Epidural analgesia during birth and adverse neonatal outcomes: A population-based cohort study.

BACKGROUND: In general, epidural analgesia is considered a safe and efficient way to relieve pain during active labour and is increasingly used in childbirth. It is well documented that epidural analgesia during birth has benefits but also adverse effects. However, evidence is limited on how epidural analgesia influences neonatal outcome in a low-risk population of birthing women. AIM: To examine low Apgar score, foetal hypoxia and admission to the neonatal intensive care unit in neonates of low-risk women receiving epidural analgesia during birth. METHODS: A cohort study using registry data to investigate a population of 23,272 low-risk women giving birth at a university hospital. RESULTS: Epidural analgesia was used in 21.6% of low-risk women during birth. Low Apgar score, foetal hypoxia, and admission to the neonatal intensive care unit were found in 0.6%, 0.6%, and 10.0%, respectively in neonates of mothers receiving epidural analgesia during birth compared to 0.3%, 0.6%, and 5.6%, respectively in the non-exposed group. Epidural analgesia was associated with low Apgar score, adjusted odds ratio 1.76 (95% CI 1.07-2.90) and admission to the neonatal intensive care unit, adjusted odds ratio 1.43 (95% CI 1.26-1.62). A mediation analysis indicates the impact of epidural analgesia on adverse neonatal outcomes was mediated by obstetric complications like maternal fever, labour augmentation, and foetal malpresentation. CONCLUSION: This study found use of epidural analgesia during birth in low-risk pregnant women was associated with infant low Apgar score and admission to the neonatal intensive care unit.

[Neurotoxic effect of toluene on background of prenatal hypoxic brain damage to white rats].

Comparative study covered influence of toluene on behavioral parameters, cognitive abilities and brain bioelectric activity in white rats with normal embryonic development or with prenatal hypoxia. Prenatal hypoxia was simulated by subcutaneous injection of 50 mg/kg sodium nitrite into female white rats on day 13-14 of gestation. The offspring at the age of 2, 5-3 months was exposed to toluene (concentration of 560 mg/m3, 4 hours per day, 5 days per week, over 4 weeks). After the exposure, the animals were estimated for individual and intraspecific behaviour in "open fields and "resident-intruder" tests, for cognitive abilities in "radial maze" training, EEG with visual and auditory evoked potentials. Acute hypoxia at early stages of organogenesis appeared to be burdening factor and to influence consequences of toluene intoxication.

[A 25-year study (1983-2008) of children's health outcomes after hyperbaric oxygen therapy for carbon monoxide poisoning in utero]. / Devenir des enfants intoxiqués au monoxyde de carbone en période foetale et traités par oxygéno- thérapie hyperbare--etude d'une cohorte constituée sur 25 ans de 1983 a 2008.

Carbon monoxide (CO) poisoning during pregnancy can be fatal for the fetus, or cause bone malformations or encephalopathy, depending on the stage of pregnancy at which the poisoning occurs. Fewer cases of death and encephalopathy have been reported since the adoption of maternal hyperbaric oxygen (HBO) therapy in this setting, but these children's long-term psychomotor development and growth remains to be documented. A prospective single-center cohort study spanning 25 years (1983 - 2008) included all pregnant women living in the Nord-Pas-de-Calais region of France who received HBO for CO poisoning and who gave birth to a living child. A descriptive analysis of the women and children was performed first. A control group of children was created by matching with anonymous files from local authorities. The results of the children's compulsory health & development assessments were used to compare the two groups. 406 women were included in the study, of whom 6 were expecting twins. The psychomotor development of 412 children was monitored, up to the day 8 assessments in 388 cases, the year 2 assessments in 276 cases, and the year 6 assessments in 232 cases. Sixty children have not yet reached the age of 6 years. No significant differences in psychomotor or height/weight criteria (p > 0.05 for both) were found between the exposed and unexposed children. No malformations were reported. These findings support the use of HBO therapy for all expectant mothers exposed to CO poisoning. No specific follow-up of the children is necessary if their neonatal status is normal.

