Search PubMed⌕ Search

Biomedical subjects

D G Porter

Publications and source records attributed to D G Porter.

At least 55 records · Page 3Linked to original sources
PubMed1982

Plasma concentrations of prolactin, progesterone, relaxin and oestradiol-17 beta in sows treated with progesterone, bromocriptine or indomethacin during late pregnancy.

Pregnant gilts (3/group) were given no treatment, 10 mg bromocriptine twice daily by mouth, from Day 111 of pregnancy to 1 day post partum, 25 mg progesterone s.c. at 6-h intervals from Days 111 to 116 inclusive or 400 mg indomethacin by mouth at 6-h intervals from Day 111 to 116 inclusive. Before spontaneous delivery maternal plasma prolactin and relaxin concentrations started to rise almost simultaneously between 58 and 47 h before the first piglet and both hormones reached peak values when the plasma progesterone concentration had started to decline rapidly (approximately 21-23 h). Suppression of prolactin levels by bromocriptine prevented the onset of lactation completely but had no obvious influence on changes of the other hormone concentrations and the course of parturition. Progesterone treatment delayed the onset of expulsion of the piglets but did not delay the simultaneous increase in prolactin and relaxin concentrations. These changes in hormone levels were prevented by indomethacin treatment but occurred essentially unchanged when the treatment was ended. The results support the concept that parturition in the pig is preceded by a biphasic increase of plasma prostaglandin levels.

Animals↗
PubMed1982

Effect of uterine distension and oestrogen treatment on gap junction formation in the myometrium of the rat.

Gap junctions were present in the myometrium of 1 out of 5 rats on Day 21 of pregnancy, 4 out of 5 on the morning of Day 22, 7 out of 7 during parturition and 1 out of 3 on Day 1 post partum. Their frequency (number per mm membrane) at these time periods increased from 0.30 to 2.20 and 6.48 and then decreased to 0.31. Ten ovariectomized post-partum rats were fitted with an intrauterine balloon in one horn for recording pressure changes. Control rats maintained continuous pressure cycles. In rats given 7.5 micrograms oestradiol-17 beta the frequency of intrauterine pressure cycles decreased from about 50 per hour to 4.3 per hour 15 h later, but the maximum rate of rise of uterine pressure cycles increased significantly from 7.2 +/- 0.95 to 11.3 +/- 1.85 mmHg sec-1 (n = 5, P less than 0.05). The overall number of gap junctions per mm membrane in the oestrogen-treated rats was 7.37 in the horns equipped with balloons and 1.03 in the empty horns, compared with 0.97 and none respectively in the control rats. The increased rate of rise of pressure in the oestrogen-treated myometrium indicated improved coupling between cells and this was associated with a high frequency of gap junctions. Both oestrogen treatment and distension (from the balloon) appeared to cause some gap junctions to form, but numbers equivalent to those at parturition were only obtained in animals in which these two treatments were combined.

Action Potentials↗
PubMed1981

Myometrial activity in rats during the oestrous cycle and pseudopregnancy: interaction of oestradiol and progesterone.

1. Oestradiol 17 beta inhibits the rat myometrium but the role of progesterone is uncertain. We have examined the interaction of the two steroids in the control of uterine activity in pseudopregnancy and the oestrous cycle. 2. Progesterone reversed the oestradiol-induced inhibition of the myometrium in ovariectomized rats in vivo, but had little inhibitory effect of its own unless treatment was continued for several days. 3. The frequency and amplitude of intra-uterine pressure cycles was unaffected by pseudopregnancy, but during the oestrous cycle frequency fell abruptly during late dioestrous and did not recover until early oestrus. 4. It is suggested that oestradiol is the major regulator of myometrial activity during the cycle and that progesterone interferes with the action of oestradiol, thereby paradoxically increasing uterine activity.

Animals↗
PubMed1981

Relaxin inhibits myometrial activity in the ovariectomized non-pregnant ewe.

Myometrial activity was abolished abruptly but reversibly in 4 out of 5 ewes by the intravenous injection of 1 mg (500 GPU) porcine relaxin. Recovery began only after about 90 min and was not complete until 3-4 h after the injection. During the relaxin-induced inhibition the myometrium responded to oxytocin administered intravenously in doses of 250 mU. One ewe received intrauterine infusions of 2.5 and 5.0 microgram PGF-2 alpha per min during the period of relaxin inhibition: the former dose evoked a slight, and the latter a marked, response from the myometrium. The rate of rise of intrauterine pressure and the mean amplitude of pressures cycles were significantly depressed at 1, 1.5 and 2 h after the relaxin injection.

