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G G Power

Publications and source records attributed to G G Power.

At least 55 records · Page 3Linked to original sources
PubMed1989

Errors in microsphere determination of cardiac output: a computer simulation in fetal sheep.

Through use of a compartmental model, we simulated the measurement of cardiac output and distribution by means of radioactively labeled microspheres in fetal lambs with weights between 0.5 and 3 kg. A systematic error in measured cardiac output caused by artifactual changes in blood volume caused by the injection and withdrawal of fluids during the procedure was less than 5% for fetal weights greater than or equal to 1 kg but increased for fetal weights less than 1 kg and when hypovolemia was simulated at all fetal weights. Sensitivity analysis disclosed no significant effect of changes in vascular resistance. We examined the effects of recirculation of microspheres and found no significant increase in error in the measured value of cardiac output due to 20% recirculation of all spheres entering a single isolated organ system; however, errors between 7 and 14% were observed with simulations of 20% recirculation in more than one compartment simultaneously. Recirculation also introduced significant errors in the measured distribution of cardiac output in certain cases. The effect on the measured cardiac output of a temporary change in the true cardiac output was dampened by the artifactual blood volume changes mentioned above and the fact that the measurement is a time-weighted average. We also evaluated four different experimental designs. We conclude that the microsphere technique provides a remarkably reliable means of quantifying cardiac output and individual organ flow in the fetus. The nonrandom errors inherent in the procedure examined in this study are of the order of 10%, which is likely to be less than the moment-to-moment variation in the true cardiac output.

Algorithms↗
PubMed1989

Temperature dependence of the maternal-fetal electrical potential difference in guinea pigs.

An electrical potential difference (PD) is measured between maternal organism and fetus in the pregnant guinea pig. To investigate whether the PD is generated by active or passive forces these studies examined the temperature dependence of the PD in guinea pigs at 55-61 days gestation. Anesthesia was induced (ketamine, 44 mg/kg) and maintained (halothane, 1.5%) in 5 pregnant guinea pigs. The animals were subjected to alternating 1 hour periods of cooling and recovery, changing core body and intrauterine temperature about 5 degrees C. PD was monitored continuously with Ag/AgCl electrodes placed in the maternal abdominal cavity and the amniotic fluid. The resting PD (+/- SEM) was 24.1 +/- 2.8 mV. Analysis of covariance indicated that PD decreased slowly with time and increased significantly with lowered temperature. A second group of 4 guinea pigs was studied after beta blockade with propranolol (0.1 mg iv, repeated hourly). In this group the resting PD was 20.7 +/- 3.6 mV. The PD decreased gradually with time and decreased consistently during cooling. In the propranolol group the relation between PD and temperature yielded a calculated activation energy of 11.7 +/- 0.8 kcal/mol (Q10 = 1.9, 30-40 degrees C). These results are consistent with the hypothesis that at least some of the PD is generated by an energy-dependent electrogenic ion pump, or by selective passive diffusion of ions across a lipid membrane during which a significant energy barrier is overcome. They are not consistent with the generation of the PD exclusively by passive streaming of ions through water-filled channels. During cooling catecholamines are presumably released, favoring the generation of the PD.

Action Potentials↗
PubMed1989

Umbilical cord occlusion but not increased plasma T3 or norepinephrine stimulate brown adipose tissue thermogenesis in the fetal sheep.

