In vitro studies suggest that the female sex steroid hormones [estrogen (E) and progesterone (P)] can affect the myoelectric and mechanical activity of colonic smooth muscle. The present study was designed to examine the influence of the hormones on colonic transit in vivo. Transit was assessed by quantifying the distribution within the colon of a radiolabeled marker (0.5 microCi Na251CrO4), using the geometric center method of analysis. Studies were performed with adult male rats and the following groups of female rats: nonpregnant, ovariectomized, ovariectomy plus hormone pretreatment (100 micrograms X kg-1 X day-1 E + 2.5 mg X kg-1 X day-1 P for 4 days), and pregnant (day 18). Hormone-pretreated animals were studied 24 h following the fourth injection. The data can be summarized as follows. 1) Colonic transit was affected by the timing of the estrus cycle. Rats determined to be in proestrus-estrus had a geometric center value (1.97 +/- 0.50) significantly less than that of metestrus-diestrus animals (4.25 +/- 0.57). 2) Ovariectomy eliminated the biphasic transit pattern observed in estrus-cycling females and resulted in a geometric center value (4.19 +/- 0.17) comparable with that of the metestrus-diestrus animals. 3) E + P pretreatment of ovariectomized rats resulted in a significant decrease in the geometric center (1.94 +/- 0.19) compared with the untreated ovariectomized rats. 4) The geometric center value in pregnant animals (2.22 +/- 0.20) closely resembled the transit data for proestrus-estrus animals and hormone-pretreated animals.(ABSTRACT TRUNCATED AT 250 WORDS)
The aims of this study were to determine regional differences and the mechanism of gastric contractile effects of erythromycin. Rabbit gastric circular muscle strips were studied in vitro. The threshold dose for erythromycin was significantly less and the maximum contraction greater in the antrum (1 microM and 0.9 +/- 0.3 kg/cm2) than in the fundus (10 microM and 0.3 +/- 0.1 kg/cm2). Erythromycin-induced antral contractions were decreased by motilin tachyphylaxis but unaffected by tetrodotoxin, atropine, hexamethonium, or ondansetron. At a subthreshold dose (0.1 microM), erythromycin increased the frequency, but not the amplitude, of bethanechol (10 +/- 3%)-and substance P-induced (13 +/- 5%) phasic antral contractions. This chronotropic effect was inhibited with tetrodotoxin, atropine, or motilin tachyphylaxis. Erythromycin (10 microM) and motilin (1 microM) enhanced the amplitude of substance P-induced tonic fundic contractions by 38 and 32%, respectively, without effect on bethanechol-induced contractions. In summary, erythromycin contracts antral muscle more potently and forcefully than fundic muscle. Erythromycin increases antral contractility by two mechanisms: an inotropic effect acting on smooth muscle motilin receptors, and, at lower doses, a cholinergic chronotropic effect mediated through neuronal motilin receptors.
In a factorially designed experiment (N = 321), 0, 800 or 1600 I.U. pregnant mare serum gonadotrophin (PMSG) were administered in combination with 0, 12 or 18 mg follicle stimulating hormone (FSH-P) to superovulate Merino ewes in autumn and spring. A moderate dose of PMSG (800 I.U.) in conjunction with 12 or 18 mg FSH-P increased the ovulation rate above that observed when FSH-P was used alone. This was accomplished by (i) increasing the proportion of ewes that exhibited a superovulatory response (greater than 3 corpora lutea (CL) or persistent large follicles (LF): 69/70 (99%) v. 55/74 (74%), P less than 0.001), and (ii) in those ewes that exhibited a superovulatory response, by an additive effect of exogenous gonadotrophin (14.8 +/- 0.9 CL (69) v. 11.3 +/- 0.9 CL (55), P less than 0.01) without increasing the incidence of LF. The use of 1600 I.U. PMSG in conjunction with 12 or 18 mg FSH-P was characterized by an increase in the number of LF and, in comparison with 800 I.U. PMSG, a reduction in ovulation rate. Season had no effect on the numbers of CL, but total ovarian response (CL + LF) was higher in autumn than in spring (P less than 0.01), because of a greater incidence of LF (P less than 0.001). The proportion of ewes with regressed CL was higher in autumn than in spring (53/143 (37%) v. 32/156 (21%), P less than 0.01), and increased with increased dose of gonadotrophin. Furthermore, a nutritional component to the incidence of ewes with regressed CL was suggested by the observation that the mean concentration of plasma glucose was higher for ewes with normal CL than for ewes with regressed CL (P less than 0.05). Rates of ova or embryo recovery, fertilization and embryo development generally declined with an increase in the incidence of LF as a result of increases in the dose of gonadotrophin and season of administration.
