Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One overt sign of clinical coliform mastitis in dairy cows is the failure to eject milk normally or to "milk out" the udder. The effect, if any, of coliform mastitis on oxytocin release is unknown. Therefore, the objective of this study was to determine the effect of endotoxin mastitis on milking-induced release of oxytocin in lactating cows. Fifteen multiparous pregnant lactating Holstein cows were divided into three groups of 5 cows each. Cows in group 1 served as controls and received an intramammary infusion of sterile physiological saline. Cows in groups 2 and 3 received intramammary infusions of 12.5 and 25 micrograms of Escherichia coli endotoxin, respectively. Serum concentrations of oxytocin were measured by radioimmunoassay before, during, and after milkings commencing at 6 and 12 h after treatment. Rectal temperatures and milk SCC were monitored to follow the course of inflammation and to verify the biological activity of infused endotoxin. Endotoxin resulted in a 1.5- to 2-fold increase in milking-induced oxytocin release compared with that of control treatments. The effect was most prominent during the first 6 h after infusion and coincided with the peak pyretic response. This study shows that endotoxin-induced mastitis potentiates, rather than inhibits, milking-induced oxytocin release.
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PMID:Effects of intramammary endotoxin infusion on milking-induced oxytocin release. 846 85

A survey on veterinary drug use and residues in milk was carried out in Hyderabad (India) and surrounding suburban villages. Mastitis was the most common disease reported; oxytocin and oxytetracycline were frequently used in veterinary formulations. Of 205 milk samples analysed, 9% of market samples and 73% of individual animal milk samples contained oxytetracycline residues. None of the government dairy samples contained oxytetracycline residues. Maximum oxytetracycline consumption through milk was calculated to be 0.045 mg/kg bw/day. The levels ranged from 0.2 to 1.4 micrograms/ml in market milk samples and from 0.2 to 6.7 micrograms/ml in samples obtained from individual buffaloes. It was found that the oxytetracycline residues affect curd setting, the extent depending on the amount of residue.
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PMID:A survey on veterinary drug use and residues in milk in Hyderabad. 852 29

For two large California dairy herds with twice daily milking, 171 infected quarters of lactating cows with mild clinical mastitis were randomly assigned to one of three treatment groups. Group A (50 cows) was treated with 62.5 mg of intramammary amoxicillin every 12 h for three milkings. Group C (50 cows) was treated with 200 mg of intramammary cephapirin every 12 h for two milkings. Group O (71 cows) was treated with 100 U of intramuscular oxytocin every 12 h for three milkings. Clinical cure rates did not differ among treatment groups. The cost per episode of clinical mastitis was higher ($54.47) for group C than for groups A ($38.53) or O ($34.88). Group O had a higher incidence of relapse (41%), and a greater percentage of group O cows (65%) experienced an additional mastitic event in the enrolled lactation than did cows in groups A and C. Treatment had no effect on the mean number of nonsalable milkings (24.7) associated with mastitis in the lactation interval subsequent to enrollment on the trial. Twenty-two percent of the cows accrued more than 30 nonsalable milkings and produced 55% of the total nonsalable milkings associated with mastitis. There was no treatment effect on total milk production, fat production, or time to removal of the enrolled cows from the herd.
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PMID:Financial analysis of alternative treatments for clinical mastitis associated with environmental pathogens. 855 Sep 18

During a three-year study, 54 cows with toxic mastitis were allocated randomly to one of three treatment groups (A, B and C). Each cow was re-examined within 24 hours of the initial examination, and, during this time, group A received fluid therapy (45 liters of intravenous isotonic electrolyte solution) and flunixin meglumine (2000 mg), group B received fluid therapy only, and group C received flunixin meglumine only. In addition all the cases were treated with parenteral and intramammary tetracyclines, oxytocin and calcium boroglucoanate. There was no significant difference in the rate of survival between the treatment groups and 29 of the cows (53.7 per cent, 95 per cent confidence interval of 39 to 67 per cent) survived.
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PMID:Comparison of fluid and flunixin meglumine therapy in combination and individually in the treatment of toxic mastitis. 905 Jan 77

A particular failure of the milk-ejection reflex in dairy cows is described on the base of own experiences in farms and reports from literature. Four cases are reported more in detail. Quantity and fat content of cisternal, alveolar and residual milk fractions, oxytocin content in blood serum, milk-ejection after manual teat stimulation, after massage of the clitoris or rectal stimulation of the vagina and cervix were investigated. This failure of the milk-ejection is observed mostly in primiparous cows and always at the begin of the lactation period. It is complete and permanent unless successfully treated, and seems to be based on an central inhibition of the oxytocin release. Treatment consists of thorough udder stimulation and milking followed by an i.v. application of oxytocin in order to remove the residual milk portion. The condition has a good prognosis, if the treatment is carried out regularly for some days and even weeks. Acute Mastitis is the main differential diagnosis.
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PMID:[Failure of milk ejection reflex in primiparous cows from the differential diagnostic and therapeutic aspects]. 969 50

