiment ◽  
Luteinized Unruptured Follicle Syndrome ◽  
Cox 2 ◽  
Luteinized Unruptured Follicle

Luteinized unruptured follicle (LUF) syndrome is a recurrent anovulatory dysfunction that affects up to 23% of women with normal menstrual cycles and up to 73% with endometriosis. Mechanisms underlying the development of LUF syndrome in mares were studied to provide a potential model for human anovulation. The effect of extended increase in circulating LH achieved by administration of recombinant equine LH (reLH) or a short surge of LH and decrease in progesterone induced by prostaglandin F2α (PGF2α) on LUF formation (Experiment 1), identification of an optimal dose of COX-2 inhibitor (flunixin meglumine, FM; to block the effect of prostaglandins) for inducing LUFs (Experiment 2), and evaluation of intrafollicular endocrine milieu in LUFs (Experiment 3) were investigated. In Experiment 1, mares were treated with reLH from Day 7 to Day 15 (Day 0=ovulation), PGF2α on Day 7, or in combination. In Experiment 2, FM at doses of 2.0 or 3.0 mg/kg every 12 h and human chorionic gonadotropin (hCG) (1500 IU) were administered after a follicle ≥32 mm was detected. In Experiment 3, FM at a dose of 2.0 mg/kg every 12 h plus hCG was used to induce LUFs and investigate the intrafollicular endocrine milieu. No LUFs were induced by reLH or PGF2α treatment; however, LUFs were induced in 100% of mares using FM. Intrafollicular PGF2α metabolite, PGF2α, and PGE2were lower and the ratio of PGE2:PGF2α was higher in the induced LUF group. Higher levels of intrafollicular E2 and total primary sex steroids were observed in the induced LUF group along with a tendency for higher levels of GH, cortisol, and T; however, LH, PRL, VEGF-A, and NO did not differ between groups. In conclusion, this study reveals part of the intrafollicular endocrine milieu and the association of prostaglandins in LUF formation, and indicates that the mare might be an appropriate model for studying the poorly understood LUF syndrome.

253 THE MARE MODEL FOR LUTEINIZED UNRUPTURED FOLLICLE SYNDROME: INTRAFOLLICULAR ENDOCRINE MILIEU

2016 ◽  
Vol 28 (2) ◽  
pp. 259
Author(s):  
E. L. Gastal ◽  
S. T. Bashir ◽  
M. O. Gastal ◽  
S. G. S. de Tarso ◽  
S. P. Tazawa ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Repeated Measures ◽  
Mixed Model ◽  
Single Point ◽  
Prostaglandin F2α ◽  
Optimal Dose ◽  
Sequential Data ◽  
Flunixin Meglumine ◽  
Cox 2 ◽  
Luteinized Unruptured Follicle

Mechanisms underlying the development of luteinized unruptured follicle (LUF) syndrome in mares were studied to provide a model for human anovulation. The aims of the present study were (1) to determine the effect of recombinant equine LH (reLH) and prostaglandin F2α (PGF2α) on LUF formation (Experiment 1), (2) to identify an optimal dose of COX-2 inhibitor (flunixin-meglumine; FM) required to experimentally induce LUF (Experiment 2), and (3) to evaluate the intrafollicular endocrine milieu in induced LUF (Experiment 3). In Experiment 1, mares (n = 30) were treated with reLH from Days 7 to 15 (Day 0 = ovulation), with PGF2α on Day 7 or in combination. In Experiment 2 (n = 18 mares), FM at doses of 2.0 or 3.0 mg kg–1 every 12 h and hCG (1500 IU) were administered after a follicle ≥32 mm was detected. In Experiment 3 (n = 23 mares), FM at a dose of 2.0 mg kg–1 every 12 h plus hCG was used to induce LUF and investigate the intrafollicular endocrine milieu. Shapiro-Wilk tests were used for analysing data for normal distribution, and data not normally distributed were transformed to ranks before any further analyses. For sequential data, mixed model repeated-measures ANOVA were used. For single-point data, Student’s t-tests were used. No LUF were induced in mares treated with reLH or PGF2α, in combination or separately. However, LUF were induced in 100% of mares using FM at the dose rate of 2.0 and 3.0 mg kg–1 of body weight in combination with 1500 IU of hCG. Intrafollicular PGF2α metabolite (PGFM), PGF2α, and prostaglandin E2 (PGE2) were lower, and the ratio of PGE2 : PGF2α was higher in induced LUF. Higher levels of intrafollicular growth hormone, cortisol, oestradiol, testosterone, and total primary sex steroids were observed in the induced LUF group; however, LH, prolactin, vascular endothelial growth factor-A, and nitric oxide did not differ between the control and induced LUF groups. In conclusion, COX-2 inhibitors used in conjunction with hCG can be used to pharmacologically induce LUF with 100% success in mares. This study revealed part of the intrafollicular endocrine milieu and the association of prostaglandins in LUF formation. We postulated that LUF result from decreased intrafollicular prostaglandin concentrations or altered prostaglandin synthesis, as indicated by disparity in PGE2 : PGF2α ratio. Increased intrafollicular oestradiol, testosterone, cortisol, and growth hormone were associated with LUF formation; however, further studies are necessary to ascertain the cause-effect relationship. The effect of LH on LUF formation remains unclear. This study further encourages the use of intrafollicular v. systemic biomarkers for evaluating ovulatory disorders. Finally, results from this study support the use of the mare as a model for investigating the poorly understood LUF syndrome in women.

