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Biomedical subjects

D Rurak

Publications and source records attributed to D Rurak.

11 recordsLinked to original sources
PubMed2004

Do commonly used oral antihypertensives alter fetal or neonatal heart rate characteristics? A systematic review.

OBJECTIVE: To examine fetal (FHR) and neonatal heart rate patterns following use of common oral antihypertensives in pregnancy. METHODS: A systematic review of randomized controlled trials (RCTs), observational studies (N >/= 6 women), and animal studies. Data were abstracted (two reviewers) to determine relative risk (RR) (or risk difference (RD) for low event rates) and 95% CI. RESULTS: Eighteen RCTs (1858 women), one controlled observational study (N = 22), and seven case series (N = 117) were reviewed. Most hypertension was pregnancy-induced (N = 14 studies). The FHR was assessed by cardiotocogram (CTG) (N = 17 studies (visual interpretation); 1 study (computerized CTG), or umbilical artery velocimetry (N = 4). Four studies examined neonatal heart rate. In placebo-controlled RCTs (N = 192 women), adverse FHR effects did not differ between groups [9/101 (drugs) vs. 7/91 (placebo); RD 0.02, 95% CI (- 0.06, 0.11); chi2 = 1.02]. In six drug vs. drug RCTs (295 women), adverse FHR effects did not differ between groups [29/144 (methyldopa) vs. 42/151 (other drugs); RR 0.72, 95% CI (0.49, 1.07); chi2 = 0.69]. In one labetalol vs. placebo trial, neonatal bradycardia did not differ between groups [4/70 (labetalol) vs. 4/74 (placebo); OR 1.06, 95% CI (0.26, 4.39)], while in three drug vs. drug RCTs, neonatal bradycardia was not observed (0/24 vs. 0/26). CONCLUSIONS: Available data are inadequate to conclude whether oral methyldopa, labetalol, nifedipine, or hydralazine adversely affect fetal or neonatal heart rate and pattern. Until definitive data are available, FHR changes cannot be reliably attributed to drug effect, but may be due to progression of the underlying maternal or placental disease.

Administration, Oral↗
PubMed2001

Fetal behavioural state changes following maternal fluoxetine infusion in sheep.

Clinical depression is diagnosed in 5-15% of women during pregnancy, increasing the risk of negative outcomes. Fluoxetine (FX), a selective serotonin reuptake inhibitor, is prescribed during pregnancy. In adults, FX alters sleep patterns with single doses decreasing total sleep time and rapid eye movement sleep. The effects of FX on sleep in the fetus are unknown. However, 5-hydroxytryptophan, the precursor of serotonin, has been reported to prolong high-voltage (HV) electrocortical (ECoG) activity and increase the incidence of fetal breathing movements (FBM) in the sheep fetus. We hypothesize that FX exposure will decrease the incidence of LV ECoG in the fetus. Twenty-one pregnant sheep were surgically prepared for chronic study of blood gases, ECoG activity, eye movements and FBM. After 3 days of recovery, ewes received a 70-mg bolus i.v. infusion of FX or sterile water followed by continuous infusion at a rate of 0.036 mg/min for 8 days. The incidence of low-voltage (LV) ECoG decreased from 54+/-4% on the preinfusion day to 45+/-5% on infusion day 1 in the FX group and remained decreased throughout the infusion period. In addition, the incidence of both eye movements and FBM was decreased on infusion day 1 compared to preinfusion day in the FX group. HV ECoG increased from 39+/-3% on preinfusion day to 68+/-14% on FX infusion day 1 and remained elevated throughout the infusion period. These data show that maternal FX administration alters fetal behavioural state.

Animals↗
PubMed2000

Altered fetal pituitary-adrenal function in the ovine fetus treated with RU486 and meloxicam, an inhibitor of prostaglandin synthase-II.

