Reduction In Uterine Blood Flow Research Articles

Vasopressors in obstetrics: what should we be using?

Historically, ephedrine has been recommended as the best vasopressor in obstetrics because animal studies showed it caused less reduction in uterine blood flow compared with alpha-agonists. Recent clinical evidence, however, suggests that this is not as important as initially thought. This review evaluates current data with a focus on spinal anesthesia for cesarean section. Ephedrine and phenylephrine have been most investigated. Advantages of ephedrine include familiarity, long history and low propensity for uteroplacental vasoconstriction. Ephedrine, however, has limited efficacy, is difficult to titrate, causes maternal tachycardia and depresses fetal pH and base excess. Advantages of phenylephrine include high efficacy, ease of titration and the ability to use liberal doses to maintain maternal blood pressure near normal and then prevent nausea and vomiting without causing fetal acidosis. Phenylephrine, however, may decrease maternal heart rate and cardiac output and few data are available on its use in high-risk cases. Combination of a phenylephrine infusion and rapid crystalloid cohydration is the first method described that reliably prevents hypotension. When current evidence is considered, in the authors' opinion, phenylephrine is the vasopressor that most closely meets the criteria for the best vasopressor in obstetrics.

Fluoxetine during pregnancy: impact on fetal development

Women are at greatest risk of suffering from depression during the childbearing years and thus may either become pregnant while taking an antidepressant or may require a prescription for one during pregnancy. The antidepressant fluoxetine (FX) is a selective serotonin reuptake inhibitor (SSRI), which increases serotonin neurotransmission. Serotonin is involved in the regulation of a variety of physiological systems, including the sleep-wake cycle, circadian rhythms and the hypothalamic-pituitary-adrenal axis. Each of these systems also plays an important role in fetal development. Compared with other antidepressant drugs, the SSRIs, such as FX, have fewer side effects. Because of this, they are now frequently prescribed, especially during pregnancy. Clinical studies suggest poor neonatal outcome after exposure to FX in utero. Recent studies in the sheep fetus describe the physiological effects of in utero exposure to FX with an 8 day infusion during late gestation in the sheep. This is a useful model for determining the effects of FX on fetal physiology. The fetus can be studied for weeks in its normal intrauterine environment with serial sampling of blood, thus permitting detailed studies of drug disposition in both mother and fetus combined with monitoring of fetal behavioural state and cardiovascular function. Fluoxetine causes an acute increase in plasma serotonin levels, leading to a transient reduction in uterine blood flow. This, in turn, reduces the delivery of oxygen and nutrients to the fetus, thereby presenting a mechanism for reducing growth and/or eliciting preterm delivery. Moreover, because FX crosses the placenta, the fetus is exposed directly to FX, as well as to the effects of the drug on the mother. Fluoxetine increases high-voltage/non-rapid eye movement behavioural state in the fetus after both acute and chronic exposure and, thus, may interfere with normal fetal neurodevelopment. Fluoxetine also alters hypothalamic function in the adult and increases the magnitude of the prepartum rise in fetal cortisol concentrations in sheep. Fetal FX exposure does not alter fetal circadian rhythms in melatonin or prolactin. Studies of the effects of FX exposure on fetal development in the sheep are important in defining possible physiological mechanisms that explain human clinical studies of birth outcomes after FX exposure. To date, there have been insufficient longer-term follow-up studies in any precocial species of offspring exposed to SSRIs in utero. Thus, further investigation of the long-term consequences of in utero exposure to FX and other SSRIs, as well as the mechanisms involved, are required for a complete understanding of the impact of these agents on development. This should involve studies in both humans and appropriate animal models.

