dinoprost has been researched along with Mastitis--Bovine* in 17 studies
17 other study(ies) available for dinoprost and Mastitis--Bovine
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Lipopolysaccharides, cytokines, and nitric oxide affect secretion of prostaglandins and leukotrienes by bovine mammary gland during experimentally induced mastitis in vivo and in vitro.
The aim of the study was to determine the effects of lipopolysaccharide (LPS), tumor necrosis factor alpha (TNF), interleukin-1-alpha (IL-1α), and nitric oxide donor (NONOate) on both in vivo and in vitro secretion of prostaglandin (PG)E2, PGF2α, leukotriene (LT)B4, and LTC4 by the bovine mammary gland. In the first experiment, tissues isolated from the teat cavity and lactiferous sinus were treated in vitro with LPS (10 ng/mL), TNF (10 ng/mL), IL-1α (10 ng/mL), NONOate (10(-4) M), and the combination of TNF + IL-1α + NONOate for 4 or 8 h. PGE2 or PGF2α secretion was stimulated by all treatments (P < 0.05) excepting NONOate alone, which did not stimulate PGF2α secretion. Moreover, all factors increased LTB4 and LTC4 secretion (P < 0.05). In the second experiment, mastitis was experimentally mimicked in vivo by repeated (12 h apart) intramammary infusions (5 mL) of (1) sterile saline; (2) 250-μg LPS; (3) 1-μg/mL TNF; (4) 1-μg/mL IL-1α; (5) 12.8-μg/mL NONOate; and (6) TNF + IL-1α + NONOate into 2 udder quarters. All infused factors changed PGE2, 13,14-dihydro,15-keto-PGF2α, and LT concentrations in blood plasma collected from the caudal vena cava, the caudal superficial epigastric (milk) vein, the jugular vein, and the abdominal aorta (P < 0.05). In summary, LPS and other inflammatory mastitis mediators modulate PG and LT secretion by bovine mammary gland in both in vivo and in vitro studies. Topics: Animals; Cattle; Cytokines; Dinoprost; Dinoprostone; Female; Interleukin-1alpha; Leukotriene B4; Leukotriene C4; Leukotrienes; Lipopolysaccharides; Mammary Glands, Animal; Mastitis, Bovine; Nitric Oxide; Nitric Oxide Donors; Prostaglandins; Tumor Necrosis Factor-alpha | 2015 |
Lipopolysaccharides, cytokines, and nitric oxide affect secretion of prostaglandins and leukotrienes by bovine mammary gland epithelial cells.
The aims of this study were to determine the effects of lipopolysaccharides (LPS), tumor necrosis factor (TNF), interleukin 1 alpha (IL-1α), nitric oxide donor (NONOate), or the combination of TNF + IL-1α + NONOate on the following: (i) secretion of prostaglandin (PG)-F(2α), PGE(2), leukotriene (LT)-B(4), and LTC(4) by epithelial cells of the teat cavity and lactiferous sinus of bovine mammary gland; (ii) messenger RNA (mRNA) transcription of enzymes responsible for arachidonic acid (AA) metabolism (prostaglandin-endoperoxide synthase 2 [PTGS2], prostaglandin E synthase [PTGES], prostaglandin F synthase [PGFS], and arachidonate 5-lipooxygenase [ALOX5]); and (iii) proliferation of the cells. The cells were stimulated for 24 h. Prostaglandins and LT were measured by enzyme immunoassay, mRNA transcription of enzymes was determined by real-time reverse transcription polymerase chain reaction, and the cell viability was measured by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide. All factors increased PG secretion, but the highest stimulation was observed after TNF and IL-1α (P < 0.001). Tumor necrosis factor, NONOate, and TNF + IL-1α + NONOate increased LTB(4) production (P < 0.01), whereas LTC(4) was increased by LPS, TNF, and IL-1α (P < 0.01). Lipopolysaccharides, TNF, IL-1α, and the reagents combination increased PTGS2, PTGES, and PGFS mRNA transcription (P < 0.01), whereas ALOX5 mRNA transcription was increased only by TNF (P < 0.001). Lipopolysaccharides, TNF, IL-1α, NONOate, and the combination of reagents increased the cell number (P < 0.001). Mediators