scholarly journals Flunixin Meglumine Reduces Milk Isoprostane Concentrations in Holstein Dairy Cattle Suffering from Acute Coliform Mastitis

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 834
Author(s):  
Carsten C. F. Walker ◽  
Jill L. Brester ◽  
Lorraine M. Sordillo
Keyword(s):  
Medical Intervention ◽  
Systemic Involvement ◽  
Analgesic Effects ◽  
Markers Of Inflammation ◽  
Inflammatory Mediator Production ◽  
Flunixin Meglumine ◽  
Coliform Mastitis ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Oxidant Status

Dysfunctional inflammation contributes significantly to the pathogenesis of coliform mastitis and the classical pro-inflammatory enzyme cyclooxygenase-2 (COX-2) is the target of medical intervention using the non-steroidal anti-inflammatory drug (NSAID) flunixin meglumine (FM). Inhibition of COX-2 by FM can decrease concentrations of pro-inflammatory fatty acid-based mediators called eicosanoids, providing antipyretic and analgesic effects in dairy cows suffering from coliform mastitis. However, approximately 50% of naturally occurring coliform mastitis with systemic involvement results in death of the animal, even with NSAID treatment. Inadequate antioxidant potential (AOP) to neutralize reactive oxygen species (ROS) produced during excessive inflammation allows for oxidative stress (OS), contributing to tissue damage during coliform mastitis. Biomarkers of lipid peroxidation by ROS, called isoprostanes (IsoP), were used in humans and cattle to quantify the extent of OS. Blood IsoP were shown to be elevated and correlate with oxidant status during acute coliform mastitis. However, the effect of FM treatment on oxidant status and markers of OS has not been established. Blood IsoP concentrations were used to quantify systemic OS, whereas milk was used to assess local OS in the mammary gland. Results indicate that FM treatment had no effect on blood markers of inflammation but reduced the oxidant status index (OSi) by increasing blood AOP from pre- to post-FM treatment. Milk AOP significantly increased from pre- to post-FM treatment, whereas ROS decreased, resulting in a decreased OSi from pre- to post-FM treatment. The only blood IsoP concentration that was significantly different was 5-iso-iPF2α-VI, with a decreased concentration from pre- to post-FM treatment. Conversely, milk 5-iso-iPF2α-VI, 8,12-iso-iPF2α-VI, and total IsoP concentrations were decreased following FM treatment. These results indicated that administration of FM did improve systemic and local oxidant status and reduced local markers of OS. However, differential effects were observed between those animals that survived the infection and those that died, indicating that pre-existing inflammation and oxidant status greatly affect efficacy of FM and may be the key to reducing severity and mortality associated with acute coliform infections. Supplementation to improve AOP and anti-inflammatory mediator production may significantly improve efficacy of FM treatment.

Follicle growth curves and hormonal patterns in patients with the luteinized unruptured follicle syndrome

1985 ◽  
Vol 43 (4) ◽  
pp. 541-548 ◽  
Author(s):  
Carl J.C.M. Hamilton ◽  
Leo C.G. Wetzels ◽  
Johannes L.H. Evers ◽  
Henk J. Hoogland ◽  
Arno Muijtjens ◽  
...  
Keyword(s):  
Growth Curves ◽  
Follicle Growth ◽  
Luteinized Unruptured Follicle Syndrome ◽  
Luteinized Unruptured Follicle

scholarly journals Paracetamol-associated luteinized unruptured follicle syndrome: effect on intrafollicular blood flow

1991 ◽  
Vol 1 (6) ◽  
pp. 420-425 ◽  
Author(s):  
T. H. Bourne ◽  
K. Reynolds ◽  
J. Waterstone ◽  
E. Okokon ◽  
D. Jurkovic ◽  
...  
Keyword(s):  
Blood Flow ◽  
Luteinized Unruptured Follicle Syndrome ◽  
Luteinized Unruptured Follicle

Non-steroidal anti-inflammatory drug induces luteinized unruptured follicle syndrome in young female juvenile idiopathic arthritis patients

2018 ◽  
Vol 37 (10) ◽  
pp. 2869-2873 ◽  
Author(s):  
Renato B. Tomioka ◽  
Gabriela R. V. Ferreira ◽  
Nadia E. Aikawa ◽  
Gustavo A. R. Maciel ◽  
Paulo C. Serafini ◽  
...  
Keyword(s):  
Juvenile Idiopathic Arthritis ◽  
Young Female ◽  
Inflammatory Drug ◽  
Luteinized Unruptured Follicle Syndrome ◽  
Anti Inflammatory ◽  
Luteinized Unruptured Follicle
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