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Results for “Maternal Physiology”

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At least 19 recordsLinked to original sources
PubMed1988

Maternal physiologic adaptations to early human pregnancy.

This study was designed to test the hypothesis that significant maternal physiologic adaptations to pregnancy take place in multiple systems long before they are functionally necessary (during the embryonic period). To test this hypothesis, 20 women were studied serially before pregnancy and in the seventh and fifteenth postconceptional week of an accurately dated, clinically normal, singleton pregnancy. By the seventh week, significant changes were noted in body composition and cardiopulmonary and metabolic functions. Body fat and plasma volume increased 2% and 11%, respectively, accounting for all of the observed 2 kg weight gain. With the patient standing at rest after eating, heart rate increased 13 beats/min (16%) while mean arterial pressure fell 8 mm Hg (9%). Minute ventilation rose 24% and oxygen consumption increased by 27 ml/min, or 10%. The postprandial respiratory exchange ratio also increased, from 0.78 to 0.83; the whole blood glucose level was unchanged at rest, although there was a 15% decrease in whole blood lactate levels. We conclude that our hypothesis is correct, which suggests these adaptations are preparative and may have diagnostic value.

Abortion, Spontaneous↗
PubMed1987

[Influence of placental protein hormones on maternal physiology].

Our data have demonstrated that maternal LH and FSH are repressed throughout pregnancy. Beside, we have discovered and characterized a variant placental GH. Our studies on the mechanism of anovulation and on pituitary GH suppression and GH physiology in pregnant women have contributed to demonstrate the autonomy of the fetoplacental unit and its effects on maternal anabolism and physiology. More specifically, human placental GH, coded by the GH-V gene appears responsible for the anabolic and somatotropic effects mediated by SM-C in the mother. The beneficial aspect of this mechanism for the species appears likely since placental tissues in which the GH-PL genes are deleted, express alternative gene(s) resulting in the production of a placental variant closely related or identical to pituitary 22K GH.

Chromosome Deletion↗
PubMed2005

Maternal physiology and complications of multiple pregnancy.

Approximately 1% to 3% of all pregnancies in the United States are multiple gestations. The vast majority (97-98%) are twin pregnancies. Multiple pregnancies constitute significant risk to both mother and fetuses. Antepartum complications-including preterm labor, preterm premature rupture of the membranes, intrauterine growth restriction, intrauterine fetal demise, gestational diabetes, and preeclampsia-develop in over 80% of multiple pregnancies as compared with approximately 25% of singleton gestations. This article reviews in detail the maternal physiologic adaptations required to support a multiple pregnancy and the maternal complications that develop when these systems fail or are overwhelmed.

Female↗
PubMed1995

Evidence for the production of platelet-activating factor by murine embryos and its putative role in the maternal physiology.

Thrombocytopenia has been shown to be an initial maternal response to conception. We investigated a potent bioactive lipid, platelet-activating factor (PAF), as one of the candidates derived from embryos to induce the decrease of platelet counts in maternal blood. First, we examined the potential of murine embryos to liberate PAF. In brief, twenty to thirty murine two-cell embryos of C57BL/6 mice were cultured in Whitten's medium for 24 h. The supernatant of the medium was collected and the total was extracted. After developing the lipid on thin-layer chromatography, the area corresponding to authentic PAF was scraped off and the lipid was extracted. The embryo-derived PAF was quantified by platelet aggregation using rabbit whole blood, and the presence of PAF was further confirmed by the addition of a PAF-receptor antagonist, SRI63-441. The results showed that a significant amount of PAF (ca. 10 ng/ml) was recovered from the lipid extract, whereas little platelet-aggregating activity was observed in the presence of SRI63-441. Second, the physiological function of murine platelets was examined using authentic PAF. When PAF (up to 83 micrograms/ml) was added to the murine platelets suspended in the whole blood, it neither induced platelet aggregation nor reduced the number of platelets. Considering these results, it is considered that PAF released from the embryos does not directly act on maternal platelets, but transduces its signal to the maternal host via some other bioactive substance.

Animals↗
PubMed1978

Early cognitive development and its relation to maternal physiologic and behavioral responsiveness.

Data are presented which support the hypothesis that infant cognitive development is a function of maternal responsiveness to infant cues. 22 mothers whose physiologic responses to infant signals had been recorded at an earlier date participated in the follow-up study reported here. Mother-infant dyads were videotaped during a feeding session when the infant was 9 months of age. Behavioral data collected were the mother's responses to her infant's facial orientation. The statistic developed to index maternal sensitivity was the rate of maternal responding during infant gaze/the rate of responding during infant looking away. Development of the object concept was assessed at 15 months using the Uzgiris and Hunt scale. The data indicated that the development of the concept of the object is positively related to maternal behavioral sensitivity and that mothers who were behaviorally sensitive to infant cues earlier had exhibited physiologic responses to infant signals.

Adult↗
PubMed2004

Maternal asthma as a model for examining fetal sex-specific effects on maternal physiology and placental mechanisms that regulate human fetal growth.

Studying the effect of maternal asthma during pregnancy on placental function and fetal development has highlighted that there is a strong interaction between mother, placenta and fetus and these interactions appear to be sex-specific. This work has found that the female fetus alters maternal asthma during pregnancy by upregulating maternal inflammatory pathways. When asthma-associated inflammatory pathways are not treated with inhaled steroids during pregnancy, the female fetus has reduced growth and adrenal function due to alterations in placental glucocorticoid metabolism. When the mother uses inhaled steroid for the treatment of her asthma during pregnancy, female fetal growth and placental function are comparable to the control population. The growth of the male fetus appears to be unaffected by asthma or inhaled steroid use. These findings indicate there may be different mechanisms regulating placental glucocorticoid and immune mechanisms depending on fetal sex in both asthmatic and non-asthmatic pregnancies.

