ABILITY OF INTRAUTERINE BACTERIAL LIPOPOLYSACCHARIDE TO CAUSE IN-SITUUTERINE CONTRACTIONS IN PREGNANT RABBITS

Citation
Y. Katsuki et al., ABILITY OF INTRAUTERINE BACTERIAL LIPOPOLYSACCHARIDE TO CAUSE IN-SITUUTERINE CONTRACTIONS IN PREGNANT RABBITS, Acta obstetricia et gynecologica Scandinavica, 76(1), 1997, pp. 26-32
Citations number
16
Categorie Soggetti
Obsetric & Gynecology
ISSN journal
00016349
Volume
76
Issue
1
Year of publication
1997
Pages
26 - 32
Database
ISI
SICI code
0001-6349(1997)76:1<26:AOIBLT>2.0.ZU;2-M
Abstract
Background. To investigate the ability of bacterial lipopolysaccharide delivered by the intrauterine route to cause uterine contractions in rabbits, and to assess the suppressive effect of urinary trypsin inhib itor on them. Methods. Both pregnant and non-pregnant rabbits were chr onically implanted with a force-transducer to make it possible to reco rd isometric uterine contractions under unanesthetized and unrestraine d conditions. Lipopolysaccharide (10 mu g/animal) was administered via a catheter to their uteri; and then, after confirmation of lipopolysa ccharide-induced uterine contractions, urinary trypsin inhibitor (3,00 0 or 10,000 units/animal/time) or saline solution was injected through the catheter, 5 times for pregnant animals or 3 times for non-pregnan t animals at 1-hour intervals in both cases. Their uterine contraction s were continuously recorded for 3 to 5 hours. Effects of lipopolysacc haride (10 mu g/ml) and urinary trypsin inhibitor (100 and 1,000 units /ml) on the contraction of isolated uteri from pregnant mice were also measured, as was their production of prostaglandin E2 and prostagland in F2 alpha by an enzyme immunoassay method. Results. Lipopolysacchari de augmented the in situ uterine contractions in both pregnant and non -pregnant rabbits, as well as the in vitro contractions of isolated ut eri from pregnant mice. Lipopolysaccharide also increased the uterine prostaglandin production. Urinary trypsin inhibitor inhibited signific antly the lipopolysaccharide-induced uterine contractions and the pros taglandin production. Conclusions. Lipopolysaccharide enhanced uterine contractions through, at least partly, a direct mechanism via uterine prostaglandin production, which action could explain the onset of pre term delivery due to intrauterine bacterial infection. As urinary tryp sin inhibitor suppressed the lipopolysaccharide-induced uterine contra ctions, this inhibitor may be a hopeful candidate of a drug for preven tion of preterm delivery.