of acute-clinical Escherichia coli mastitis locally modulate PG and LT secretion by the epithelial cells of the teat cavity and lactiferous sinus, which might be a useful first line of defense for the bovine mammary gland. Moreover, the modulation of PG and LT secretion and the changing ratio of luteotropic (PGE(2), LTB(4)) to luteolytic (PGF(2α), LTC(4)) metabolites may contribute to disorders in reproductive functions. Topics: Animals; Arachidonate 5-Lipoxygenase; Arachidonic Acids; Cattle; Cell Proliferation; Cytokines; Dinoprost; Dinoprostone; Epithelial Cells; Female; Hydroxyprostaglandin Dehydrogenases; Interleukin-1alpha; Intramolecular Oxidoreductases; Leukotriene B4; Leukotriene C4; Leukotrienes; Lipopolysaccharides; Mammary Glands, Animal; Mastitis, Bovine; Nitric Oxide; Nitric Oxide Donors; Prostaglandin-E Synthases; Prostaglandin-Endoperoxide Synthases; Prostaglandins; RNA, Messenger; Tumor Necrosis Factor-alpha | 2012 |
Subclinical, chronic intramammary infection lowers steroid concentrations and gene expression in bovine preovulatory follicles.
Chronic, subclinical intramammary infection depresses fertility. We previously found that 30% of subclinical mastitic cows exhibit delayed ovulation, low circulating estradiol levels, and delayed luteinizing hormone surge. We examined the function of preovulatory follicles of cows experiencing subclinical mastitis or a past event of acute clinical mastitis. Cows were diagnosed for mastitis by somatic cell count and bacteriological examination. All clinical infections were caused by Escherichia coli, and most subclinical infections were caused by Streptococcus dysgalactiae and coagulase-negative staphylococci. On day 6 of the cycle, cows received PGF2α; 42 h later, follicular fluids and granulosa cells or theca cells were aspirated from preovulatory follicles in vivo or following slaughter, respectively. Overall, follicular estradiol and androstenedione concentrations in the subclinical group (n = 28) were 40% lower (P < 0.05) than those in uninfected cows (n = 24) and lower than in past clinical mastitic cows (n = 9). Distribution analysis revealed a clear divergence among subclinical cows: one-third (9/28) exhibited low follicular estradiol; the other two-thirds had normal levels similar to all uninfected (P < 0.01) and most clinical cows (P < 0.08) that had normal follicular estradiol levels. Subclinical normal-estradiol cows had twofold higher (P < 0.05) circulating estradiol concentrations and sevenfold and fourfold higher (P < 0.05) follicular androstenedione levels and estradiol-to-progesterone ratio, respectively, than subclinical low-estradiol cows. Follicular progesterone level was not affected. Reduced expression (P < 0.05) of LHCGR in theca and granulosa cells, CYP11A1 (mRNA and protein) and CYP17A1 in theca cells, and CYP19A1 in granulosa cells may have contributed to the lower follicular steroid production in the subclinical low-estradiol subgroup. StAR and HSD3B1 in theca cells and FSHR in granulosa cells were not affected. Mastitis did not alter follicular growth dynamics, and no carryover effect of past clinical mastitis on follicular function was detected. These data indicate that a considerable proportion (one-third) of subclinical mastitic cows have abnormal follicular steroidogenesis, which can explain the reproductive failure associated with this disease. Topics: Animals; Base Sequence; Cattle; Dinoprost; Escherichia coli; Escherichia coli Infections; Female; Gene Expression; Mammary Glands, Animal; Mastitis, Bovine; Membrane Proteins; Ovarian Follicle; Staphylococcal Infections; Staphylococcus; Steroid Hydroxylases; Steroids; Streptococcal Infections; Streptococcus | 2011 |
Effect of bST and reproductive management on reproductive performance of Holstein dairy cows.
