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Doctoral thesis2001Open access

Induced parturition and retained placenta in the cow : inhibition of prostaglandin F2[alpha] synthesis and antibiotic therapy

Königsson, Kristian

Abstract

In order to study rapid changes in 1 5-kctodihydro-PGF2, (PG-metabolite), in the period preceding parturition in cattle, prc-term parturition was induced by dcxamcthasonc injection in four heifers on days 254 to 265 in gestation. Blood samples were collected at least every hour until 12 hours after parturition and during the second stage of labour at least 6 times per hour. The average time from injection to parturition was 7.7 days (mean). Two of the heifers had retained foetal membranes (RFM). At the start of the experiment the levels of PG-metabolite were low and increased slowly to levels between 1000 and 2000 pmoliL at one day before parturition. During the last day, however, the levels increased rapidly and the highest levels (>10000 pmoliL) were reached at the time of delivery. No pulsatile PG-metabolite elevations were seen. Immediately after foetal expulsion the PG-metabolite levels decreased rapidly in all animals. In two animals with RFM, however, this decline ceased within a few hours postpartum (pp). Instead the PG- metabolite levels started to increase and reached levels as high as during parturition. In another experiment the effects of the prostaglandin synthesis inhibitor, flunixin (F) and oxytetracycline (T) was evaluated in cows with RFM. As a model for RFM, pre-term parturition was induced by injections of PGF2,. 22/24 cows had RFM. After parturition the cows were divided into different groups according to the treatment. Cows were treated with F, T, T+F or conservatively. There were two experiments with two different treatment periods (3-6 d pp, before placental shedding and 11-14 d pp, after placental shedding). Animals treated with T on days 1 1 -14 had a quicker recovery from the uterine infection than other cows. T or T+F treatment on days 3-6 did not shorten the uterine infection but altered the bacterial flora. Furthermore, T or T+F treatment at this time led to improved appetite and increased energy consumption. However, T or T+F before placental shedding delayed the detachment of the retained foetal membranes compared with other cows. F did not influence clinical signs, recovery from infection or uterine involution. F suppressed PG-metabolite levels signifkantly during periods of treatment. However, treatment on days 3-6 suppressed PG synthesis only partially. T and T+F before placental shedding significantly altered the kinetics of the early PG-metabolite profile compared with other treatments. Late PG-metabolite elevation was significantly correlated to the duration of the uterine infection and to the cervical involution. In a final study, we wanted to evaluate meloxicam (M) as an inhibitor of the inflammatory response elicited by endotoxin (ET). Furthermore, we wanted to evaluate a possible effect of meloxicam on A"-rcductasc and 15-hydroxy prostanoatc dehydro- gcnasc, which catalysc the flrst steps of the metabolism of PGF2,. Four heifers in mid luteal phase were used in the experiment. ET elicited a rapid PG and cortisol release. White blood cells, iron, zinc and calcium were affected as well. The clinical effect was dramatic. Prc-treatment with M was found to abolish the PG-release totally. Furthermore, the cortisol release was reduced and the effect on general appearance and several blood parameters were suppressed. M did not prevent the pyrogenic effect of ET. M seems to have no major influence on the metabolism of

Keywords

PGF2u; parturition; retained foetal membranes; flunixin; meloxicam; oxytctracyclinc; endotoxin

Published in

Acta Universitatis Agriculturae Sueciae. Veterinaria
2001, number: 106
ISBN: 91-576-5933-8
Publisher: Swedish University of Agricultural Sciences

      SLU Authors

    • Königsson, Kristian

      • Department of Obstetrics and Gynaecology, Swedish University of Agricultural Sciences

    UKÄ Subject classification

    Clinical Science

    Permanent link to this page (URI)

    https://res.slu.se/id/publ/107605