Electromyographic properties of the myometrium of the pony mare during pregnancy

Haluska, George J.; Lowe, Jillian E.; Currie, W. B.

doi:10.1530/jrf.0.0810471

Cited by 10 publications

(6 citation statements)

References 17 publications

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“…In the present study, control mares from experiment 1 exhibited spike burst clusters for approximately 25% of the time of each recording session (11 h recording daily) until 6 days before delivery when evening activity increased to approximately 30% of the recording time. These findings are in agreement with Haluska et al (1987) who found that the myometrium is electrically active 30% of the time in the mare in late gestation.…”

Section: Discussionsupporting

confidence: 93%

“…Visual assessment of myoelectrical data files that were recorded in the last 8 h of gestation showed long periods of decreased activity followed by very short, rhythmic bursts of activity. This supports the findings of Haluska et al (1987) that there is a decrease in uterine activity 2 -4 h before foaling. This period of quiescence is thought to be the time when the foal rotates from the dorso-pubic position to the dorso-sacral position.…”

Section: Discussionsupporting

confidence: 91%

“…Relatively little is known about the uterine contractility pattern in the late-gestational mare. In a small study in which myoelectrical activity was analyzed for 2 h daily in two pony mares in late gestation, Haluska et al (1987) observed that the change in the percent myoelectrical activity per hour was a function of the frequency of the myoelectrical bursts, and frequency of spike bursts increased as parturition approached.…”

Section: Introductionmentioning

confidence: 99%

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Alteration in uterine contractility in mares with experimentally induced placentitis

McGlothlin

Lester²,

Hansen³

et al. 2004

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An experimental model of ascending placentitis was developed in the mare to characterize the uterine myoelectrical pattern in late gestation and determine how ascending placentitis altered this pattern. In experiment 1, myometrial electrical activity was analyzed during the early morning, late morning and evening hours in four mares in the last 15 days of gestation to identify patterns of activity. In experiment 2, nine mares received intra-cervical inoculations of Streptococcus equi subspecies zooepidemicus. Myoelectrical activity in the early morning and evening hours in these mares was compared with four control mares. In experiment 1, the number of spike burst clusters >30 s was greater in the evening than in the late morning hours (P < 0.04). Spike burst activity (number 3 duration) of mares in experiment 1 was similar during day and night recordings until the last 6 days of gestation when it gradually increased each evening until parturition (P < 0.05). In experiment 2, control mares experienced a gradual increase in the number of small spike burst clusters in the last 6 days (P 5 0.008) and an increase in large and small spike burst clusters in the evening hours in the last 4 days of gestation (P 5 0.03). Mares with experimentally induced placentitis never exhibited a rise in spike burst clusters but had an increase in the mean duration and activity index of large spike burst clusters in the 4 days before parturition (P < 0.04). In conclusion, control mares had a progressive, reversible rise in myoelectrical activity at night in the week preceding parturition. This was not observed in mares with experimentally induced placentitis. They exhibited an increase in the intensity and duration of large spike burst clusters possibly in response to local inflammation.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Alteration in uterine contractility in mares with experimentally induced placentitis

McGlothlin

Lester²,

Hansen³

et al. 2004

Reproduction

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“…8,9 Internally, during this period, the mare's uterus begins more active contractions beginning at the end of the uterus near the ovary and progressing posteriorly toward the cervix. Prior to this increase, mares may demonstrate decreased activity that could last for several weeks.…”

Section: Mare Prepartum Changesmentioning

confidence: 99%

Parturition and Dystocia

Threlfall¹

2007

Current Therapy in Large Animal Theriogenology

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“…Might it serve a protective role during sporadic hypoxic episodes that occur during normal pregnancy? In placental mammals, transient hypoxia accompanies spontaneous uterine contractions, called contractures, and has been observed throughout gestation in large mammals [31,[41][42][43][44] and rodents [45,46] . In rabbit, contractures lasting between 4 and 5 min were recorded from day 1 of gestation and continued to term [45] .…”

Section: Ne Blunts Hypoxia-induced Bradycardiamentioning

confidence: 99%

β<sub>1</sub>-Adrenergic Receptors Maintain Fetal Heart Rate and Survival

et al. 2006

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β-Adrenergic receptor (βAR) activation has been shown to maintain heart rate during hypoxia and to rescue the fetus from the fetal lethality that occurs in the absence of norepinephrine. This study examines whether the same subtype of βAR is responsible for survival and heart rate regulation. It also investigates which βARs are located on the early fetal heart and whether they can be directly activated during hypoxia. Cultured E12.5 mouse fetuses were treated with subtype-specific βAR antagonists to pharmacologically block βARs during a hypoxic insult. Hypoxia alone reduced heart rate by 35–40% compared to prehypoxic levels. During hypoxia, heart rate was further reduced by 31% in the presence of a β₁AR antagonist, CGP20712A, at 100 nM, but not with a β₂ (ICI118551)- or a β₃ (SR59230A)-specific antagonist at 100 nM. Survival in utero was also mediated by β₁ARs. A β₁ partial agonist, xamoterol, rescued 74% of catecholamine-deficient (tyrosine-hydroxylase-null) pups to birth, a survival rate equivalent to that with a nonspecific βAR agonist, isoproterenol (87%). Receptor autoradiography showed that β₁ARs were only found on the mouse heart at E12.5, while β₂ARs were localized to the liver and vasculature. To determine if the response to hypoxia was intrinsic to the heart, isolated fetal hearts were incubated under hypoxic conditions in the presence of a βAR agonist. Heart rate was reduced to 25–30% by hypoxia alone, but was restored to 63% of prehypoxic levels with 100 nM isoproterenol. Restoration was completely prevented if β₁ARs were blocked with CGP20712A at 300 nM, a concentration that blocks β₁ARs, but not β₂- or β₃ARs. Our results demonstrate that β₁ARs are located on the heart of early fetal mice and that β₁AR stimulation maintains fetal heart rate during hypoxia and mediates survival in vivo.

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Electromyographic properties of the myometrium of the pony mare during pregnancy

Cited by 10 publications

References 17 publications

Alteration in uterine contractility in mares with experimentally induced placentitis

Alteration in uterine contractility in mares with experimentally induced placentitis

Parturition and Dystocia

β<sub>1</sub>-Adrenergic Receptors Maintain Fetal Heart Rate and Survival

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