The objective was to determine the effects of bovine somatotropin (bST) and two artificial insemination (AI) protocols on reproductive performance of Holstein cows. Lactating cows (n = 840) were assigned at 37 d in milk (DIM) to one of four treatments in a 2 x 2 factorial arrangement. Treatments consisted of either bST (500 mg/14 d) starting at 63 +/- 3 DIM or no bST (control), with cows either submitted for timed AI following a synchronized ovulation (Ovsynch) protocol or assigned to receive AI based on estrus detection (ED). Two injections of PGF2, at 37 +/- 3 and 51 +/- 3 DIM were used to presynchronize estrous cycles. Cows then received an injection of GnRH at 63 +/- 3 DIM, followed 7.5 d later by PGF2. Cows assigned to ED treatments were inseminated after observed estrus during a 7-d period. Cows in Ovsynch treatments received a second GnRH injection 48 h after the last PGF2alpha and received timed AI 16 to 18 h later. Pregnancy was diagnosed by ultrasound at 31 d after AI and confirmed 14 d later. Frequency of anovulation (18.5%) at 63 DIM was similar across treatments, but proportions of anovulatory cows decreased quadratically as body condition at 70 DIM increased from 2.25 to 3.75. Estrus detection rate after PGF2alpha tended to be lower in multiparous cows receiving bST, and bST reduced returns to estrus in nonpregnant cows. Conception rates were higher in cows receiving AI after ED and bST improved conception rates to first AI in cyclic cows by reducing embryonic mortality. Pregnancy loss was similar for cows inseminated following ED or the Ovsynch protocol. There was a positive impact of bST on fertility of cyclic cows inseminated at fixed time or at detected estrus, but effective resynchronization protocols are needed to optimize reinsemination of non-pregnant bST-treated cows. Topics: Abortion, Spontaneous; Animals; Body Composition; Cattle; Cattle Diseases; Cell Count; Dairying; Dinoprost; Estrus Detection; Estrus Synchronization; Female; Growth Hormone; Insemination, Artificial; Lactation; Mastitis, Bovine; Milk; Ovulation Induction; Postpartum Period; Pregnancy; Reproduction; Reproductive Techniques, Assisted | 2004 |
Identification of possible mediators of embryonic mortality caused by mastitis: actions of lipopolysaccharide, prostaglandin F2alpha, and the nitric oxide generator, sodium nitroprusside dihydrate, on oocyte maturation and embryonic development in cattle.
Mastitis and immunization against constituents of organisms causing mastitis can reduce fertility of cattle and sheep, respectively. For the current experiments, it was hypothesized that these effects are mediated via actions of lipopolysaccharide (LPS), prostaglandin F2alpha (PGF2), and nitric oxide on oocyte maturation and embryonic development.. To evaluate effects on oocyte maturation, oocytes were matured with various concentrations of LPS, PGF2alpha, or the nitric oxide (NO) generator, sodium nitroprusside (SNP). Following maturation, oocytes were fertilized and cultured until day 8 after fertilization. To test effects on embryo growth, oocytes were matured and fertilized and cultured after fertilization with LPS, PGF2alpha, or SNP.. Addition of 100 and 1000 ng/mL LPS and 50 and 100 ng/mL PGF2alpha to oocyte maturation medium reduced the proportion of oocytes that became blastocysts at day 8 after fertilization. When added after fertilization, in contrast, neither LPS nor PGF2alpha reduced development to the blastocyst stage. Unlike for LPS and PGF2alpha, addition of SNP during oocyte maturation was without effect on the proportion of oocytes that became blastocysts at day 8 after fertilization. However, addition of 10 microM SNP to culture medium after fertilization completely prevented development to the blastocyst stage while 0.1 and 1 microM SNP did not affect development.. Results indicate that increased local concentrations of LPS, PGF2alpha, and NO can have deleterious consequences on oocyte function (LPS, PGF2alpha) and embryonic development (NO). Thus, these molecules are putative mediators of effects of infectious disease or inflammation, including mastitis, on fertility of cattle. Topics: Animals; Cattle; Dinoprost; Embryo Loss; Embryo, Mammalian; Embryonic and Fetal Development; Female; Lipopolysaccharides; Mastitis, Bovine; Nitric Oxide Donors; Nitroprusside; Oocytes; Pregnancy | 2003 |
Endocrine profiles of dairy cows following experimentally induced clinical mastitis during early lactation.