Animals↗
PubMed1981

Tamoxifen and the role of oestrogen in the timing of parturition in the rat.

After tamoxifen treatment 'spontaneous' pressure cycles were resumed in conscious rats in which myometrial activity had been inhibited with oestradiol benzoate, demonstrating an anti-oestrogenic effect of this compound. Tamoxifen did not shorten the length of pseudopregnancy to less than 11 days when administered to rats 4 days after cervical stimulation. The effect of oestradiol benzoate (OB) treatment of pregnant rats depended on the day of administration. On Day 18 OB injection (5 micrograms) advanced the mean time of parturition by 5-6 h (P less than 0.001) whereas injection on Days 19 or 20 delayed delivery by more than 6.5 and 8.5 h respectively (P less than 0.05). It is suggested that the ability of tamoxifen given on Days 20 or 21 to advance the time of parturition in rats is due to its anti-oestrogenic activity.

Animals↗
PubMed1981

Demonstration of some of the physiological properties of rat relaxin.

Relaxin was extracted from the ovaries of pregnant rats. Material possessing uterine relaxing activity in vitro was eluted in three peaks from Sephadex G.50 columns. The 'G3 peak' material eluting in a position comparable to that of porcine relaxin inhibited myometrial activity of rats in vivo, improved the rate of rise of pressure of intrauterine pressure cycles in vivo, and, when administered to rats following progesterone and oestrogen priming, increased the distensibility of the cervix in vitro. This material also stimulated inter-pubic ligament formation in the mouse.. This rat relaxin material therefore exhibits biological actions in the rat similar to those previously assigned to porcine relaxin.

Animals↗
PubMed1981

Inhibition of oxytocin-or prostaglandin F2alpha-driven myometrial activity by relaxin in the rat is oestrogen-dependent.

Relaxin in doses of 5 microgram i.v. completed but reversibly abolishes "spontaneous' myometrial activity in anaesthetized ovariectomized rats. Similar levels of myometrial activity, evoked in oestrogen-treated rats (which normally have quiescent uteri) by infusions of oxytocin or prostaglandin F2alpha (PGF2alpha), were also reduced to complete quiescence by relaxin in small doses. However when spontaneous myometrial activity in untreated ovariectomized rats was slightly stimulated by oxytocin the uterus became completely refractory to the inhibitory effects of relaxin even at doses of 50 microgram. Relaxin was also ineffective in reducing myometrial activity in similar rats during intra-arterial infusion of PGF2alpha. It is suggested that the ability of relaxin to inhibit uterine smooth muscle during exogenous stimulation is oestrogendependent.

Animals↗
PubMed1980

Oestrogen-induced myometrial quiescence in the post-partum rat is not mediated by adrenaline or by alpha- or beta-adrenoceptor activation.

Ovariectomized post-partum rats exhibit in vivo continuous stable myometrial activity with a frequency of 45--50 pressure cycles per h, and a mean maximum amplitude of 45--50 mmHg for many days. Oestradiol benzoate (5 micrograms) reduced the frequency of intra-uterine pressure cycles to 5 cycles per h by 20 h after treatment. The decrease in frequency was due to increased periods of uterine quiescence. Pretreatment with reserpine caused significant reductions in the concentration of uterine adrenaline and noradrenaline as measured by a fluorometric assay but had no effect on the extent or time-course of oestrogen-induced myometrial quiescence. Neither intravenous infusion of the adrenergic beta-blocker, propranolol, altered the extent or the time-course of the reduction of intra-uterine pressure cycles after oestrogen treatment. These results suggest that the mechanism by which oestrogen induces myometrial quiescence does not involve adrenaline mediation or alpha- or beta-adrenoceptor activation.

Animals↗
PubMed1979

Relaxin inhibits spontaneous and prostaglandin-driven myometrial activity in anaesthetized rats.

