Biomedical subjects
Publications and source records attributed to T Ikenoue.
Twenty-one days of magnesium sulfate tocolysis were performed on a 28-year-old woman because of preterm labor at 31 weeks gestation. In association with this tocolysis, urinary calculus of magnesium ammonium phosphate occurred at 34 weeks gestation.
This study is the first approach to evaluate whether human atrial natriuretic peptide (hANP) is involved in the pathophysiology in transient puerperal hypertension (TPH). Five women who were normotensive throughout pregnancy, labor, and delivery developed hypertension between the first and sixth postpartum day. hANP (pg/ml) and plasma renin activity (PRA, ng/ml/h), angiotensin I, II (AI, II, pg/ml), and aldosterone (Aldo, pg/ml) in plasma were quantified by radioimmunoassay. Ten women without hypertension were also studied on hANP, PRA, AI, AII, and Aldo sequentially as the control group. hANP was apparently lower in women with TPH than in normotensive women. The levels of PRA, AI, AII, and Aldo were also clearly decreased in women with TPH, whereas those values in normotensive women were not altered from nonpregnant levels. Maternal natriuresis usually reaches the peak at 3-5 days postpartum. The decrease of hANP and PPA, AI, AII, and Aldo in TPH coincides with this natriuretic period. This observation suggests that hANP may serve an important role in the pathogenesis of TPH.
OBJECTIVE: Our purpose was to investigate the relationship between the birth weights and 24-h urinary C-peptide in infants of diabetic mothers. METHODS: Sixty pregnancies with gestational diabetes mellitus (DM) were enrolled. Neonatal urine was collected for the first and second 24 h for measuring C-peptide. Birth weights were classified into 3 categories according to the Japanese standard curves; heavy-for-date (HFD), appropriate-for-date (AFD), and light-for-date (LFD). Unpaired t-test was used for comparison of 24-h urinary C-peptide in the 3 birth weight categories, with P-value <0.05. There were 7 HFD, 47 AFD, and 6 LFD infants. Birth weight averaged 3.9+/-0.7, 3.0+/-0.4, and 2.3+/-0.3 kg, respectively. RESULTS: Insulin concentrations of the umbilical artery were significantly higher in HFD than in AFD, and significantly higher in AFD than in LFD (49.5+/-45.1, 16.8+/-15.2, and 6.3+/-6.1 microU/ml). During the first 24 h, urinary C-peptide was significantly higher in HFD than in AFD (2.73+/-1.52 vs. 0.76+/-0.81 microg/day), and significantly higher in AFD than in LFD (0.27+/-0.27). On the second day, there was no longer statistical significance. CONCLUSIONS: Measurement of 24-h urinary C-peptide revealed that, among infants of diabetic mothers, HFD infants continue to secrete more insulin than AFD and LFD infants for the first 24 h.
OBJECTIVE: The effects of magnesium sulfate on fetal heart rate (FHR) response during acute hypoxemia in goats were investigated. METHODS: The FHR responses due to hypoxemia during magnesium sulfate infusion (Mg study) were compared with those during vehicle infusion (controls) in six chronically instrumented goat fetuses at 125-130 days' gestation. RESULTS: Four-hour infusions of magnesium sulfate significantly increased fetal plasma concentrations of magnesium from 2.3 to 6.5 mg/dL. During the hypoxemic period, the fetal arterial oxygen pressure was significantly decreased from 29.0 +/- 2.5 to 14.6 +/- 2.6 torr in the controls, and from 28.9 +/- 3.9 to 13.7 +/- 4.7 torr during the Mg study. Neither arterial carbon dioxide pressure nor pH was significantly altered. In the controls, FHR was significantly decreased by hypoxemia, accompanied by increases in variability. In the Mg study, FHR was not significantly decreased by hypoxemia. Acute hypoxemia also increased the FHR variability during magnesium infusion, which was significantly reduced compared with those in the control population. CONCLUSION: Magnesium sulfate masks FHR-slowing responses during acute hypoxemia in fetal goats.
OBJECTIVE: To determine if fetal heart rate (FHR) decelerations periodically occur with uterine contractures during 6 hours' induced hypoxemia in goats. METHODS: In five chronically catheterized goat fetuses at 125-130 days' gestation, incidence of FHR decelerations was compared between 6 hours' control time and 6 hours' induced hypoxemia with two-way ANOVA and Duncan's multiple range test. Three other fetuses were used as controls for circadian rhythm. RESULTS: Fetal PaO2 was significantly decreased from 26.1 to 16.3 mmHg without acidemia. During hypoxemia, 42 decelerations were induced along with 5 initial decelerations during the acute phase hypoxemia. Incidence of decelerations increased significantly from 0.07 +/- 0.15 per hour in 6-hour controls to 1.40 +/- 0.28 per hour during 6 hours' induced hypoxemia. Short-term variability and long-term variability of the 42 decelerations were significantly increased. These variabilities were also increased during the 5 initial decelerations. Frequency of uterine contractures did not change during hypoxemia. There was an observable association of FHR decelerations with uterine contractures during hypoxemia. CONCLUSION: Fetal heart rate decelerations occurred periodically in association with uterine contractures during induced 6 hours' hypoxemia, which were characterized by slow onset and recovery with increases in variability.