Concentrations of LH, cortisol, estradiol-17beta (E(2)), prolactin and 13,14-dihydro-15-keto-prostaglandin F(2alpha) (PGFM) were determined in cows with experimentally induced clinical mastitis during early lactation. Cows free of intramammary infection (IMI) and in the luteal phase of the estrous cycle were balanced by lactation number and days in milk and assigned to either control (n=5) or treatment (n=5) groups. Treated cows were infected experimentally (day 0), in two mammary quarters, with Streptococcus uberis and developed clinical mastitis within 60 h after inoculation as evidenced by increased mastitis scores, elevated rectal temperatures, mammary swelling and isolation of S. uberis pathogen. Four days following bacterial challenge, blood samples were collected every 20 min for 8 h for determination of PGFM and LH following administration of oxytocin and GnRH, respectively. Blood samples were also collected on days 0, 4 and 7 of the experiment to determine concentrations of E(2), prolactin and cortisol. Four days after bacterial challenge, concentrations of cortisol were higher (P=0.04) in experimentally infected cows than controls. Experimentally challenged cows had increased (P=0.02) concentrations of cortisol on days 4 and 7 compared with day 0. Control cows had no significant increase in blood cortisol during the experimental period. Baseline concentrations of PGFM did not differ between groups; however, peak concentrations of PGFM following oxytocin challenge were elevated (P=0.006) in cows with clinical mastitis compared with control animals. Prolactin, E(2) and LH did not differ between cows with clinical mastitis or controls. Experimentally induced mastitis during early lactation elevated concentrations of cortisol during the luteal phase of the estrous cycle. Furthermore, mastitic cows demonstrated an increased PGFM response following oxytocin administration. Altered reproductive efficiency in cows with clinical mastitis caused by Gram-positive pathogens may be the result of increased uterine sensitivity to prostaglandin F(2alpha) (PGF(2alpha)). Topics: Animals; Cattle; Dairying; Dinoprost; Estradiol; Female; Lactation; Luteal Phase; Luteinizing Hormone; Mastitis, Bovine; Ovulation | 2000 |
Bovine acute mastitis: effects of intravenous sodium salicylate on endotoxin-induced intramammary inflammation.
Effects of the nonsteroidal antiinflammatory agent sodium salicylate on endotoxin-induced mastitis were evaluated in lactating cows. Escherichia coli endotoxin was administered to a mammary quarter 1 h after initiation of a 12-h i.v. infusion of sodium salicylate. Milk SCC, BSA concentrations in milk, mammary inflammation, rectal temperature, appetite, milk production, and plasma and lymph PGF2 alpha were monitored. Gross mammary inflammation was not reduced by salicylate infusion, nor did sodium salicylate prevent increased milk SCC or BSA concentrations in milk, although treatment tended to decrease the magnitude of these responses. Sodium salicylate decreased subcutaneous abdominal vein PGF2 alpha metabolite, and PGF2 alpha metabolite tended to be reduced in lymph during the acute phase of inflammation. The increased rectal temperature after endotoxin infusion was reduced in cows treated with sodium salicylate. Appetite was reduced after endotoxin infusion in untreated cows and those treated with sodium salicylate. Milk production declined after endotoxin challenge in all cows. Although sodium salicylate did not substantially reduce mammary inflammation, it had an antipyretic effect and reduced PGF2 alpha metabolite in mammary blood. Topics: Animals; Cattle; Dinoprost; Endotoxins; Escherichia coli; Female; Infusions, Intravenous; Lactation; Lymph; Mastitis, Bovine; Sodium Salicylate | 1993 |
Effects of voltages on cows over a complete lactation. 2. Health and reproduction.
