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.
Aortic rings from male and female Sprague-Dawley rats were placed in organ chambers filled with Krebs solution, and the isometric tension was recorded. There were no gender differences in responses to potassium chloride or phenylephrine in either intact or endothelium-denuded rings from control animals. Treatment with 10 mg/kg of lipopolysaccharide (LPS) attenuated the contractile response to potassium chloride in intact, but not in endothelium-denuded rings, and suppressed the phenylephrine contractions in rings both with and without endothelium from male and female rats. Endothelium-dependent and -independent relaxation by acetylcholine and the nitric oxide donor diethylamine/NO, respectively, did not depend on gender and were equally suppressed by LPS treatment. Treatment with LPS accentuated the effects of oxyhemoglobin in rings with and without endothelium and this was significantly larger in rings from females compared to males. Thus, gender differences were present in the effect of LPS on vascular responses. LPS induced a greater increase in basal release of nitric oxide and a greater inhibition of depolarization by potassium chloride, but not receptor-activated contractions, in aortic rings from female versus male rats.
Objective: The aim of this study was to illuminate the mechanism of a redistribution of blood flow in fetuses. Nitric oxide (NO) is now known to play important functional roles in the vasculature. We measured plasma nitrate (the metabolites of nitric oxide) concentrations in maternal and fetal sheep at term, and compared the effect of NO donors on isolated carotid and renal arteries from fetuses. Methods: (1) Blood samples were taken from maternal and fetal arteries in sheep at 132 ± 2 days’ gestation, and were collected for nitrate determination with Griess reagent. (2) Rings of carotid and renal arteries with intact endothelium from fetal sheep were positioned in organ chambers filled with Krebs‐Henseleit solution (37°C) bubbled with 5% CO 2 in air (pH: 7.4) and isometric tension was recorded. Concentration‐response relationships to sodium nitroprusside (SNP), nitroglycerine (NTG) and diethylamine nitric oxide (DEA/NO) with pretreatment NO scavenger, oxyhemoglobin (10 –5 M), and vehicle were determined. Results: (1) Plasma nitrate levels were significantly higher in fetuses than in maternal sheep. (2) Nitric oxide donor concentrations dependently inhibited in phenylepherine‐precontracted carotid and renal arteries. The relaxation of both rings was attenuated by previous treatment with oxyhemoglobin. Nitric oxide sensitivity was greater in carotid arteries than in renal arteries. The order of potency was SNP > NTG > DEA/NO in the two types of arteries. Conclusion: These observations indicate that NO may play an important role in the redistribution of blood flow in fetuses.
Primary aldosteronism rarely complicates pregnancy. We present a woman with primary aldosteronism in pregnancy associated with severe preeclampsia. A 33-year-old Japanese woman with hypertension was referred to our hospital at 25 weeks of gestation. Her blood pressure was 180/100 mmHg, and laboratory tests identified a low serum potassium level and moderate proteinuria on urinalysis. The fetus was diagnosed with growth restriction. Plasma renin activity (PRA) value was 2.2 ng/mL/h and plasma aldosterone concentration (PAC) was elevated (260 pg/mL). The patient was treated medically. At 27 weeks of gestation, we noted persistent late fetal heart rate decelerations associated with uterine contractions. Therefore, elective caesarean section was performed and she was delivered of a 698-g female. After delivery, PRA declined and PAC remained elevated. Abdominal computerized tomography scan and I-iodochoresterol scan revealed a tumor in the left adrenal gland. Laparoscopic adrenalectomy was performed and confirmed the clinical diagnosis.