Anaesthetic considerations for non-obstetric surgery during pregnancy.

Surgery during pregnancy is complicated by the need to balance the requirements of two patients. Under usual circumstances, surgery is only conducted during pregnancy when it is absolutely necessary for the wellbeing of the mother, fetus, or both. Even so, the outcome is generally favourable for both the mother and the fetus. All general anaesthetic drugs cross the placenta and there is no optimal general anaesthetic technique. Neither is there convincing evidence that any particular anaesthetic drug is toxic in humans. There is weak evidence that nitrous oxide should be avoided in early pregnancy due to a potential association with pregnancy loss with high exposure. There is evidence in animal models that many general anaesthetic techniques cause inappropriate neuronal apoptosis and behavioural deficits in later life. It is not known whether these considerations affect the human fetus but studies are underway. Given the general considerations of avoiding fetal exposure to unnecessary medication and potential protection of the maternal airway, regional anaesthesia is usually preferred in pregnancy when it is practical for the medical and surgical condition. When surgery is indicated during pregnancy maintenance of maternal oxygenation, perfusion and homeostasis with the least extensive anaesthetic that is practical will assure the best outcome for the fetus.

Third trimester fetal heart rate and Doppler middle cerebral artery blood flow velocity characteristics during prenatal selective serotonin reuptake inhibitor exposure.

Prenatal selective serotonin reuptake inhibitor (SSRI) exposure increases the risk for adverse neonatal behavioral outcomes; although it is unknown whether altered brain function is present before birth. We investigated fetal vascular and heart rate changes at 36-wk gestation in SSRI-treated women with mood disorders (n = 29) [exposed (EXP)] and controls (n = 45) [non-EXP (NEXP)]. Fetal middle cerebral artery (MCA) flow parameters and heart rate characteristics were obtained during pre-SSRI dose morning and postdose afternoon sessions. Maternal mood and cord Hb and hematocrit were measured. Basal fetal heart rate (fHR) did not differ between groups or across the day. The fHR short- and long-term variations, accelerations, and duration of high variability episodes remained lower and did not change across the day in EXP, whereas all increased significantly in NEXP. In both groups, MCA flow velocity and volume flow increased significantly across the day. EXP MCA pulsatility index was significantly lower, as was MCA cross-sectional area. EXP cord Hb and hematocrit were significantly increased. Prenatal SSRI exposure reduced fetal MCA flow resistance and fHR variability, before and after an SSRI dose, controlling for maternal mood. These changes and the SSRI-related increased red cell indices suggest possible fetal hypoxia.

Carbohydrate and energy metabolism in the brain of rats with thromboxane A2-induced fetal growth restriction.

Fetal growth restriction (FGR) remains a cause of perinatal brain injury, sometimes leading to neurological and intellectual impairment. Although the mechanisms and pathophysiology of CNS injuries have not been elucidated completely, it is possible carbohydrate and energy metabolism may have an important role in the FGR brain. In this study, FGR was induced in rats by administration of synthetic thromboxane A2 (STA2). Pups were delivered by cesarean section. After killing, samples were obtained from the fetuses of both control and FGR rats for evaluation of carbohydrate and energy metabolism in brain tissue. Lactate and pyruvate levels in brain were reduced significantly in the FGR group. Glucose content in brain tissue tended to be increased in the FGR group. In contrast, glycogen content in brain tissue tended to be lower in the FGR group. However, these differences in glucose and glycogen content did not reach statistical significance. Brain high-energy reserves, including ATP, ADP, AMP, and phosphocreatine (P-Cr), were similar in the control and FGR groups. Gluconeogenesis compensated for chronic fetal hypoxia and decreased glycogen storage. Energy metabolism in the FGR brain is likely to be disrupted as a consequence of lower reserves of energy substrates.

Erythropoietin protects the developing retina in an ovine model of endotoxin-induced retinal injury.

