Uterine motor responses to an α-adrenergic agonist (phenylephrine) in the ewe during oestrus and at the end of gestation

Abstract

Summary. The a-adrenergic activity of the myometrium was studied by recording the electromyographic activity (EMG) of the uterus in 4 conscious cyclic ewes during oestrus and in 8 conscious pregnant ewes during the last 6 days of gestation.In the cyclic ewes, changes in intra-uterine pressure were recorded at the same time as the EMG. Motor responses to perfusions of phenylephrine, a specific a-adrenergic agonist, were studied at three uterine sites. In the ewes in oestrus, uterine activity was stimulated at the three sites by perfusions with phenylephrine (0.6, 2.5, 5 or 10 pg/kg/min). The whole uterine horn was a-adrenergic-responsive. The effect of the drug was dosedependent in that the uterine response increased with the dose and reached a plateau at 5 pg/kg/min.In the late pregnant ewes, the motor responses to the perfusion of phenylephrine at 10 wg/kg/min were studied at three uterine sites once a day during the last 6 days of gestation. Plasma levels of progesterone and total oestrogens were measured at the same time.Up to 48 h before parturition, the effect of phenylephrine depended on the uterine site. The drug had no or little effect at the tubal end of the horn. Phenylephrine stimulated uterine activity at the cervical end of the horn in at least 50 % of the ewes. Thus, during this part of gestation, the a-adrenergic sensitivity of the myometrium was greater at the cervical than at the tubal end of the uterine horn. Forty-eight hours before parturition, phenylephrine stimulated uterine activity at all three uterine sites in all the ewes. Thus, a-adrenergic sensitivity developed over the uterine horn beginning 48 h before parturition at the same time that the oestrogen level increased.Introduction.

Long-Term Observations of Uterine Contractions in Nonpregnant Dogs

“…The uterine contractile responses to these neurotransmitters have been studied widely, mostly in vitro, in various experimental animal species [3,10,14,19,25,26,[31][32][33] as well as in humans [4,7,8,34]; considerable information about the mechanism or mechanisms by which these neurotransmitters stimulate contraction has been gathered. With respect to the contractile response of the uterus to cholinomimetics, many studies have indicated the existence of abundant muscarinic receptors in the uterine smooth muscle [3,4,7,8,[35][36][37][38].…”

“…With regard to other adrenergic receptors, phenylephrine (atl agonist) [13,14,25], clonidine (at2 agonist) [13], and butoxamine (2 antagonist) were found to enhance uterine spontaneous contractile activity, whereas prazosin (a 1 antagonist) [10], yohimbine (a 2 antagonist) [10], dobutamine (1 agonist), and atenolol ([3 antagonist) did not influence the spontaneous contractions at all.…”

“…Furthermore, the methods utilized in most studies on uterine contractile activity were measurement of the contractile activity of the isolated myometrium in vitro [1][2][3][4][5][6][7][8] and electromyogram [9][10][11][12][13][14][15] and intrauterine pressure [16][17][18][19][20][21][22] recording in vivo. Although removal of the tissue from its natural environment and elimination of the numerous complex interactions make it easy to perform experiments and understand the underlying mechanisms, in vitro experiments have considerable limitations with respect to understanding the overall picture of uterine contractile activity control.…”

The Effect of Detomidine Hydrochloride on the Electrical Activity of Uterus in Pregnant Mares

“…It activates nrreceptors of the adrenergic system (Savo/a 1986, Salonen 1986, Virtanen 1986. Previous information indicates that the a-receptor agonist xylazine and phenylephrine induce uterine contractions in cows and ewes (Le Bfac et al 1984, Prudhomme 1986. Thus the use of n-agonists during pregnancy can create the risk of abortion.…”