| Summary: | 博士 === 國立陽明大學 === 臨床醫學研究所 === 83 ===
It has been shown that men have more rapid gastric emptying of liquid meals and higher gastric acid secretory capacity than premenopausal women. A prolongation of gastrointestinal (Gl) transit has been reported during pregnancy or during the luteal phase of the menstrual cycle. In addition, symptoms of peptic ulcer usually subside during pregnancy but flare up after parturition or at the time of the menopause. These clinical observations have led to speculation about the possible roles of ovarian hormones on Gl function. However, the current conclusions from the studies about sex and pregnancy-related alterations in gastric emptying and Gl transit are based on indirect evidence, and the role of male sex hormone is unclear. Also the studies concerning the effect of ovarian steroids on acid secretion are controversial. The purpose of present study is to examine (1) the effect of ovarian steroids on gastric emptying, Gl transit, and gastric acid secretion in ovariectomized (OVX) rats, (2) the effect of lactation on gastric emptying, Gl transit, and gastric acid secretion, and (3) the effect of testosterone on gastric emptying, Gl transit, and acid secretion in male rats. In another experiment the role of placenta in regulating acid secretion during pregnancy was evaluated by examining the presence of gastric inhibitory polypeptide (GIP), both immunoreactivity and biological activity, in the rat placenta extract (RPE). Gastric emptying was expressed by determing the amount of labeled chromium contained in the small intestine 15 min after instillation as a percentage of the initial amount received. Gastrointestinal transit was assessed by calculating both the geometric center of distribution of the radiolabeled marker and the charcoal transit in the small intestine. Acid output was determined by titration of the flushed perfusate with O.O1N NaOH to pH7.0. Basal secretion was collected for 45 min before infusion ofpentagastrin (8μg/ml/300 g BW/30 min) with a peristaltic pump for 90 min. Concentration of plasma GIP, estradiol (E), progesterone (P), and prolactin (PRL) were measured by radioimmunoassay (RIA). Our results showed that E inhibited while P enhanced gastric emptying dosedependently. E plus P inhibited gastric emptying. Both E and P did not affect Gl transit. Testosterone had no effect either on gastric emptying and Gl transit or on basal and pentagastrin-stimulated acid secretion. The values of gastric emptying and plasma P concentrations remained high during lactation, and decreased rapidly to the levels of non-pregnant diestrus rats at day 7 of postweaning. The values of geometric center, charcoal transit, small intestine length, and plasma prolactin levels were greater in the early stage of lactation. There was no difference in E concentrations among lactating, postweaning, and diestrus rats. There was no difference in basal and pentagastrin-stimulated acid secretion among OVX rats replaced with E, P, E+P or vehicle (sesame oil). Pentagastrin-stimulated acid secretion was greater while uterine weight was lower in lactating than in non-pregnant rats. Plasma P concentrations were higher on days 7 and 14 of lactation, and decreased to non-pregnant levels on day 21-22 of lactation. There was no difference in either basal or pentagastrin-stimulated acid secretion, and uterine weight between 1st, 2nd, and 3rd week of lactation. There was no correlation between acid secretion and plasma P concentrations or uterine weight in lactating rats. A dose-response immunoreactivity of GIP-like substance was found in the rat placenta extract. RPE inhibited the pentagastrin-stimulated acid secretion in male rats. These results suggest that (1) ovarian steroid hormones could modulate gastrointestinal motor activity, (2) rising of plasma P and PRL concentrations in lactating rats is resulted from lactation. Elevation of plasma P levels may contribute to the quicker gastric emptying observed in lactating rats, (3) the change of plasma E and P concentrations could not explain the hypersecretion of acid during lactation, (4) E, P, or testosterone has no effect on basal and pentagastrin-stimulated acid secretion, and (5) the normalization of pentagastrin-stimulated acid secretion in late pregnant rats is at least in part due to the production of GIP-like substance from placenta.
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