Mastitis was induced in dairy cows by infusion of 500 cfu of Streptococcus uberis into the mammary gland. Most infections developed to clinical disease, and the majority were predicted by changes in the electrical conductivity of the foremilk. The benefits of clinical prognosis and bacteriological cure were determined for cases that were treated when predicted to develop into clinical mastitis and compared with cases that were allowed to develop until milk clotted or until pyrexia before intramammary antibiotic treatment was used. Treatment prior to clinical mastitis included use of intramammary antibiotic or intramuscular oxytocin to allow stripping of residual milk to remove bacteria. All infections in which treatment was delayed resulted in clinical mastitis that was cured clinically and bacteriologically by sustained treatment using a broad-spectrum intramammary antibiotic preparation once daily but requiring a mean treatment time of 10 d. It was possible to prevent clinical mastitis from developing and to eliminate all infections in cows that were treated early when the developing disease was predicted by changes in the electrical conductivity of quarter foremilk and was treated aggressively by administering an intramammary antibiotic at each milking for 3 d. Treatment of 20 IU of oxytocin at six successive milkings of cows that were predicted to develop disease eliminated 25% of the infections, but 75% of the cows developed clinical mastitis. Those cases were resolved by sustained daily treatment using the same intramammary antibiotic. Elimination (100% clinical and bacteriological cure) of all infections caused by Strep. uberis was possible with early and aggressive or sustained use of the intramammary antibiotic. The early intervention using an intramammary antibiotic, when infection was first indicated by changes in the electrical conductivity of milk, was the most efficient method to achieve cure and led to quicker recovery of milk quality to a saleable standard.
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PMID:Comparison of treatment of mastitis by oxytocin or antibiotics following detection according to changes in milk electrical conductivity prior to visible signs. 1002 11

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)).
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PMID:Endocrine profiles of dairy cows following experimentally induced clinical mastitis during early lactation. 1070 98

Tight junctions form a narrow, continuous seal that surrounds each endothelial and epithelial cell at the apical border, and act to regulate the movement of material through the paracellular pathway. In the mammary gland, the tight junctions of the alveolar epithelial cells are impermeable during lactation, and thus allow milk to be stored between nursing periods without leakage of milk components from the lumen. Nonetheless mammary epithelial tight junctions are dynamic and can be regulated by a number of stimuli. Tight junctions of the mammary gland from the pregnant animal are leaky, undergoing closure around parturition to become the impermeable tight junctions of the lactating animal. Milk stasis, high doses of oxytocin, and mastitis have been shown to increase tight junction permeability. In general changes in tight junction permeability in the mammary gland appear to be the results of a state change and not assembly and disassembly of tight junctions. Both local factors, such as intramammary pressure and TGF-beta, and systemic factors, such as prolactin, progesterone, and glucocorticoids, appear to play a role in the regulation of mammary tight junctions. Finally, the tight junction state appears to be closely linked to milk secretion. An increase in tight junction permeability is accompanied by decrease in the milk secretion rate, and conversely, a decrease in tight junction permeability is accompanied by an increase in the milk secretion rate.
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PMID:Tight junction regulation in the mammary gland. 1081 11

Antibiotic regimens (intramammary antibiotic, penicillin-based parenteral treatment) and intramuscular oxytocin were tested for effectiveness against experimental infection by Streptococcus uberis with the following results from 54 animals: a) no treatment led to deterioration of infected quarters, requiring intervention within 48 h for cow health; b) aggressive intramammary antibiotic at every milking achieved 70% clinical cure in 3 d and 100% cure within 6 d; overall bacteriological cure was 80%; c) parenteral treatment alone used about 14 times as much antibiotic with 18% clinical cure in 3 d and 91% within 6 d; overall bacteriological cure was 80%; d) combination of aggressive intramammary and parenteral treatments achieved 61% clinical cure in 3 d and 100% within 6 d; overall bacteriological cure was 72%; e) intramammary antibiotic at labeled rates (1x for 3 d) achieved 27% clinical cure in 3 d but 91% within 6 d of treatment; overall bacteriological cure was 64%; f) use of oxytocin alone for 3 d failed to achieve clinical improvement with an increase in the severity of mastitis; g) combining oxytocin with labeled use of intramammary antibiotic (1x for 3 d) was unsuccessful: 0% clinical cures in 3 d, 10% in 6 d; significantly poorer than intramammary antibiotic alone. Extended treatment periods with parenteral or intramammary antibiotics resulted in positive inhibitory tests for milk from individual quarters up to 8 d after treatment. Aggressive intramammary antibiotic was the most effective treatment for fastest cure clinically and bacteriologically using least antibiotic.
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PMID:Effective treatment of Streptococcus uberis clinical mastitis to minimize the use of antibiotics. 1201 12

The objectives of the study were to purify porcine beta-casein from sow's milk, to determine N-terminal amino acid sequence, to develop specific antisera against porcine beta-casein, and to use that antisera to evaluate milk samples from a mastitis study. Milk was collected by hand milking a Yorkshire by Duroc crossbred sow following oxytocin administration on d 27 of lactation. A casein-enriched fraction was then prepared by iso-electric precipitation. Porcine beta-casein was then purified by liquid chromatography on a Mono Q anion-exchange column, and checked for purity with SDS-PAGE. An apparent molecular weight of 29,000 Da was estimated from SDS-PAGE. N-Terminal amino acid sequence was determined by Edman degradation to be RAKEELNASGETVE. Rabbits (n = 2) were immunized with beta-casein mixed with Freund's complete (primary) or incomplete (boosters) adjuvant at 4-wk intervals. Antiserum collected from one rabbit 112 d after primary immunization detected 30 to 100 ng beta-casein by Western blot procedure when used at a dilution of 1:2 x 10(6). The antiserum was specific for porcine beta-casein, but showed some cross-reactivity with equine casein. It was determined by Western blot procedure that mammary inflammation induced by lipopolysaccharide infusion resulted in a 41% decrease in the beta-casein concentration of sow milk.
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PMID:Purification of porcine beta-casein, N-terminal sequence, quantification in mastitic milk. 1216 53


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