For the effects of voltages on health and reproduction, 40 cows in second to fifth lactation were divided into four groups of 10. These included a control group that was not subjected to voltages and three treatment groups that were given either 1, 2, or 4 V at the water bowl. Cows in the treatment groups were exposed during the entire lactation to voltage whenever they drank. Voltages did not sufficiently affect milk yield. General health parameters studied were mastitis, hoof problems, and changes in body weight. Reproductive and calving parameters examined were days to first breeding, days open, services per conception, response to PGF2 alpha, calving intervals, visible abortion, and calves born dead. Voltages did not significantly influence cow health or reproductive performance. Topics: Abortion, Veterinary; Animals; Body Weight; Cattle; Cattle Diseases; Dinoprost; Electricity; Female; Fetal Death; Foot Diseases; Hoof and Claw; Lactation; Mastitis, Bovine; Pregnancy; Reproduction | 1992 |
The combined use of lipoxygenase and cyclooxygenase inhibitors in Klebsiella pneumoniae-induced bovine mastitis.
The effect of combined administration of flunixin meglumine (FM) and nordihydroguaiaretic acid (NDGA) on milk prostaglandin F2 alpha (PGF2 alpha) and leukotriene B4 (LTB4) concentrations, and inflammatory indicators of bovine mastitis was examined. Mastitis was induced in six Holstein cows by the inoculation of Klebsiella pneumoniae via the teat canal. Four cows were intravenously treated with FM (1.1 mg/kg) and NDGA (10 mg/kg) 1 hour prior to bacterial inoculation and again at post inoculation hour (PIH) 11. Two control cows were intravenously treated with equivalent volume doses of sterile isotonic saline solution at the same post inoculation time points. Combined use of FM and NDGA was effective in reducing elevations in milk PGF2 alpha levels and slightly effective in reducing elevations in milk LTB4 levels in the mastitic cows. Elevations in milk bovine serum albumin (BSA) levels were partially reduced during the early post inoculation time period in the FM and NDGA treated cows as compared to the saline treated control cows. Milk somatic cell counts from inoculated quarters were not significantly altered by FM and NDGA treatment. Elevations in rectal temperature were not reduced by FM and NDGA treatment, but clinical signs of quarter inflammation (warmth and swelling) were reduced by FM and NDGA treatment. Topics: Animals; Cattle; Clonixin; Dinoprost; Female; Klebsiella Infections; Klebsiella pneumoniae; Leukotriene B4; Masoprocol; Mastitis, Bovine | 1991 |
Physiological responses to intramammary or intravenous treatment with endotoxin in lactating dairy cows.
Twenty-one, middle to late lactation Holstein cows were assigned to one of three treatments in a completely randomized design to examine physiological changes associated with intramammary or intravenous administration of Escherichia coli endotoxin. Treatments were 1) Hank's balanced salt solution infusion in two contralateral quarters (control), 2) E. coli endotoxin infusion in two contralateral quarters, and 3) intravenous infusion of E. coli endotoxin. Blood was sampled and rectal temperature was measured at 30-min intervals. Endotoxin treatment was at 0900 h and sampling continued until 1700 h. Serum prolactin, cortisol, and 13,14-dihydro-15-keto-prostaglandin F2 alpha were measured. A pyretic response was observed in intravenous and intramammary treatment groups after endotoxin treatment. Response peak was higher (41.1 vs. 40.3 degrees C) and occurred later (6 vs. 4.5 h posttreatment) in the intramammary than the intravenous treatment group. Significant prolactin peaks were observed also in intravenous and intramammary endotoxin treatment groups. Prolactin peaked higher (288 vs. 112 ng/ml) and occurred sooner (1 vs. 4 h posttreatment) in the intravenous than in the intramammary treatment group. Cortisol followed a trend similar to prolactin. Cortisol peaked higher (100 vs. 82 ng/ml) and sooner (2.5 vs. 4.5 h posttreatment) in the intravenous than in the intramammary treatment group. Concentrations of 13,14-dihydro-15-keto-prostaglandin F2 alpha increased rapidly posttreatment in the intravenous group only. Topics: Abortion, Veterinary; Animals; Body Temperature; Cattle; Dinoprost; Endotoxins; Female; Hydrocortisone; Injections, Intravenous; Lactation; Mastitis, Bovine; Pregnancy; Prolactin; Random Allocation | 1990 |
Role of eicosanoids, histamine, and serotonin in the pathogenesis of Klebsiella pneumoniae-induced bovine mastitis.