PURPOSE: Intrauterine infection is a common antecedent of preterm birth. Infants born very preterm are at increased risk for neurologic dysfunction, including visual deficits. With increasing survival of very preterm infants, there is a need for therapies that prevent adverse neurologic outcomes. Using an ovine model, the authors investigated the neuroprotective potential of recombinant human erythropoietin (rhEPO) on retinal injury induced by intrauterine inflammation. METHODS: At 107 ± 1 days of gestational age (DGA), chronically catheterized fetal sheep received either of the following on 3 consecutive days: intravenous (IV) bolus dose of lipopolysaccharide (LPS; ∼0.9 µg/kg; n = 8); IV bolus dose of LPS, followed at 1 hour by 5000 IU/kg rhEPO (LPS + rhEPO; n = 8); rhEPO alone (n = 5). Untreated fetuses (n = 8) were used for comparison with the three treatment groups. Fetal physiological parameters were monitored. At 116 ± 1 DGA, fetal retinas were assessed quantitatively for morphologic and neurochemical alterations. RESULTS: Exposure to LPS alone, but not to rhEPO alone, resulted in fetal hypoxemia and hypotension (P < 0.05). Exposure to LPS alone caused retinal changes, including reductions in thickness of the inner nuclear layer (INL), somal areas of INL neurons, process growth in the plexiform layers, and numbers of ganglion and tyrosine hydroxylase immunoreactive (TH-IR) dopaminergic amacrine cells. Treatment of LPS-exposed fetuses with rhEPO did not alter the physiological effects of LPS but significantly reduced alterations in retinal layers and ganglion and TH-IR cell numbers. CONCLUSIONS: rhEPO treatment was beneficial in protecting the developing retina after LPS-induced inflammation. Retinal protection could occur by the antiapoptotic or anti-inflammatory actions of EPO.

Erythropoietin is neuroprotective in a preterm ovine model of endotoxin-induced brain injury.

Intrauterine infection and inflammation have been linked to preterm birth and brain damage. We hypothesized that recombinant human erythropoietin (rhEPO) would ameliorate brain damage in anovine model of fetal inflammation. At 107 +/- 1 day of gestational age (DGA), chronically catheterized fetal sheep received on 3 consecutive days 1) an intravenous bolus dose of lipopolysaccharide ([LPS] approximately 0.9 microg/kg; n = 8); 2) an intravenous bolus dose of LPS, followed at 1 hour by 5,000 IU/kg of rhEPO (LPS + rhEPO, n = 8); or 3) rhEPO (n = 5). Untreated fetuses (n = 8) served as controls. Fetal physiological parameters were monitored, and fetal brains and optic nerves were histologically examined at 116 +/- 1 DGA. Exposure to LPS, but not to rhEPO alone or saline, resulted in fetal hypoxemia, hypotension (p < 0.05), brain damage, including white matter injury, and reductions in numbers of myelinating oligodendrocytes in the corticospinal tract and myelinated axons in the optic nerve (p < 0.05 for both). Treatment of LPS-exposed fetuses with rhEPO did not alter the physiological effects of LPS but reduced brain injury and was beneficial to myelination in the corticospinal tract and the optic nerve. This is the first study in a long-gestation species to demonstrate the neuroprotective potential of rhEPO in reducing fetal brain and optic nerve injury after LPS exposure.

Low doses of nicotine-induced fetal cardiovascular responses, hypoxia, and brain cellular activation in ovine fetuses.

Prenatal exposure to nicotine is associated with a variety of adverse outcomes. The present study investigated the effect of low doses of nicotine during pregnancy on fetal blood gases, cardiovascular system, and cellular activation in the brain. Intravenous administration of nicotine 10 or 25 microg/kg into ewe did not affect maternal blood gases, blood pressure, and heart rate. Maternal administration of nicotine also had no effect on fetal blood electrolyte concentrations, osmolality levels, and lactic acid levels. However, it significantly reduced fetal blood pO2 levels and oxygen saturation, increased fetal arterial blood pressure and decreased heart rate in utero. In addition, exposure to low doses of nicotine increased the expression of Fos in the paraventricular nucleus (PVN) and subfornic organ (SFO) in the fetal brain. The data demonstrated that even low doses of nicotine could impact significantly on fetal cardiovascular and central nervous systems, as well as oxygen status, and suggested a toxic risk to fetuses of exposure to low levels nicotine or second-hand smoking during pregnancy.