Adult↗
PubMed1985

The effect of constant light on maternal physiology and behavior.

In contrast to previous findings in nonlactating rats, constant light does not disrupt maternal water or food intake. Mothers and pups in constant light, however, gained less weight than their counterparts in the light-dark cycle. While mothers did not differ in their total daily contact time or daily bout frequency, the distribution of the contact time was shifted in constant light. These data may be consistent with the idea that mothers maintain a free-running rhythm under such conditions.

Animals↗
PubMed2006

Meloxicam effectively inhibits preterm labor uterine contractions in a chronically catheterized pregnant sheep model: impact on fetal blood flow and fetal-maternal physiologic parameters.

OBJECTIVE: Preterm birth occurs in 5% to 10% of all pregnancies and is associated with considerable neonatal mortality and morbidity. Effective and safe drugs to prevent preterm labor are not currently available. We have hypothesized that the nonsteroidal anti-inflammatory drug meloxicam, a more selective cyclooxygenase-2 inhibitor will successfully inhibit labor but avoid the complications associated with inhibition of cyclooxygenase-1. STUDY DESIGN: Preterm labor was induced in chronically catheterized sheep by RU486 administration. Animals were then randomized to receive maternal infusions of saline (n = 5) or meloxicam (n = 4) for 48 hours or until delivery when the animals were killed and tissues and blood samples collected. RESULTS: Maternal infusion of meloxicam inhibited uterine contractions, increasing contraction duration, and attenuating frequency and amplitude. Saline-treated animals progressed to delivery. Administration of meloxicam was not associated with any change in fetal or maternal blood gas status, osmolality, arterial pressure, heart rate, or fetal blood flows. CONCLUSION: Meloxicam may represent a potentially safe and effective tocolytic agent.

Abortifacient Agents, Steroidal↗
PubMed1989

Prenatal ethanol and stress in mice: 1. Pup behavioral development and maternal physiology.

On days 12 to 17 of pregnancy, B6D2F1 mice were pair-fed liquid diets containing either 25% ethanol-derived calories or an isocaloric amount of maltose-dextrin. During this period, half the mice in each dietary condition also underwent two daily one-hour periods of restraint stress. A fifth group, given lab chow and water ad lib, was left undisturbed throughout gestation. Neither treatment affected offspring body weight on days 22 or 32 postconception, but undernutrition produced by the pair feeding procedure reduced day 32 body weight in all groups relative to the ad lib-fed group. Both prenatal ethanol and pair feeding led to delayed neurobehavioral development on day 32, while prenatal stress significantly reduced the degree of developmental delay caused by these factors. In a second study, restraint stress significantly reduced blood alcohol concentrations in pregnant dams on day 15 of gestation while elevating plasma corticosterone concentrations, and this elevation was consistent regardless of the dietary condition of the dam. The pair feeding procedure also produced corticosterone elevations but the effect of ethanol was not significant. These results suggest that prenatal stress in the presence of other physiological insults may act to counter the actions of those insults.

Animals↗
PubMed1993

Fetal development in the rat following disruption of maternal renal function during pregnancy.

Pregnant Sprague-Dawley rats received subcutaneous injections of mercuric chloride (1-4 mg/kg) on either gestation day 7, 9, 11, or 13 to determine effects of altered maternal renal function on embryonic and fetal development. Maternal renal function, assessed by urinalysis, was markedly disrupted for at least 48 hours after treatment and resulted in decreased maternal body weight gain. Residual effects on maternal kidney weight were evident on GD 21 when the females were killed and the fetuses removed and examined for visceral and skeletal development. We did not observe an increased incidence of malformations in the offspring for exposure on any day of gestation. Maternal exposure to mercuric chloride slightly impaired fetal growth over several gestational exposures periods and changed the pattern of rib formation when exposure occurred early in organogenesis. The extent of the changes could not, however, be related to the immediate degree or duration of altered maternal renal function. Rather, we found correlations between lasting effects of exposure as measured by maternal renal weight on GD 21 and super-numerary lumbar rib induction on GD 7 and 9; while for the relationship with fetal weight, the strongest correlation with maternal kidney weight occurred following exposure on GD 9 (P < 0.01), with weaker correlations (P < 0.10) for GD 7 and 13 exposures. Maternal serum urea was negatively correlated with fetal weight from the GD 7 exposure. This study supports the concept that some specific forms of maternal toxicity may be associated with limited manifestations of developmental toxicity, but, in general, embryonic development was observed to proceed normally in the presence of marked disruptions in maternal renal physiology. Maternal toxicity, especially as routinely measured in developmental toxicity studies, cannot be looked upon as a single disease. Instead, each manifestation must be examined for what it signifies to the physiology and well being of the female and for cause-and-effect relationships with fetal observations. Maternal toxicity and developmental toxicity should not be etiologically linked solely because of their concurrent appearance on the dose-response curve.

Acute Kidney Injury↗
PubMed1981

Maternal hyperoxia greatly reduces the incidence of phenytoin-induced cleft lip and palate in A/J mice.

The A/J mouse has been used to study the teratogenic affects of phenytoin. The developmental abnormalities produced in offspring of this model are similar to some of the malformations observed in cases of human "fetal hydantoin syndrome." Placing pregnant A/J mice in a hyperoxic chamber after phenytoin injection greatly reduces the incidence of phenytoin-induced cleft lip and palate. These results suggest that phenytoin may affect embryonic development indirectly by altering maternal physiology. This maternally mediated mechanism, and the protection against it afforded by hyperoxia, has general implications for the effects of maternal toxicity on teratogenesis.

Abnormalities, Drug-Induced↗