Maternal Insufflation during the Second Trimester Equivalent Produces Hypercapnia, Acidosis, and Prolonged Hypoxia in Fetal Sheep

Anecdotal reports suggest that the second trimester is the safest time to conduct a laparoscopic procedure on a pregnant patient, but this supposition has not been tested empirically. Previously instrumented preterm sheep (total n = 8) at gestational day 90 (term, 145 days) were anesthetized and then insufflated with carbon dioxide for 60 min at a pressure of 15 mmHg. Cardiovascular parameters were continuously recorded while blood gas status was determined before and at 15-min intervals during and up to 2 h after insufflation. Insufflation produced minimal maternal blood gas or cardiovascular changes except for a significant reduction in uterine blood flow. The decrease in perfusion increased fetal arterial blood partial pressure of carbon dioxide and decreased fetal pH, oxygen saturation, and oxygen content; there was also progressive fetal hypotension and bradycardia. After manually deflating the ewe, uterine blood flow returned to normal, and the fetal partial pressure of carbon dioxide and pH changes resolved within 1 h. However, fetal oxygen saturation and content remained depressed, and fetal cardiovascular status continued to decline during the 2-h postinsufflation monitoring period. Previous studies with near-term sheep determined that carbon dioxide pneumoperitoneum produces respiratory acidosis but does not decrease fetal oxygenation. In contrast, the current findings indicate that in the preterm fetus, insufflation-induced hypercapnia and acidosis are accompanied by prolonged fetal hypoxia and cardiovascular depression. This result suggests that additional work should be conducted to confirm the presumed safety of conducting minimally invasive procedures during the second trimester.

The oestrous cycle and early pregnancy – a new concept of local endocrine regulation

Facts discovered in recent decades have compelled us to revise long-established views on the physiological regulation of cyclic adjustments to the reproductive system in preparation for pregnancy in females. Evidence has been presented to show that changes in the uterine blood supply induced by the oestrogen/progesterone ratio in the blood and cytokines are important in the regulation of the secretory function of the endometrium. Progressive reduction in uterine blood flow during the luteal phase of the oestrous cycle causes regressive changes in endometrial cells and release of prostaglandin (PG) F 2α, resulting in initiation of luteolysis. Retrograde transfer of PGF 2α in the area of the mesometrium vasculature is an important element in the mechanism protecting the corpora lutea against luteolysis before day 12 of the porcine oestrous cycle and during early pregnancy and pseudopregnancy. Results of many studies presented in this review indicate that PGF 2α pulses in uterine venous blood during the follicular phase of the oestrous cycle may not be due to PGF 2α secretion by endometrial cells, but occur due to remodeling of the endometrium and pulsatile exretion of PGF 2α in accordance with rhythmic uterine contractions caused by oxytocin.

Development of foetal and neonatal simulators at the University of Porto.

Human error can be expected to play a significant role in adverse outcomes in perinatal acute care. In acute care of the adult, simulator based training is recommended and used to improve patient safety. Our general goal is to develop model-driven foetal and neonatal educational simulators and curricula. The specific objectives of this paper are to introduce the reader to the perinatal acute care context and simulator design considerations, as well as to give initial results and describe ongoing developments. A brief description of adult simulators and simulation engines is followed by a more detailed description of a foetal distress simulator (FDS) and of models for a neonatal simulator developed at the University of Porto. Ongoing developments involve the modelling of foetal baroreflexes, the effect of uterine contractions, and an adapted method for estimating foetal heart rate variability parameters. We present FDS simulation results reflecting the changes in oxygen supply to the foetus and the foetal heart rate in response to a reduction in uterine blood flow. We also present a structural diagram of a model for the educational simulation of congenital heart disease and preliminary simulation results reflecting a patent ductus arteriosus. We expect that, after initial clinical and educational validation, the presented models and simulators will play a role in simulator-based educational programmes contributing to increased perinatal safety.

Uterine blood flow—a determinant of fetal growth

An adequate increase of uterine blood flow throughout gestation is essential for uterine, placental and fetal growth. Maternal cardiovascular adaptation has to provide the uterine perfusion that is necessary to meet the requirements of the developing and growing fetus by providing transport of nutrients and oxygen to the placenta and the fetus. Thus, uterine blood flow is inextricably linked to fetal growth and survival. Reductions of uterine blood flow can occur under acute or chronic conditions or in a combination of both. Chronic reductions of uterine blood flow can be observed in pregnancy-induced hyertension (PIH), diabetes mellitus in pregnancy and intrauterine growth restriction (IUGR). Chronic restrictions in uterine blood flow will elicit a placental and fetal response in the form of growth adaptation to the reduced supply of oxygen and nutrients to the conceptus. If compensatory growth restriction reaches its limits intrauterine fetal distress can ensue. Among the great number of experimental models of intrauterine growth restriction, those involving a generalized reduction in the uteroplacental blood supply are of significance to questions relating to human pregnancy. Despite physiological differences, particularly with regard to maternal metabolism and placentation, the occlusion model in the pregnant sheep is suitable for investigating questions about fetal and placental growth.