Intramuscular fetal corticosteroid therapy: short-term effects on the fetus.

OBJECTIVE: The aim of the study was to assess the short-term effects of direct intramuscular (i.m.) corticosteroid therapy on fetal biophysical profile, baseline fetal heart rate and the nonstress test, which indicate the degree of fetal hypoxia. METHOD: We evaluated the effect of direct i.m. fetal single-dose dexamethasone (4 mg/kg) on the fetal biophysical profile 2 h before and 2-4 h after corticosteroid therapy in 41 fetuses in the 32nd week of gestation at risk of preterm delivery. Risk factors for preterm delivery included pregnancy-induced hypertension and preeclampsia. RESULT: There was a statistically significant difference between fetal breathing movements before and after corticosteroid therapy (p = 0.019; 95% confidence interval for difference -11.75, -1.12). No significant changes were observed between baseline fetal heart rate before and after corticosteroid therapy (p = 0.99; 95% confidence interval for difference -4.81, +4.81), biophysical profile before and after fetal corticosteroid therapy, p = 0.235 as well as the nonstress test before and after therapy (p = 0.564). CONCLUSION: Direct corticosteroid i.m. fetal therapy results in increasing profound short-term fetal breathing movements. There are no changes in baseline fetal heart rate, biophysical profile score, and nonstress test.

Prenatal buprenorphine exposure: effects on biochemical markers of hypoxia and early neonatal outcome.

OBJECTIVE: To evaluate the possible association between prenatal buprenorphine exposure and compromised early neonatal outcome in view of markers of perinatal hypoxia. DESIGN, SETTING AND SAMPLE: The study group consisted of 27 full-term neonates exposed to buprenorphine prenatally and prospectively followed up at a special tertiary outpatient clinic for pregnant drug abusers. Serving as controls were 27 full-term neonates exposed prenatally to illicit substances other than opioids and 38 full-term neonates from uncomplicated pregnancies of healthy parturients. METHODS AND MAIN OUTCOME MEASURES: Apgar scores, cord pH and base excess were recorded. Cord serum samples were collected at birth for analysis of biochemical markers of fetal hypoxic stress: erythropoietin (EPO; chronic hypoxia), cardiac troponin T (cardiac involvement) and S100 (neural damage). RESULTS: All infants were born in good condition according to Apgar scores and pH of cord blood. No statistically significant differences were found between the three groups in cord serum concentrations of EPO (33.0 median, range: 9.0-476.0 U/L in the buprenorphine-exposed group vs 27.0, range: 8.0-114.0 U/L in substance-abusing controls vs 28.1, range: 11.6-260.0 U/L in healthy controls) or S100 (0.47, range: 0.25-0.91 microg/L vs 0.40, range: 0.12-1.22 microg/L vs 0.47, range: 0.20-2.15 microg/L). No significant differences existed in cardiac TnT levels (0.017, range: 0.010-0.072 U/L vs 0.010, range: 0.010-0.075 U/L vs 0.024, range: 0.010-0.075 U/L). CONCLUSIONS: While no significant differences in asphyxia markers were observed between the three groups, a tendency towards higher levels of EPO emerged in the buprenorphine-exposed group.

Stress hormone responses during 24-hour hypoxemia in preterm goat fetus.