By inoculating Klebsiella pneumoniae into the teat canals of mammary glands, coliform mastitis was induced experimentally in 6 lactating cows. Release of eicosanoids, histamine, and serotonin in plasma and milk was studied in response to 2 doses of K pneumoniae. A low dose (mean, 5,000 organisms/ml) was inoculated into cows 1 through 4, and a high dose (mean, 200,000 organisms/ml) was inoculated into cows 5 and 6. Milk and blood samples were collected before inoculation (0 hours), and hourly, from 3 to 24 hours after inoculation. Concentrations of prostaglandin F2 alpha (PGF2 alpha), prostaglandin E (PGE), thromboxane B2 (TxB2), histamine, and serotonin were measured in plasma and milk obtained from control (NaCl solution-inoculated) and infected quarters. Fluorometric analysis of milk from infected quarters revealed significantly increased histamine and serotonin concentrations regardless of the dose of K pneumoniae. The mean (+/- SEM) peak concentrations of histamine were significantly (P less than 0.01) increased from the preinoculation value of 44 (+/- 12) ng/ml to 312 (+/- 104) ng/ml in milk from infected quarters and 72 (+/- 24) ng/ml in milk from control quarters. The mean peak concentration of serotonin increased significantly from the preinoculation concentration of 436 (+/- 37) ng/ml to 1,754 (+/- 662) ng/ml and 4,867 (+/- 1,248) ng/ml in milk from control (P less than 0.02) and infected (P less than 0.001) quarters, respectively. However, serotonin concentration in milk from infected quarters was approximately 2.8 times greater than that in milk from control quarters. Concentrations of PGF2 alpha, PGE, and TxB2 in milk and plasma were evaluated by radioimmunoassay.(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Animals; Cattle; Dinoprost; Female; Histamine; Histamine Release; Klebsiella Infections; Klebsiella pneumoniae; Mastitis, Bovine; Milk; Prostaglandins E; Prostaglandins F; Serotonin; Thromboxane B2 | 1987 |
Milk prostaglandins and electrical conductivity in bovine mastitis.
Prostaglandin (PG) levels in milk samples from healthy and mastitic cows were determined by radioimmunoassay. In composite milk the PG levels were rather high both in healthy and mastitic samples, and the only significant difference was in thromboxane B2 (TXB). In quarter milk samples classified according to the degree of mastitis by use of somatic cell counts, PGE2 was 40, PGF2 alpha 15, and TXB2 44 per cent higher respectively in affected samples. PG levels were in good correlation with somatic cell counts (r = 0.63-0.68, p less than 0.01) and electrical conductivity (r = 0.36-0.52, p less than 0.01), two established criteria for diagnosis of mastitis. PGE2 also correlated with protein, TXB2 with fat content. PGF 2 alpha was in a negative correlation with milk yield. The good correlation of PGs with somatic cell counts and electrical conductivity suggests that PGs might be used as markers of mastitic inflammation. Topics: Animals; Cattle; Dinoprost; Dinoprostone; Electric Conductivity; Female; Mastitis, Bovine; Milk; Prostaglandins E; Prostaglandins F; Radioimmunoassay; Thromboxane B2 | 1987 |
Endotoxin-induced bovine mastitis: arachidonic acid metabolites in milk and plasma and effect of flunixin meglumine.