Anaesthesia for fetal surgery.

*Department of Anesthesia, Children’s Hospital, Harvard Medical School, Boston, MA,**Department of Anesthesiology and Critical Care, The Children’s Hospital of Philadelphia,University of Pennsylvania School of Medicine, Philadelphia and †Department of Anesthesia andCritical Care, The Hospital of the University of Pennsylvania, University of Pennsylvania Schoolof Medicine, Philadelphia, PA, USA

Fetal umbilical vascular response to chronic reductions in uteroplacental blood flow in late-term sheep

Objective: The present study was designed to determine the effects of chronic reduction in uterine blood flow (UBF) on umbilical blood flow (UmbBF) and fetal cardiovascular hemodynamics and oxygenation. Study Design: Sixteen sheep with singleton pregnancies were instrumented on gestational day (GD) 110; an externally adjustable vascular occluder was placed on the common internal iliac artery. UBF in control animals rose from 867 ± 61 mL/min on GD 115 to 1520 ± 158 mL/min (n = 8) on GD 138, whereas UBF in restricted animals was maintained at 750 ± 50 mL/min (n = 8). Results: UmbBF in control animals increased from 472 ± 25 mL/min to 744 ± 58 mL/min over the study period from GD 115 to GD 138. This was associated with normal gestational increases in fetal arterial pressure and significant reductions in calculated umbilical vascular resistance. Although restricted animals initially had a similar UmbBF on GD 115, UmbBF rose only to 545 ± 43 mL/min over the study period (control vs restricted, P <.008). Although fetal arterial pressure showed normal gestational changes, umbilical vascular resistance failed to decrease over gestation in restricted animals as it did in control animals. Fetal heart rate and oxygenation showed normal changes in both groups. Conclusion: Chronic reduction in UBF prevents umbilical vascular resistance from undergoing normal gestational decreases, leading to significantly lower UmbBF. This altered umbilical perfusion pattern would be expected to significantly affect fetal delivery of oxygen and nutrients and ultimately fetal growth. (Am J Obstet Gynecol 2002;187:178-86.)

Leptin in the ovine fetus correlates with fetal and placental size

Objective: The purpose of this study was to detect the presence of leptin and its receptor in ovine fetal tissues and to examine the relationship between circulating leptin concentrations and fetal and placental weights on gestational day 138 (GD138) of ovine pregnancy (term, 145 days). Study Design: Pregnant sheep (n = 18) were instrumented on GD 110 to facilitate measurement and chronic reduction of uterine blood flow and produce intrauterine growth restriction. Four animals that served as controls were euthanized on GD 138 to obtain fetal tissues to determine the presence of ovine leptin and its receptor by reverse transcriptase–polymerase chain reaction. Seven instrumented animals were randomized into the control group, and 7 instrumented animals were randomized into the uterine blood flow restricted group (reduction equaled approximately 50% on GD 138). Maternal and fetal blood samples were obtained on day 138 to measure plasma leptin concentrations, and animals were euthanized for the determination of fetal morphometrics and placental weight. Results: Expression of RNA for ovine leptin and its receptor were observed in fetal liver, skeletal muscle, kidney, heart, and placenta. Fetal body weight, ponderal index, and placental weight were significantly decreased by approximately 40% in the blood flow restricted group as compared with controls. Fetal leptin concentrations were increased by 45% in the uteroplacental blood flow restricted group (P =.01). Maternal leptin concentrations were not significantly different between the 2 groups and did not correlate with fetal concentrations. Fetal leptin concentrations had an inverse relationship with uterine blood flow (r = -0.73; P =.004), fetal body weight (r = -0.78; P =.002), and placental weight (r = -0.68; P =.01). Conclusion: Ovine fetal tissues express RNA for leptin and its receptor. Circulating leptin concentrations in the ovine intrauterine growth restriction fetus were significantly elevated on gestational day 138 compared with controls. Fetal leptin concentrations were inversely related to uterine blood flow and fetal and placental weight. These findings suggest that fetal leptin may be involved in an adaptive response to intrauterine growth restriction. (Am J Obstet Gynecol 2001;185:786-91.)