Fetal endocrinological responses to chronic hypoxemia are useful in elucidating the process of growth restriction at earlier stages of fetal development. The purpose of this study was to observe endocrinological responses to prolonged (24-h) non-acidemic hypoxemia in preterm goat fetuses. Fetal hormonal changes were examined in chronically instrumented goat fetuses at gestational day 96-102 (0.7 gestation) during continuous nitrogen infusion into the maternal trachea to create prolonged fetal hypoxemia. Plasma levels of arginine vasopressin (AVP), epinephrine, norepinephrine, adrenocorticotropic hormone (ACTH) and cortisol were measured, along with fetal heart rate (FHR) and fetal blood pressure (FBP). Fetal arterial pO(2) declined significantly from 25.0 +/- 1.0 mmHg at baseline to 15.3 +/- 1.0 mmHg after 2 h of hypoxemia, then remained at this level. FHR increased significantly throughout the experiment, but FBP remained unchanged. AVP and ACTH levels rose significantly after 2 h of hypoxemia, and declined to the control values after 12 h. There was no significant increase in the epinephrine level during 24-hr hypoxemia. In contrast, norepinephrine significantly increased after 2 h of hypoxemia and remained at the elevated levels throughout the remainder of the experiment. Thus, preterm fetuses could respond to acute hypoxic stress by increasing the plasma levels of AVP, norepinephrine and ACTH. However, despite the rapid increase in ACTH, the level of cortisol in the fetal plasma was significantly elevated only after 18 h of hypoxemia. The chemoreceptors of preterm fetuses, which regulate the release of cortisol or epinephrine, may be less sensitive to hypoxic insults.

The effect of prenatal nicotine on mRNA of central cholinergic markers and hematological parameters in rat fetuses.

A number of studies have demonstrated the influence of nicotine on fetal development. This study determined the expression of choline acetyltransferase (ChAT), vesicular acetylcholine transporter (VAChT), and high-affinity choline transporter (CHT1) in the forebrain and hindbrain following chronic prenatal nicotine exposure in the rat fetus (maternal rats were subcutaneously injected with nicotine at different gestation periods). We also measured the effect of chronic nicotine exposure on fetal blood pO(2), pCO(2), pH, Na(+) and K(+) concentrations, as well as lactic acid levels. Maternal nicotine exposure during pregnancy was associated with a decrease in fetal pO(2) coupled with a significant increase in pCO(2) and lactic acid as well as restricted fetal growth. Additionally, maternal nicotine administration also reduced ChAT, VAChT, and CHT1 mRNA levels in the fetal brain. Nicotine-induced fetal hypoxic responses and reduced cholinergic marker expression in the brain were more severe when nicotine was started in early gestation. Our results provide new information about the effects of repeated exposure to nicotine in utero on the expression of central ChAT, VAChT, and CHT1 in the rat fetus. These results indicate that repeated hypoxic episodes or/and a direct effect of nicotine on the central cholinergic system during pregnancy may contribute to brain developmental problems in fetal origin.

Prenatal exposure to nicotine with associated in utero hypoxia decreased fetal brain muscarinic mRNA in the rat.

Prenatal exposure to nicotine can be associated with fetal abnormal development and brain damage. This study determined the effect of administration of nicotine with associated in utero hypoxia in maternal rats from early, middle, and late gestation on fetal blood hemoglobin, and expression of cholinergic receptor subtypes in the fetal brain. Our results demonstrated that maternal subcutaneous nicotine from the early gestation increased fetal hemoglobin and hematocrit, associated with reduction of PO(2). Although exposure to nicotine during late gestation had no effects on fetal brain weight, nicotine administration from the early gestation significantly decreased fetal brain muscarinic receptor (M1, M2, M3, and M4) mRNA expression, associated with restricted brain growth. Nicotine-altered muscarinic receptor subtype expression in the fetal forebrain and hindbrain showed regional differences. In addition, there were gestational differences for fetal brain muscarinic suppression by prenatal nicotine. Together, the results demonstrate that nicotine-induced in utero hypoxia is associated with poor development of muscarinic receptors in the fetal brain and restricted brain growth, and that either prolonged prenatal exposure to nicotine or critical "window" period for the brain development during pregnancy may play a role in prenatal nicotine-induced fetal muscarinic-receptor deficiency in the fetal brain.

Cloprostenol, a prostaglandin F(2alpha) analog, induces hypoxia in rat placenta: BOLD contrast MRI.

