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In this thesis the importance of UCA in uterine clearance was demonstrated by converting the uterus of a genitally normal mare, using clenbuterol, into a susceptible uterus, after bacterial infusion. All clenbuterol-treated mares had intrauterine fluid collections 48 h after the infusion. Uterine contractile activity is mainly controlled by the action of the ecbolic hormones, oxytocin (OT) and prostaglandin F2α (PGF2α). The profiles of these two hormones were investigated in resistant and susceptible mares around AI and after OT injection. Other stimuli applied only to resistant mares included oestrous and dioestrous testing, natural service, intrauterine saline infusion and manual manipulation of the genital tract. All stimuli caused OT release and there were no differences in OT profiles between resistant and susceptible mares. However significantly were susceptible mares release dPGF2α in response to endogenous OT release or exogenous OT administration. Qualitative measurement of UCA has been reported in mares using ultrasonography and its effect on ecbolic hormone release and subsequently UCA was investigated. There was no evidence to show any effect of ultrasonography on UCA. Utilizing the same technique, differences in UCA before and after OT administration in oestrous resistant and susceptible mares were investigated. Oestrous resistant mares had higher baseline UCA and OT administration caused uterine spasm in all oestrous mares. However the repeated use of OT at short time intervals caused uterine refractoriness. Daily OT administration in the early postovulatory period significantly affected UCA up to day 3 postovulation. It was finally concluded that UCA is responsible for the clearance of uterine fluid from the uterus. Mares susceptible to endometritis have lower baseline uterine motility and UCA is restored slower after OT administration. There are no differences in the OT profiles between resistant and susceptible mares and different mechanical and psychogenic stimuli associated with reproductive events, seem to trigger OT release. However, most susceptible mares do not release PGF2α in response to endogenous OT release or exogenous OT. Oestrous resistant mares respond to OT administration with uterine spasm and PGF2α release. However in dioestrus, OT stimulates UCA only up to day 3 postovulation.

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