Effects of chronic reduction in uterine blood flow on fetal and placental growth in the sheep.

Pregnancy is associated with a significant increase in uteroplacental blood flow (UBF), which is responsible for delivering adequate nutrients and oxygen for fetal and placental growth. The present study was designed to determine the effects of vascular insufficiency on fetal and placental growth. Thirty-nine late-term pregnant ewes were instrumented to investigate the effects of chronic UBF reduction. Animals were split into three groups based on uterine blood flow, and all animals were killed on gestational day 138. UBF, which began at 851 +/- 74 ml/min (n = 39), increased in controls (C) to 1,409 +/- 98 ml/min (day 138 of gestation) and in the moderately restricted (R(M)) group to 986 +/- 69 ml/min. In the severely restricted (R(S)) group, UBF was only 779 +/- 79 ml/min on gestational day 138. This reduction in UBF significantly affected fetal body weight with R(M) fetuses weighing 3,685 +/- 178 g and R(S) fetuses weighing 2,920 +/- 164 g compared with C fetal weights of 4,318 +/- 208 g. Fetal brain weight was not affected, whereas ponderal index was significantly reduced in R(M) (2.94 +/- 0.09) and R(S) fetuses (2.49 +/- 0.08) compared with the value of the C fetuses (3.31 +/- 0.08). Placental weight was also significantly reduced in the R(M) group, being 302 +/- 24 g, whereas the R(S) group placenta weighed 274 +/- 61 g compared with the C values of 414 +/- 57 g. Fetal heart, liver, lung, and thymus were all significantly smaller in the R(S) group. Thus the present study shows a clear relationship between the level of UBF and both fetal and placental size. Furthermore, the observation that fetal brain weight was not affected, whereas fetal body weight was significantly reduced suggests that this experimental preparation may provide a useful model in which to study asymmetric fetal growth restriction.

Uterine perfusion and fetal growth

An adequate increase of uterine blood flow throughout gestation is essential for uterine, placental and fetal growth. Maternal cardiovascular adaptation has to provide the uterine perfusion that is necessary to meet the requirements of the developing and growing fetus by providing transport of nutrients and oxygen to the placenta and the fetus. Thus uterine blood flow is inextricably linked to fetal growth and survival. Reductions of uterine blood flow can occur under acute or chronic conditions or in a combination of both. Chronic reductions of uterine blood flow can be observed in pregnancy induced hyertension (PIH), diabetes mellitus in pregnancy and intrauterine growth restriction (IUGR). Chronic restrictions in uterine blood flow will elicit a placental and fetal response in the form of growth adaptation to the reduced supply of oxygen and nutrients to the conceptus. If compensatory growth restriction reaches its limits intrauterine fetal distress can ensue.

Altered fetal cardiovascular responses to prolonged hypoxia after sinoaortic denervation.

