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In order to clarify the mechanism of preterm labor induced by intrauterine infection, we studied the effect of endotoxin on oxytocin sensitivity of the myometrium in the pregnant rat. We administrated bacterial endotoxin obtained from Escherichia coli to the pregnant rat at preterm. By using a myometrial strip, we determined the effect of oxytocin on contractility, production of prostaglandins (PGs) and phosphoinositide hydrolysis. 1. Endotoxin increased myometrial sensitivity to oxytocin in the pregnant rat at preterm. The pD2 value was equal to that of myometrium taken from term pregnant rat. This hypersensitivity was significantly inhibited by indomethacin. 2. In the myometrial strips from rats to which endotoxin was administered, the concentrations of PGF2 alpha and PGE2 had already developed a tendency to increase during spontaneous contractions, when compared to the controls. There was seen a significant additional increase due to oxytocin. PGF2 alpha production was also significantly inhibited by indomethacin. 3. Oxytocin significantly stimulated total inositol phosphate production in a dose-dependent manner in myometrium taken from preterm pregnant rat. The inositol 1.4.5-trisphosphate production stimulated by oxytocin significantly increased in comparison to the controls. These results suggest that not only the production of PGs but phosphoinositide hydrolysis of transmembrane signaling pathways would play an important role in the mechanism of myometrial contraction at preterm when intrauterine bacterial infection developed.
H Suzuki, and
T Okawa, and
C Endo, and
K Hoshi, and
A Sato
December 1968,
American journal of obstetrics and gynecology,
H Suzuki, and
T Okawa, and
C Endo, and
K Hoshi, and
A Sato
January 1985,
British journal of pharmacology,
H Suzuki, and
T Okawa, and
C Endo, and
K Hoshi, and
A Sato
September 1990,
European journal of pharmacology,
H Suzuki, and
T Okawa, and
C Endo, and
K Hoshi, and
A Sato
August 1983,
Endocrinology,
H Suzuki, and
T Okawa, and
C Endo, and
K Hoshi, and
A Sato
September 2012,
Reproductive sciences (Thousand Oaks, Calif.),
H Suzuki, and
T Okawa, and
C Endo, and
K Hoshi, and
A Sato
July 2014,
European journal of obstetrics, gynecology, and reproductive biology,
H Suzuki, and
T Okawa, and
C Endo, and
K Hoshi, and
A Sato
March 1993,
Endocrinology,
H Suzuki, and
T Okawa, and
C Endo, and
K Hoshi, and
A Sato
February 1996,
Endocrinology,
H Suzuki, and
T Okawa, and
C Endo, and
K Hoshi, and
A Sato
December 1987,
General physiology and biophysics,
H Suzuki, and
T Okawa, and
C Endo, and
K Hoshi, and
A Sato
May 1995,
European journal of pharmacology,