We report a rare case of an umbilical cord hemangioma diagnosed by ultrasound at 16 weeks of gestation. The umbilical cord consisted of a hemangioma nodule and pseudocysts near the placental insertion, a large gelatin-like swelling adjacent to the nodule on its fetal side, and a short normal part extending to the navel. At 17 weeks of gestation, this condition resulted in the intrauterine death of the fetus. Microscopically, there were communications between the capillary of the hemangioma and the umbilical vessels, verifying the origin of the tumor. Moreover, the umbilical vein and one of the arteries changed stenotically due to the intravascular proliferation of the hemangioma. These findings indicate the possibility of a pathological association between the umbilical cord hemangioma and fetal demise due to impaired umbilical circulation.
OBJECTIVE: We investigated the effect of hyperthermic pretreatment 24 hours before hypoxic-ischemic exposure on neuronal cell damage in 7-day-old rats. METHODS: Newborn rats were separated on postnatal day 7 into two groups: 1) preheated (those exposed to 2 hours of hyperthermic pretreatment at 42-43C) (n = 29), and 2) nonheated (n = 20). At 24 hours after the hyperthermic stress, rats from both groups were subjected to left carotid artery ligation followed by 2 hours of hypoxia (8% oxygen/92% nitrogen) at 33C. All rats were killed 1 week after hypoxia-ischemia, and brains were extracted for histologic study. A different group of 7-day-old rats (n = 8) was placed in the same hyperthermic environment as mentioned above for 2 hours, and 24 hours after heat exposure brains were extracted for immunohistochemistry of heat-shock protein 70. RESULTS: The total incidence of hypoxic-ischemic brain damage significantly decreased in the preheated group (12 of 25 [48%]) compared with the nonheated group (17 of 20 [85%]; P < .03). The induction of immunoreactive heat-shock protein 70 was observed mainly in glial and vascular endothelial cells and, in a lesser amount, in neuronal cells of the cerebral cortex and hippocampus. CONCLUSION: Incidence of hypoxic-ischemic brain damage is consistently reduced by 2 hours of hyperthermic pretreatment in 7-day-old rats.
OBJECTIVE: We measured fetal plasma concentrations of epinephrine, norepinephrine, and vasopressin during acute hypoxemia in goats and tested whether hypermagnesemia altered these endocrine responses. METHODS: Five chronically catheterized goat fetuses at 124-129 days' gestation were used. After 4 hours of infusion (magnesium or vehicle as controls), 30 minutes of hypoxemia was induced by infusing nitrogen gas through a maternal tracheal catheter. Fetal plasma concentrations of epinephrine, norepinephrine, and vasopressin were measured before and during hypoxemia. Both magnesium sulfate and vehicle infusions were performed in each animal. Repeated-measures analysis of variance (ANOVA) and two-way ANOVA with post hoc test were used to determine statistical significance. RESULTS: During hypoxemia, fetal PO(2) decreased significantly from 30 to 14 mmHg with no significant changes in fetal pH or PCO(2) in both groups. Fetal heart rate was reduced significantly by hypoxemia, but to a lesser extent in the magnesium group (change in decrease in fetal heart rate: 41 beats per minute [bpm] in controls versus 26 bpm with magnesium). Mean blood pressure did not change significantly during hypoxemia in both groups. Fetal plasma concentrations of epinephrine, norepinephrine, and vasopressin significantly increased from the prehypoxemic values both with magnesium and in controls. There were no significant differences in these hormone concentrations between magnesium and the controls. CONCLUSION: Magnesium sulfate had no effect on fetal plasma concentrations of vasopressin, epinephrine, and norepinephrine during acute hypoxemia.
The ductus arteriosus of 19 premature infants with intrauterine growth retardation (IUGR) (study group) was compared histologically with that of 22 infants without IUGR (control group). The two groups exhibited no significant differences in gestational age, age at death, and frequency of disseminated intravascular coagulation. Maternal complications, that is, pregnancy-induced hypertension, cesarean section, and low umbilical artery oxygen tension values, were seen more frequently (p < 0.01) in the study group than in the control group. The histologic changes of ductus arteriosus, such as fragmentation, coagulation necrosis of the intimal elastic lamina, hemorrhage with necrosis, and loosening of elastic fibers and muscles in the tunica media, were seen more frequently in the study group. These findings are suggestive of both the maturation process and the prenatal hypoxic response of premature IUGR fetuses with chronic hypoxia. These changes may have produced subsequent patent ductus arteriosus, which in turn may have induced pulmonary hemorrhage.