This study examines the role of the peripheral chemoreceptors in mediating fetal cardiovascular responses to prolonged hypoxia secondary to reduced uterine blood flow (RUBF). Fetal sheep were chronically instrumented for continuous heart rate (FHR), blood pressure (FBP), and carotid blood flow (CBF) measurements after bilateral sectioning of the carotid sinus and vagus nerves (denervated, n = 7) or sham denervation (intact, n = 7). Four days postoperatively, uterine blood flow was mechanically restricted, reducing fetal arterial oxygen saturation by 47.3% (P < 0.01). An initial bradycardia was observed in intact (184.0 +/- 10.7 to 160.5 +/- 10.7 beats/min, not significant) but not denervated fetuses, followed by a tachycardia (180.0 +/- 2.2 to 193.7 +/- 2.7 beats/min, P < 0.05). FHR increased in denervated fetuses (175.5 +/- 8.7 to 203. 0 +/- 17.9 beats/min, P < 0.05). FBP increased transiently in intact fetuses from 45.1 +/- 1.0 to 55.4 +/- 3.0 mmHg at 2 h (P < 0.01), whereas denervated fetuses demonstrated a decrease in FBP from 47.1 +/- 4.2 to 37.2 +/- 3.7 mmHg (not significant). CBF increased (P < 0. 05) in both intact and denervated fetuses from 39.3 +/- 2.8 and 29.7 +/- 3.8 ml. min-1. kg-1 to 47.7 +/- 0.4 and 39.1 +/- 0.3 ml. min-1. kg-1, respectively, whereas carotid vascular resistance decreased only in denervated fetuses (1.7 +/- 0.1 to 1.1 +/- 0.02 mmHg. ml-1. min. kg-1, P < 0.05). We conclude that the peripheral chemoreceptors play an important role in mediating fetal cardiovascular responses to prolonged RUBF.

Prostaglandin E2 inhibition of fetal breathing movements is not sustained during prolonged reduced uterine blood flow in sheep

Fetal breathing movements (FBM) are inhibited by both exogenous prostaglandin E2 (PGE2) and ethanol in sheep. Maternal ethanol exposure in late-gestation sheep also increases fetal [PGE2]. However, during prolonged reduced uterine blood flow (RUBF) when [PGE2] in fetal plasma is already elevated, FBM are not inhibited by ethanol. These experiments were designed, therefore, to test the hypothesis that the FBM response to PGE2 is also diminished during RUBF. PGE2 (594 ± 19 ng·min-1·kg-1 fetal body weight) was infused for 6 h into the jugular vein of RUBF (PO2 = 14 ± 1 mmHg (1 mmHg = 133.3 Pa); n = 7) and control (PO2 = 22 ± 1 mmHg (p &lt; 0.01); n = 7) ovine fetuses, and the effect on FBM, electrocortical (ECoG), and electroocular activities was determined. The infusion of PGE2 increased plasma [PGE2] from 881 ± 162 to 1189 ± 114 pg·mL-1 in RUBF fetuses and from 334 ± 72 to 616 ± 118 pg·mL-1 (p &lt; 0.05) in control fetuses. FBM were initially inhibited by PGE2 from 22.5 ± 9.4 and 17.9 ± 6.5% of the time to 6.9 ± 2.4 and 0.5 ± 0.4% (p &lt; 0.01) in RUBF and control fetuses, respectively. FBM remained inhibited in control fetuses throughout the infusion but returned to baseline incidence in RUBF fetuses in the last 2 h of the infusion. These results are consistent with the hypothesis that one component of the adaptative mechanisms of the fetus to prolonged RUBF is an altered response of FBM to exogenous PGE2. We speculate that the lack of a sustained inhibition in FBM during RUBF with infusion of PGE2 may be a result of an alteration in brainstem receptor function or number or local PGE2 removal.Key words: fetal breathing movements, prostaglandin E2, hypoxia, reduced uterine blood flow, ethanol, fetal behaviour.

Supplemental Oxygen and Glucose During Prolonged Uterine Blood Flow (UtBF) Reduction Prevents Fetal Growth Restriction in Sheep. • 1576

We have shown that 7 days of UtBF reduction in sheep results in a 38% decrease in fetal linear growth rate (LGR) from 6 mm/day to 3.7 mm/day (Am J Physiol, 1996). This decrease in LGR correlates with the fetal concentrations of oxygen and glucose. Subsequent studies, in which fetal PaO2 was increased by providing supplemental oxygen to the ewe during UtBF reduction, failed to prevent the development of fetal growth restriction. The present study was undertaken to test the hypothesis that fetal growth restriction might be prevented by providing supplemental O2 and glucose during UtBF reduction. Six sheep with singleton pregnancies at 115-117 days gestation were prepared with vascular catheters, a fetal crown-rump length measuring device, a vascular occluder on the maternal terminal aorta, and a catheter in the maternal trachea. Fetal LGR was measured daily after surgery. The sheep were recovered for 8-14 days after which serial studies were performed 7 days apart. Following a basal study UtBF was reduced and sheep were supplemented with 100% O2 at 2-2.5 lpm via the maternal tracheal catheter. In addition, a variable glucose infusion was begun through the middle uterine artery with the goal of increasing the fetal arterial glucose concentration by 25-50%. UtBF reduction and O2 and glucose concentrations were checked twice daily between the Basal and Day 7 studies.