Blood oxygen level dependent (BOLD) contrast was used to monitor hypoxia induced by cloprostenol, a prostaglandin F(2alpha) (PGF(2alpha)) analog, in the rat embryo-placental unit (EPU). It is shown that administration of cloprostenol (0.025 mg/rat) at mid-gestation (day 16) reduced EPU oxygenation, as detected by BOLD contrast MRI, in correlation with induction of vascular endothelial growth factor (VEGF) gene (Vegfa) expression in the corresponding placenta (r = 0.56, p = 0.03). Elevated VEGF mRNA expression in response to cloprostenol treatment was also observed at early gestation (day 9) in the forming placenta (p = 0.04) and uterus (p = 0.03). Cloprostenol increased the expression levels of endothelin-1 (ET-1) gene (Edn1) (p = 0.03) and its corresponding peptide (p = 0.02) in the forming placenta, as well as the expression of the endothelin receptor type A (ETA) gene (Ednra) in both the forming placenta (p = 0.009) and the uterus (p = 0.01). The levels of the endothelin receptor type B (ETB) gene (Ednrb) were not affected in response to cloprostenol, but a significant elevation in the expression level of this receptor was observed in the uterus at mid- and late gestation (day 22) (p = 0.04 and 0.01 respectively), suggesting a role for ETB in the vasodilatory status of the pregnant uterus. It is suggested that PGF(2alpha) induces uteroplacental vasoconstriction in the rat, and that ET-1 may take part in mediating this effect, probably via activation of ETA receptor. The uteroplacental vasoconstriction induces hypoxia, as manifested by significant changes in BOLD MRI and by upregulation of VEGF.

Vitamin E supplementation in phenytoin induced developmental toxicity in rats: postnatal study.

OBJECTIVES: The aim of this study was to test the effect of supranutritional dosage of the natural antioxidant vitamin E (VitE) on phenytoin (PHT) induced developmental toxicity and possible long-term effects in rat offspring. METHODS: PHT (150 mg/kg) was administered by oral gavage daily from day 7 to 18 of gestation and VitE prior to PHT orally on the same days. RESULTS: PHT administration alone resulted in decreased survival rate and lower body weight of pups on day 21 post partum (PP). Moreover, PHT slightly changed somatic growth and pups failed to present dynamic air righting on days 15-20 PP. VitE supplementation did not alleviate these changes but rather induced persisting body weight reduction on the days 21 PP and 100 PP. We observed also decreased brain wet weight in the PHT and VitE + PHT groups compared to controls. CONCLUSIONS: We concluded that prenatal supplementation with 500 mg/kg of VitE did not ameliorate the developmental toxicity of PHT and failed to protect postnatal development of rat offspring. Further, in the group supplemented with VitE, the occurrence of persistent body weight gain depression up to adulthood indicates its possible interference with somatic growth regulation.

The relationship between cleft lip, maxillary hypoplasia, hypoxia and phenytoin.

Cleft lip (CL) is a common malformation that has both genetic and exogenous causes. The main pharmaceutical cause is exposure to phenytoin during early facial development in the 5th to 6th weeks of gestation. Phenytoin also causes CL if administered to pregnant rats during the period of early facial development. Evidence is presented that in the pregnant rat, a teratogenic dose of phenytoin slows the early embryonic heart and causes a prolonged period of embryonic hypoxia. It is proposed that this hypoxia, through an undefined downstream mechanism, leads to the development of CL. The involvement of hypoxia in the pathogenesis of CL is in agreement with studies in mouse strains with a spontaneous rate of CL in which exposure to hypoxia has been shown to increase the rate and hyperoxia to decrease the rate. Other exogenous risk factors during pregnancy for human CL include maternal cigarette smoking, residence at high altitude and exposure to corticosteroids. It is suggested that these exposures all involve an increased risk of embryonic hypoxia. It has been proposed that phenytoin affects the embryonic heart by inhibition of the human-ether-a-go-go (HERG) potassium channel. Phenytoin also inhibits sodium and calcium channels and these properties may also be involved in the observed effect on the embryonic heart. Phenytoin-induced bradycardia leading to embryonic hypoxia may be an important mechanism by which phenytoin causes birth defects.