Arachidonic acid metabolites (AAM) were measured in milk and plasma during the course of acute endotoxin-induced mastitis in 12 lactating cows. Mastitis was induced by intramammary challenge exposure with 10 micrograms of Escherichia coli (026:B6) endotoxin. Endotoxin was injected into the teat cistern via the teat canal of a single randomly selected rear quarter of each cow. Concentrations of prostaglandin (PG) F2 alpha and thromboxane (Tx) B2 in fat-free unextracted milk and of 15-keto-13,14-dihydro-PGF2 alpha in plasma were measured by radioimmunoassay. Total production of AAM in milk was determined by measuring quarter milk production. The AAM were compared in 6 cows administered flunixin meglumine (1.1 mg/kg of body weight) and in 6 cows administered saline solution. Concentrations of TxB2 in milk were significantly (P less than 0.001) increased during the early course of acute mastitis in endotoxin-treated quarters of cows not administered flunixin meglumine. Peak concentrations of TxB2 in milk occurred at 8 hours after endotoxin inoculation. Flunixin meglumine treatment produced significant (P less than 0.05) reductions in milk TxB2 and plasma 15-keto-13,14-dihydro-PGF2 alpha concentrations. Concentrations of PGF2 alpha in milk and total PGF2 alpha and TxB2 production per quarter per milking were not significantly influenced by endotoxin challenge or by flunixin meglumine treatment. Topics: Animals; Arachidonic Acid; Arachidonic Acids; Cattle; Clonixin; Dinoprost; Endotoxins; Escherichia coli; Female; Mastitis, Bovine; Milk; Nicotinic Acids; Prostaglandins F; Thromboxane B2 | 1986 |
Prostaglandins and glutathione peroxidase in bovine mastitis.
Prostaglandin (PG) levels in milk and plasma samples from mastitic cows were determined by radioimmunoassay and compared with erythrocyte glutathione peroxidase (GSH-Px) and other relevant parameters in milk and blood. The overall levels of PGE2, PGF2 alpha and thromboxane B2 (TXB2) in milk were two to four times higher than in blood plasma both in healthy and diseased animals (P less than 0.01). In mastitic milk the PG levels were 24 to 55 per cent and in blood plasma 41 to 95 per cent higher than in healthy animals. The changes were significant and largest for the PGF2 alpha values. In milk, the PG concentrations correlated with the markedly elevated cell count (r = 0.49 to 0.57), and TXB2 values also correlated with milk yield. In blood, PGE2 and PGF2 alpha correlated positively with serum albumin, and PGE2 also correlated with glutathione (GSH). PGE2 and PGF2 alpha correlated negatively with GSH-Px and gamma-glutamyl transferase. The substantial decline in GSH-Px in mastitic animals (P less than 0.01) may be related to changes in lipid peroxidation and PG formation. The possible implications of these findings in the treatment of mastitis are discussed. Topics: Animals; Cattle; Dinoprost; Dinoprostone; Erythrocytes; Female; Glutathione Peroxidase; Mastitis, Bovine; Milk; Prostaglandins E; Prostaglandins F; Radioimmunoassay; Thromboxane B2 | 1986 |
Arachidonic acid metabolites in milk of cows during acute coliform mastitis.
Concentrations of prostaglandin F2 alpha (PGF2 alpha) and thromboxane B2 (TXB2) were evaluated in the milk of cows with naturally occurring (n = 3) and experimentally induced (n = 5) acute coliform mastitis. These arachidonic acid metabolites were measured by radioimmunoassay in unextracted milk. Experimental infections were induced by inoculating 600 to 1,200 colony-forming units of Escherichia coli into 1 mammary quarter per experimental cow. In the experimental cows, milk was collected before inoculation and at 12, 24, 36, 48, 60, and 72 hours after inoculation. Somatic cell concentrations, bovine serum albumin, and concentrations of PGF2 alpha and TXB2 were determined in milk collected at each sampling. Mild-to-moderate increases in milk PGF2 alpha and TXB2 concentrations were observed in cows with naturally occurring mastitis. the increases corresponded to the clinical severity and course of mastitis. In the experimental cows, increases in milk PGF2 alpha and TXB2 concentrations were observed, but the increases were not significant, using a statistical model that included factors of treatment, cows, hours after inoculation, cows-by-treatment and hours-by-treatment interactions, and random error (residual). Results of the present study indicated a large biological variability in milk arachidonic acid metabolite concentrations in cows with acute coliform mastitis, and that arachidonic acid metabolites may be important in the pathophysiologic process of acute coliform mastitis. Topics: Acute Disease; Analysis of Variance; Animals; Arachidonic Acid; Arachidonic Acids; Cattle; Dinoprost; Escherichia coli Infections; Female; Lactation; Mastitis, Bovine; Milk; Pregnancy; Prostaglandins F; Radioimmunoassay; Thromboxane B2; Thromboxanes | 1985 |
Role of prostaglandins in pathogenesis of bovine mastitis induced by Escherichia coli endotoxin.