Term and preterm labor are associated with increased fetal hypothalamic-pituitary-adrenal (HPA) activation and synthesis of prostaglandins (PGs) generated through the increased expression of prostaglandin H synthase-II (PGHS-II) in the placenta. Inhibition of PGHS-II has been advocated as a means of producing uterine tocolysis, but the effects of such treatment on fetal endocrine functions have not been thoroughly examined. Because PGE(2) is known to activate the fetal HPA axis, we hypothesized that administration of meloxicam, a PGHS-II inhibitor, to sheep in induced labor would suppress fetal HPA function. Chronically catheterized pregnant ewes were treated with RU486, a progesterone receptor antagonist, to produce active labor, and then treated with either high-maintenance-dose meloxicam, graded-maintenance-dose meloxicam, or a saline infusion. Maternal uterine contraction frequency increased 24 h after the RU486 injection and the animals were in active labor by 48 +/- 4 h. RU486 injection led to increased concentrations of PGE(2), ACTH, and cortisol in the fetal circulation, and increased concentrations of 13,14 dihydro 15-ketoprostaglandin F(2 alpha) (PGFM) in the maternal circulation. Uterine activity was inhibited within 12 h of beginning meloxicam infusion at both infusion regimes. During meloxicam infusion there were significant decreases in fetal plasma PGE(2), ACTH, and cortisol concentrations, and PGFM concentrations in maternal plasma. In control animals, frequency of uterine contractions, maternal plasma PGFM, fetal plasma PGE(2), ACTH, and cortisol concentrations increased after RU486 administration, and continued to rise during saline infusion until delivery occurred. We conclude that RU486-provoked labor in sheep is associated with activation of fetal HPA function, and that this is attenuated during meloxicam treatment to a level considered compatible with pregnancy maintenance.

6-Ketoprostaglandin F1 alpha↗
PubMed1999

Preoperative dextrose does not affect spinal-induced hypotension in elective Cesarean section.

PURPOSE: To determine if preoperative intravenous dextrose affects the incidence and ease of treatment of spinal-induced hypotension in parturients having elective Cesarean section under spinal anesthesia. METHODS: In this prospective, double-blind study, following informed consent, 119 ASA I, II parturients for elective Cesarean section were randomized to receive intravenously either dextrose 5% in normal saline (Group D) or normal saline (Group NS) at 125 ml x hr(-1) for two hours prior to delivery. Following a bolus of 15 ml x kg(-1) normal saline iv, spinal anesthesia was induced with hyperbaric bupivacaine 0.75%, fentanyl and morphine. Hypotension (systolic blood pressure <100 mm Hg or >20% decrease) was treated with fluids and/or vasopressor. DATA COLLECTED: demographics, blood glucose concentrations (fasting, time of spinal, delivery), blood pressure (baseline, one minute intervals from spinal to delivery), neonatal Apgar scores, umbilical blood gas analyses, glucose and lactate concentrations. RESULTS: There was no difference between the two groups in the rate of hypotension (P = 0.272). All parturients who experienced hypotension received fluids, and there was also no difference between the groups in vasopressor requirement [mean dose of ephedrine: Group D = 21.6 mg (95% CI 15.1-28.2), Group NS = 16 mg (95% CI 12.0-20.5)]. CONCLUSION: The routine administration of dextrose 5% at a rate of 5.22 g x hr(-1) preoperatively does not affect the hypotension rate, or make it easier to treat.

Adult↗
PubMed1996

Tissue blood flow distribution and the effect of chronic vascular catheterization in the hind limb of the fetal lamb.

In six chronically instrumented fetal lambs, hind-limb skin, bone, and muscle comprised 22.5 +/- 1.3, 35.3 +/- 1.6, and 42.3 +/- 1.1% of total limb weight, respectively. As estimated using radionuclide-labeled microspheres, blood flow to these tissues averaged 30.4 +/- 4.9, 30.1 +/- 3.3, and 14.0 +/- 3.1 mL.min-1.100 g-1, respectively, and they received 29.5 +/- 3.3, 45.3 +/- 3.6, and 25.2 +/- 4.5% of total limb blood flow. Thus, muscle has a lower blood flow in relation to its weight in comparison with the other tissues, while bone receives the largest fraction of hind-limb blood flow. The higher perfusion rate to bone may by due to a high rate of hematopoiesis in late gestation, whereas muscle flow may be lower than that reported immediately after birth because of limited limb movement and lack of shivering thermogenesis. There were no significant differences in tissue weights between the limb in which femoral arterial and lateral tarsal venous catheters were implanted (nonstudy limb) and the leg that had smaller diameter catheters placed in the pudendoepigastric artery and vein (study limb). However, nonstudy limb blood flow was 13.4 +/- 1.8% less than in the study limb, although the flow distribution to hind-limb tissues was not different between the two limbs. This suggests that the longer, larger diameter catheters inserted into the nonstudy limb had an adverse effect on hind-limb blood flow but not on overall limb growth or blood flow distribution. More attention should be paid to the effects of chronic fetal vascular catheterization on the tissues or organs normally perfused by the catheterized vessel.

Animals↗
PubMed1989

Cerebral oxidative metabolism during sustained hypoxaemia in fetal sheep.