Fetal endocrine responses to prolonged reduced uterine blood flow are altered following bilateral sectioning of the carotid sinus and vagus nerves.

The present study examines the effect of carotid sinus/vagosympathetic denervation on fetal endocrine responses to prolonged reduced uterine blood flow (RUBF). Fetal sheep had vascular catheters inserted following bilateral sectioning of the carotid sinus and vagus nerves (denervated, n = 7) or sham denervation (intact, n = 7). Uterine blood flow was mechanically restricted at 126.1 +/- 0.7 days (mean +/- S.E.M.) for 24 h, decreasing arterial oxygen saturation by 47.3 +/- 2.6% (P < 0.01). Fetal plasma samples were obtained at -1, 3, 6, 12 and 24 h for subsequent analyses of arginine vasopressin (AVP), angiotensin II and catecholamines. The AVP response to prolonged RUBF was markedly attenuated in denervated fetuses (15.6 +/- 3.6 to 34.9 +/- 6.0 pg/ml) when compared with intact (10.0 +/- 1.4 to 127.3 +/- 28.4 pg/ml). In contrast, intact fetuses demonstrated no change in plasma angiotensin II concentrations with RUBF whereas denervated fetuses demonstrated a marked increase from 47.5 +/- 18.9 to 128.7 +/- 34.2 pg/ml. The norepinephrine and epinephrine responses to prolonged RUBF were attenuated in denervated fetuses (950.1 +/- 308.9 and 155.8 +/- 58.5 to 1268.3 +/- 474.6 and 290.6 +/- 160.2 pg/ml respectively) when compared with intact (1558.3 +/- 384.4 and 547.3 +/- 304.7 pg/ml to 3289.2 +/- 1219.8 and 896.8 +/- 467.8 pg/ml respectively). These results support a role for the peripheral chemoreceptors in mediating fetal endocrine responses to prolonged RUBF, which may in part lead to the altered cardiovascular responses observed in denervated fetuses under these conditions.

Prostaglandin E2 inhibition of fetal breathing movements is not sustained during prolonged reduced uterine blood flow in sheep.

Fetal breathing movements (FBM) are inhibited by both exogenous prostaglandin E2 (PGE2) and ethanol in sheep. Maternal ethanol exposure in late-gestation sheep also increases fetal [PGE2]. However, during prolonged reduced uterine blood flow (RUBF) when [PGE2] in fetal plasma is already elevated, FBM are not inhibited by ethanol. These experiments were designed, therefore, to test the hypothesis that the FBM response to PGE2 is also diminished during RUBF. PGE2 (594+/-19 ng.min(-1).kg(-1) fetal body weight) was infused for 6 h into the jugular vein of RUBF (PO2 = 14+/-1 mmHg (1 mmHg = 133.3 Pa); n = 7) and control (PO2 = 22+/-1 mmHg (p < 0.01); n = 7) ovine fetuses, and the effect on FBM, electrocortical (ECoG), and electroocular activities was determined. The infusion of PGE2 increased plasma [PGE2] from 881+/-162 to 1189+/-114 pg.mL(-1) in RUBF fetuses and from 334+/-72 to 616+/-118 pg.mL(-1) (p < 0.05) in control fetuses. FBM were initially inhibited by PGE2 from 22.5+/-9.4 and 17.9+/-6.5% of the time to 6.9+/-2.4 and 0.5+/-0.4% (p < 0.01) in RUBF and control fetuses, respectively. FBM remained inhibited in control fetuses throughout the infusion but returned to baseline incidence in RUBF fetuses in the last 2 h of the infusion. These results are consistent with the hypothesis that one component of the adaptative mechanisms of the fetus to prolonged RUBF is an altered response of FBM to exogenous PGE2. We speculate that the lack of a sustained inhibition in FBM during RUBF with infusion of PGE2 may be a result of an alteration in brainstem receptor function or number or local PGE2 removal.