Comparative routes of oxytocin administration in crated farrowing sows and its effects on fetal and postnatal asphyxia.

Oxytocin is used to induce and control parturition; nevertheless, an increase in uterine contractions decreases blood flow and gaseous exchange through the uterus predisposing to intra-partum mortality in pigs. The objective of the present study was to evaluate the effect of different oxytocin administration routes on myometrial activity, fetal intrauterine hypoxia and postnatal asphyxia in crated farrowing sows. Yorkshire x Landrace hybrid sows (n = 300), that were approaching the time of parturition, were randomly assigned into six groups. Each group included 50 sows, 10 for each of the parities from one to five. A 40-IU oxytocin dosage was administered by intramuscular (IM), or intravulvar (IVU) routes, or 20 IU was administered via intravenous (IV) route. Groups 1 (G1), 3 (G3) and 5 (G5) were administered 0.9% saline solution (NaCl) IM, IVU and IV, respectively, whereas groups 2 (G2), 4 (G4) and 6 (G6) were treated with oxytocin IM, IVU and IV, respectively. There was a significantly (P < 0.05) greater number of intra-partum stillbirths (IPS) for the oxytocin treatments, as compared with the control groups, especially with the IVU and IV routes; a lesser number of IPS and lesser IPS with broken umbilical cords was observed with the IM administration route. Oxytocin and control IV administration resulted in longer farrowing durations. Administration of IV-oxytocin resulted in a greater number (P < 0.05) of intrauterine distressed neonates compared with its corresponding control and interpreted through dips II, a fetal cardiac frequency deceleration which determines acute fetal suffering. Independent of the route of oxytocin administration, the treatments resulted in twice as many dips II compared with the respective control groups. The use of the cardiotocograph proved to be an excellent tool for establishing the oxytocin response dose in farrowing sows. A greater number of piglets born alive, which had undergone bradycardia, also showed severe acidosis and greater meconium staining in oxytocin-treated sows, indicating that the administration time (at birth of the first piglet) as well as the dosage used were not adequate treatment regimens in the present study. Further studies will be conducted to evaluate different dosages and oxytocin administration timing to determine the most desirable treatment regimen to increase myometrial contractibility without compromising fetal welfare and neonatal survival.

Uterine and fetal asphyxia monitoring in parturient sows treated with oxytocin.

Oxytocin is used to induce and control parturition, nevertheless, the increase of uterine contractions decreases blood flow and gaseous exchange through the womb predisposing to intra-partum mortality. The objective of the present study was to evaluate the effect of oxytocin on myometrial activity, fetal intrauterine hypoxia and postnatal asphyxia in sows during farrowing. Hybrid (n = 120) sows approaching the time of farrowing were randomly assigned in two groups of 60 animals each. Group I (G(1): control) was treated IM with saline solution and Group II (G(2)) was injected IM with oxytocin (1IU/6kg LW) as a single dose at birth of the first piglet. Both average number of myometrial contractions and intensity in G(2) were greater (P < 0.01) as compared with G(1). The mean of intra-partum stillbirths (IPS's) and those where fetal cardiac frequency (FCF) or heart beats, could not be detected after birth, were greater (P < 0.01) in G(2) as compared with G(1). The average decelerations of FCF known as dips II, which indicate severe hypoxia, was greater in G(2) (P < 0.01) as compared with that of G(1). There was a greater (P < 0.01) number of intra-partum stillbirths, stained with severe meconium in G(2) when compared with G(1). Oxytocin treatment increased (P < 0.01) the number of pigs born alive with ruptured umbilical cords and those with different grades of meconium staining on their skin. It was concluded that administration of oxytocin at the onset of parturition increased the myometrial activity, decreased fetal cardiac frequency, predisposed the rupture of umbilical cords and the degree of meconium staining, and increased intra-partum mortality.

Maternal insufflation during the second trimester equivalent produces hypercapnia, acidosis, and prolonged hypoxia in fetal sheep.

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.