Administration of gonadotrophin releasing hormone (GnRH) 24 h after sponge withdrawal did not affect the numbers of corpora lutea (CL) or persistent large follicles (LF) in ewes superovulated with 400 I.U. pregnant mare serum gonadotrophin and 12 mg follicle stimulating hormone in spring (11.6 +/- 0.9 v. 13.0 +/- 0.9 CL and 0.8 +/- 0.9 v. 0.9 +/- 0.3 LF, for +GnRH and -GnRH ewes, respectively). However, it did increase the ovulatory response of ewes superovulated in autumn (15.8 +/- 1.2 v. 11.8 +/- 1.1 CL). The incidence of ewes with prematurely regressed CL was also greater in autumn than in spring (21/89 v. 5/88). Supplementary feeding with lupin grain in autumn had no effect on numbers of CL but did increase the incidence of ewes with LF (18/48 v. 7/46) and caused a marked reduction in the incidence of ewes with regressed CL (1/44 v. 20/45). For ewes treated in autumn, there were no effects of lupin supplementation or GnRH administration on peak oestradiol-17 beta (E2) or peak luteinizing hormone (LH) levels. However, when peak E2 concentrations in the plasma were adjusted for numbers of preovulatory follicles, higher concentrations were observed for ewes in the +lupin/-GnRH group (12.4 +/- 2.9 pg mL-1) than in other treatment groups (range 4.3 +/- 0.4 to 5.7 +/- 0.3 pg mL-1). Moreover, the time of the LH peak was advanced by both lupin supplementation and GnRH treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
This study utilized the transfer of preimplantation embryos to pseudo-pregnant mice to determine whether PAF-antagonists act primarily on the maternal or embryonic components of implantation. The first experiment used reciprocal embryo transfers, in which blastocysts from mice treated with PAF antagonist (SRI 63-441) or saline (controls), from Days 1 to 4 of pregnancy, were transferred to Day-3 pseudo-pregnant recipients which were also treated with SRI 63-441 or saline on Days 1-4 of pregnancy. The antagonist (40 micrograms) was administered at 16:00 h on Day 1 and at 09:00 h on Days 2-4 of pregnancy. The percentage of the transferred embryos which implanted was determined on Day 8 of pregnancy. Treatment of the recipient or the donor female with SRI 63-441 resulted in a reduction in implantation rate, from a control level of 45% to 33.8% or 34.7% (P less than 0.0002, P less than 0.007) respectively. These results suggest that the PAF antagonist affected implantation at the embryonic and maternal levels. However, when the blastocysts were transferred to Day-4 pseudopregnant recipients, treatment of the donor female had a dramatic effect on the implantation rate, resulting in a reduction of 64% (from 40% to 14.3%, P less than 0.04), while treatment of the recipient female had no significant effect. In this later experiment the transferred embryos were exposed to the recipient uterine environment for a shorter period before implantation. These results suggest that PAF antagonists affected implantation at the embryonic level and did not adversely affect maternal physiology.(ABSTRACT TRUNCATED AT 250 WORDS)
To determine if and how clonidine and tricyclic antidepressants affect gastric contractility. Guinea pig fundic and antral circular muscle strips were studied in vitro. The effects of clonidine or amitriptyline added in graded concentrations on contractions to electric field stimulation (EFS), acetylcholine (ACh), and SP in the presence of N(epsilon)-nitro-l-arginine methyl ester (l-NAME) were studied. EFS produced frequency dependent contractions of fundic and antral muscle that were abolished by atropine or tetrodotoxin (TTX). ACh contractions were abolished by atropine but not TTX. Clonidine reduced contractile response to EFS but had no effect on ACh contractions. The threshold concentration of clonidine to inhibit EFS contractions was lower in the fundus than in the antrum. Amitriptyline reduced contractions to both EFS and ACh but not to SP. The threshold concentration of amitriptyline to inhibit EFS contractions was lower in the antrum than in the fundus. Both clonidine and amitriptyline affect gastric contractility. At threshold concentrations, clonidine affects fundic contractility whereas amitriptyline affects antral contractility. Clonidine affects gastric contractility in response to EFS but not to ACh, suggesting alpha-2 receptors on cholinergic nerves that reduce ACh release. Amitriptyline inhibits gastric contractility to EFS and ACh suggesting an inhibitory muscle effect.
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