Placental transfer and maternal and fetal hemodynamic effects of ketanserin in the pregnant ewe

Objectives: To determine placental transfer of ketanserin and to assess the effect of serotonin-2 receptor blockade by ketanserin on serotonin- and phenylephrine-induced vasoconstriction. Study design: Five chronically instrumented pregnant ewes at 120 days gestation were injected with 20 mg ketanserin i.v., and fetal and maternal arterial samples were obtained at predetermined intervals to assess placental transfer. Maternal and fetal responses of blood flows and pressures were determined after injection of serotonin (20 μg/kg) or phenylephrine (10 μg/kg) before and after ketanserin (0.75 mg/kg). Results: In the ewe, ketanserin is transferred across the placenta and reaches measurable levels in the fetal lamb. Ketanserin blocks the maternal and fetal serotonin-induced rise in arterial pressure, but not the serotonin-induced reduction in uterine blood flow. Conclusion: In the pregnant ewe, the serotonin-induced rise in maternal and fetal blood pressure is effectively antagonized by ketanserin, whereas the serotonin-induced reduction in uterine blood flow is not.

The maternal and fetal physiologic effects of nicotine

The effects of nicotine are seen in every trimester of pregnancy, from increased spontaneous abortions in the first trimester, to increased premature delivery rates and decreased birth weights in the final trimester. The birth weight of a baby is dependent on two factors: the gestational age of the fetus at the time of delivery and the rate of fetal growth. Nicotine has been shown to affect both of these factors. Carbon monoxide, also found in tobacco, forms carboxyhemoglobin, which inhibits the release of oxygen into fetal tissues. Nicotine readily gains access to the fetal compartment via the placenta, with fetal concentrations generally 15% higher than maternal levels. The primary metabolite of nicotine, cotinine, has a half-life of 15 to 20 hours and serum concentrations that are 10-fold higher than nicotine; thus, cotinine provides a better index of nicotine exposure because of its longer half-life. Nicotine concentrates in fetal blood, amniotic fluid, and breastmilk. The fetus and neonate may also have environmental tobacco exposure that may be significant. In animal models and humans, nicotine increases maternal blood pressure and heart rate, with a concomitant reduction in uterine blood flow. An increase in fetal heart rate is also seen, which is thought to be caused by catecholamine release. The impact of nicotine on the respiratory and central nervous system is also reviewed. In conclusion, the physiological effect of tobacco on fetal growth seems to be a culmination of both the vasoconstrictive effects of nicotine on the uterine and potentially the umbilical artery and the effects on oxygenation by carboxyhemoglobin.

Prostaglandin E2 inhibits fetal breathing movements during prolonged reductions in uterine blood flow in sheep

Prostaglandin E2 inhibits fetal breathing movements during prolonged reductions in uterine blood flow in sheep

Pregnancy outcome: Physical activities inside versus outside the workplace

There is concern that the thermal, cardiovascular, metabolic, and biophysical changes which accompany physical activity may have detrimental effects on both mother and fetus. Research focused on physical activity in the workplace has identified four specific physical stresses (quiet standing, long hours, protracted ambulation, and heavy lifting) that are associated with an increased incidence of both prematurity and low birth weight. The physiological basis for these is believed to be that these activities cause intermittent but protracted reductions in uterine blood flow. Research focused on recreational physical activity during pregnancy has not identified similar associations. Indeed, these data indicate that the overall impact of regular recreational exercise on pregnancy outcome is positive for both mother and fetus. The physiological basis for these beneficial effects is believed to be that the interaction between the physiological adaptations to both exercise and pregnancy improve maternal cardiovascular reserve, maternal mechanisms for heat dissipation, and placental growth and functional capacity. Finally, there is preliminary evidence suggesting that the vibratory and auditory stimuli associated with regular recreational exercise may enhance functional maturation of the fetal brain.