Four doses (5 to 100 micrograms, 1 dose/quarter) of Escherichia coli endotoxin were introduced into lactating mammary glands of 2 cows. There was no effect on milk prostaglandin (PG) E2 concentration, except that the concentration was increased from 200 pg/ml of milk to 1,060 pg/ml at post-treatment hour (PTH) 8 in cow 1 and from 75 to 420 pg/ml at PTH 4 in cow 2 after the highest dose 100 micrograms. Endotoxin caused a dose-dependent increase in milk PGF2 alpha concentrations in both cows. After the highest dose, PGF2 alpha was maximally increased from 200 to 3,500 pg/ml at PTH 4 in cow 1 and from 250 to 2,000 pg/ml in cow 2 at PTH 8. The instillation of 50 micrograms of endotoxin in all 8 quarters of 2 more lactating cows caused no significant (P greater than 0.05) changes in milk PGE2 and thromboxane B2 concentrations, whereas milk PGF2 alpha was significantly increased from the base-line value of 642 to 2,683, 1,189, and 2,281 pg/ml at PTH 4, 8, and 12, respectively. The 6-keto-PGF1 alpha was also significantly increased from the base-line value of 305 to 871, 631, and 600 pg/ml at the corresponding times, respectively. A marked increase in vascular permeability, as judged by high concentrations of serum albumin in the whey, was observed as early as PTH 4 and peaked at PTH 12 followed by a gradual decline, although it remained significantly increased over the control for 48 hours after treatment.(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Animals; Cattle; Dinoprost; Endotoxins; Escherichia coli; Female; Mammary Glands, Animal; Mastitis, Bovine; Milk; Prostaglandins F | 1984 |
Morphometric effect of prostaglandin E1 and F2 alpha on lactating bovine mammary tissue in vitro.
Mammary explants from six lactating cows were incubated for .17, 4, 8, and 12 h in medium containing prostaglandin E1 or prostaglandin F2 alpha tromethamine salt at 0, 1, 10, or 50 micrograms/ml to determine if prostaglandins alter tissue structure. Explants were fixed, dehydrated, embedded in plastic resins, and sectioned at .5 to 1.0 mu. Tissue area was partitioned by light microscopy into normal, damaged, or debris epithelial; normal or debris lumenal; or stromal areas. All tissue samples exhibited signs of deterioration as incubation progressed. Prostaglandin E1 treatment maintained more secretory epithelium and resulted in less epithelial debris and lumenal debris than controls. Prostaglandin F2 alpha-treated tissue had less epithelial debris and normal lumenal area than tissue receiving no prostaglandin during the limited incubation. The three concentrations of prostaglandins studied did not identify optimal prostaglandins for mammary tissue incubated but indicated concentrations below 1 microgram prostaglandin E1 or F2 alpha/ml should be studied. The response of mammary tissue to prostaglandin was affected by donor milk production. Increases of normal epithelial area were correlated with decreases of damaged and debris areas. Prostaglandins E1 and F2 alpha appeared to be beneficial to healthy mammary tissue incubated under limited conditions. Topics: Alprostadil; Animals; Cattle; Dinoprost; Female; In Vitro Techniques; Lactation; Mammary Glands, Animal; Mastitis, Bovine; Pregnancy; Prostaglandins E; Prostaglandins F; Vasodilator Agents | 1984 |