Cerebral oxidative metabolism was determined in 9 unanaesthetized fetal sheep near term, during a normoxic control period and during sustained hypoxaemia induced by lowering maternal inspired O2 concentration to 11-8% with 3% CO2 added. Preductal arterial and sagittal vein blood samples were analyzed for oxygen content, blood gas tensions and pH. Cerebral blood flow was measured with a radioactively-labelled microsphere technique. Induced fetal hypoxaemia resulted in a metabolic acidaemia which was progressive over several h. Cerebral oxygen consumption was initially marginally decreased in response to induced hypoxaemia with cerebral blood flow increased thus maintaining O2 delivery coupled to cerebral oxygen consumption. With a worsening metabolic acidemia, pHa below 7.15, cerebral blood flow fell as mean arterial pressure fell, but cerebral oxygen consumption was little changed as fractional O2 extraction now increased. With sustained hypoxaemia and profound metabolic acidaemia, pHa below 7.00, fractional O2 extraction also fell resulting in a terminal fall in cerebral oxygen consumption to less than 50% of control values. Although the initial marginal decrease in cerebral oxygen consumption in response to induced hypoxia may represent a protective mechanism whereby the fetal brain decreases nonessential functions thus lowering oxidative needs, the terminal fall in cerebral oxygen consumption suggests pathological alterations within the brain at this time.

Animals↗
PubMed1987

Fetal oxygen extraction: comparison of the human and sheep.

To estimate fetal oxygen extraction in the human, the inverse, linear relationship between umbilical arterial PO2 and oxygen extraction was calculated from measurements made on cord blood samples obtained after vaginal (n = 12) and cesarean (n = 16) delivery and used to predict oxygen extraction in utero. Comparisons with similar data from fetal lambs in utero and during labor and delivery indicate that extraction in the human and sheep fetus is 47% and 27%, respectively, at PaO2 = 20 mm Hg. For the human fetus to have extraction similar to that in the fetal lamb, vascular PO2 would have to be substantially higher. This would lead to a higher umbilical venous oxygen content in the human, compensating for the lower umbilical blood flow and yielding a rate of oxygen delivery comparable with that observed in the fetal sheep. These data indicate that there may be significant quantitative differences in the fetal oxygen delivery systems in the human and sheep.

Animals↗
PubMed1986

Plasma adrenocorticotropic hormone and cortisol and adrenal blood flow during sustained hypoxemia in fetal sheep.

We examined the effect of sustained hypoxemia with progressive acidemia on pituitary-adrenal endocrine function (adrenocorticotropic hormone, cortisol) and on adrenal blood flow in fetal sheep. Hypoxemia was induced by the maternal sheep breathing a gas mixture containing 9% oxygen, with 3% carbon dioxide added. Induced hypoxemia resulted in a progressive fetal metabolic acidosis but with little change in maternal pH. During induced hypoxemia there was little change in maternal plasma adrenocorticotropic hormone or cortisol level. Fetal adrenocorticotropic hormone and cortisol increased to peak values within 2.8 hours of induced hypoxia but by 7.2 hours had begun to fall to values that were not significantly different from those at 1.4 hours. Fetal adrenal blood flow (microsphere technique) also increased significantly and remained elevated throughout the duration (7.2 hours) of hypoxemia. The maximum fetal adrenal blood flow achieved during hypoxemia was significantly correlated with the basal (prehypoxemia) flow to the adrenals. We conclude that the changes in fetal adrenocorticotropic hormone, cortisol, and adrenal blood flow seen in short-term hypoxemia are reproduced during sustained hypoxemia with acidemia. Furthermore, the noted rise in the fetal adrenocorticotropic hormone level may be an important factor contributing to the increase in adrenal blood flow during hypoxemia.

Adrenal Glands↗
PubMed1976

The distribution and clearances of hormones and metabolites in the circulation of the foetal sheep.

Plasma hormone and metabolite concentrations have been measured in the plasma of blood collected simultaneously from the femoral artery, umbilical vein and carotid artery of the exteriorized foetal sheep. The concentration of vasopressin and catecholamines was consistently lower and of glucose, lactate and corticosteroids consistently higher in the umbilical vein compared with the femoral artery. ACTH concentrations showed no consistent pattern and fluctuated widely at each site, but during synacthen infusion the concentration in the umbilical vein was consistently lower than in the femoral artery. For corticosteroids the concentration in the carotid artery was much lower than that in the umbilical vein; the converse was true for catecholamines. Concentrations in the carotid and femoral artery were similar for all compounds investigated. These results indicate that the placenta is a major site of vasopressin, catecholamine and ACTH clearance and of glucose, lactate and corticosteroid production. The foetal liver is probably a major site of corticosteroid and catecholamine clearance.

Adrenocorticotropic Hormone↗