Porcine relaxin (250 guinea-pig units/mg) infused intravenously into anaesthetized rats at 20 micrograms/h reversibly abolished spontaneous intra-uterine pressure cycles yet left the myometrium responsive to oxytocin in doses of 4--8 mu. The inhibition was found to be primarily of the frequency, rather than of the amplitude, of pressure cycles. Relaxin (5 or 10 micrograms) was capable of completely suppressing uterine activity driven by prostaglandin F2 alpha infusion in oestrogen-treated ovariectomized rats. Whereas the beta-adrenergic blocker, propranolol, had no effect on relaxin-induced inhibition, phentolamine, an alpha-blocker, significantly delayed the relaxin effect. It is unlikely, however, that relaxin operates through an alpha-inhibitory receptor. The results show that relaxin acts primarily as a frequency modulator and is capable of antagonizing an exogenous myometrial stimulant.

Animals↗
PubMed1978

Demonstration that progesterone 'blocks' uterine activity in the ewe in vivo by a direct action on the myometrium.

Intrauterine pressure was monitored in vivo in oestrogen-treated ovariectomized ewes before, during and after treatment with progesterone (50 mg s.c./day for 3 days). Progesterone reversibly reduced the frequency and amplitude of myometrial activity and abolished uterine reactivity to oxytocin (i.v.) and PGF-2alpha (intrauterine infusion). The rate of rise of intrauterine pressure during active pressure cycles was significantly reduced. These results confirm that the action of progesterone on the ovine myometrium is comparable to the classic progesterone 'block'. The intrauterine infusion of PGF-2alpha (10 microgram/min), which elicited a marked mechanical response in the control animals, failed to stimulate the progesterone-'blocked' uterus, suggesting that the inhibition produced by progesterone is due to a direct action of the hormone on the uterine muscle and not to an indirect mechanism operating through endometrial prostaglandin output.

Animals↗
PubMed1978

Evidence that a humoral factor possessing relaxin-like activity is responsible for uterine quiescence in the late pregnant rat.

When post-partum ovariectomized rats were linked to 21-day-pregnant rats by a cross-circulation system their myometrial activity was almost completely inhibited. No reduction in activity was induced by cross-circulation with other post-partum rats, or with rats in which myometrial activity had been suppressed with oestrogen. Changes in uterine activity could not be correlated with alterations in arterial blood pressure occurring during the experiments. Uteri rendered inactive by cross-circulation were found to be responsive to oxytocin. It is concluded that a humoral myometrial inhibitor is present in late pregnancy in rat blood and the possibility that it is relaxin is discussed.

Animals↗
PubMed1978

Rat myometrial activity in vivo: effects of oestradiol-17 beta and progesterone in relation to the concentrations of cytoplasmic progesterone receptors.

The amplitude, frequency and rate of rise of intra-uterine pressure cycles in rats (postpartum, ovariectomized) were unaffected by treatment with progesterone. Amplitude was also unaffected by a combination of treatments with progesterone and oestradiol-17 beta, which was adequate to ensure the survival of 84% of foetuses in ovariectomized pregnant rats. The failure of progesterone to influence myometerial activity could not be attributed to a lack of "true" progesterone receptors since these were present in the myometria of the test animals in concentrations exceeding those of oestrous animals. Evidence was obtained which suggested that a high-affinity binding protein, different from the "true" receptor may predominate in the myometrium of the pregnant rat. Oestradiol-17 beta in single or repeated doses of from 0.25 to 5 microgram, however, was found to reduce the frequency of pressure cycles but to increase significantly their rate of rise of pressure. There was a latency of 6--8 h in these effects of oestradiol. The possibility that inhibition of the myometrium by oestrogen may play a part in the preparation for parturition is discussed.

Animals↗
PubMed1978

Evidence that inhibition of myometrial activity by oestradiol in the rat is mediated by an RNA synthetic pathway.

Within some 14 h of treatment with oestradiol benzoate (5 microgram), the intra-uterine pressure cycles in ovariectomized puerperal rats were almost abolished. However, treatment with 600 microgram actinomycin D 30 min before the administration of oestradiol benzoate interfered significantly with the inhibition of uterine mechanical activity during the following 14h. Treatment of rats with actinomycin D alone produced no significant fall in the frequency of pressure cycles. These results suggest that oestrogen inhibits myometrial activity in the rat through a mechanism which involves the synthesis of protein.

Animals↗