Nonshivering thermogenesis is normally inactive in utero but increases with supplemental oxygenation and again after occlusion of the umbilical cord. To test the hypothesis that brown fat responses are triggered by the surge in triiodothyronine (T3) which occurs at birth, we studied 7 fetal sheep at 132-143 days gestation. Fetuses were first cooled 2-3 degrees C by circulating cold water through an external coil in the amniotic fluid and then ventilated with oxygen in utero to raise arterial PO2 to 109 +/- 10 (SEM) mmHg. An hour later T3 was infused intravenously to elevate and maintain plasma levels at 39.8 +/- 6.1 nmol/l, some 40-50 times basal levels. Indices of brown heat production did not rise during the next 30 min. Following snaring of the umbilical cord, however, plasma free fatty acid levels increased 400% to 423 +/- 91 mEq/l, plasma glycerol rose 350% to 766 +/- 168 mmol/1, and the temperature difference between brown fat and body core widened to 0.59 +/- 0.13 degrees C during the next 30 min. Whole body oxygen consumption peaked at 23.1 +/- 2.8 ml.min-1.kg-1 body weight. These responses to cord occlusion were similar with and without T3 administration. Changes in plasma catecholamines during these experiments did not correlate with the onset of nonshivering thermogenesis. We conclude that the rise in T3 or the changes in plasma catecholamines which occurs at birth are not causally related to the onset of nonshivering thermogenesis.

Adipose Tissue, Brown↗
PubMed1989

A microcomputer program for real-time data acquisition in the perinatal physiology laboratory.

This report describes a real-time data acquisition system using the IBM PC-AT microcomputer, and software specifically engineered for the perinatal physiology laboratory. The system samples up to sixteen analog signals at a rate ranging from 1 to 1024 Hz. Calibrated digital values are displayed on the computer monitor and stored on disk. The system can perform algebraic computations and estimate derivatives. Pattern recognition algorithms are included for the detection and characterization of uterine contractions and fetal breathing movements. Two different noise-rejection filters are implemented. Output of signals via a digital-to-analog converter is supported. The system has been used to record a broad variety of physiologic variables in a number of different studies.

Algorithms↗
PubMed1988

Disappearance of growth hormone from plasma of fetal and newborn sheep.

The disappearance of growth hormone (GH) from plasma was measured after a single intravenous injection in fetal and newborn sheep and fetal sheep after simulated birth in utero. The process was adequately described when separated into two exponential components, consistent with an inner (plasma) and outer (composite tissue) pool. Plasma clearance rate increased from 3.4 +/- 0.2 (SE, n = 6) in fetuses to 3.9 +/- 0.1 (n = 5) ml.min-1.kg-1 in newborns (P less than 0.05), but was not altered significantly after simulated delivery in utero. The volume of distribution decreased from 74 +/- 4 ml/kg before birth to 47 +/- 2 ml after natural birth (P less than 0.001). The basal secretory rate decreased from 2.4 +/- 0.2 before birth to 0.27 +/- 0.02 microgram/min after birth (P less than 0.001) and to a lesser extent after simulated delivery. The rate constant for irreversible loss, Kd, increased from 0.052 +/- 0.004 min-1 before birth to 0.093 +/- 0.002 min-1 after birth (P less than 0.001). Because plasma GH concentration in steady state equals secretory rate/(volume of distribution X Kd), one may calculate that 83% of the total decrease in GH, which occurs after birth, can be explained by diminished secretory rate, whereas 17% can be explained by more rapid loss from the plasma.

Animals↗
PubMed1988

Computer model of fetal-maternal heat exchange in sheep.

We constructed and used a mathematical model of maternal-fetal heat exchange in the sheep to explore the effects of changes in certain parameters on steady-state fetal temperatures and to determine whether the fetus in the model has any potential to control its own temperature. The model took into account both fetal and placental heat production and exchange of heat in the placenta, across the fetal skin, via amniotic fluid, and through the uterine wall. The maternal ewe was assumed to be a constant temperature heat sink. Changes in placental or fetal heat production were calculated to change the ratio of heat exiting across the placenta or fetal skin significantly but to have little effect on fetal core temperature, e.g., a rise of only 0.8 degrees C was predicted after a twofold increase in fetal heat production. Fetal placental blood flow was calculated to affect fetal temperature the most of any flow, a reduction to zero causing fetal temperature to rise 5.0 degrees C. Changes in heat conductances between fetal skin and amniotic fluid, or between amniotic fluid and uterine wall, had minimal effect on fetal temperature. From the model calculations here and because heat exchange within the sheep placenta has previously been calculated to be extremely efficient, we conclude that the fetal sheep has little ability to control its temperature by changes in heat dissipated through extraplacental pathways. Thus the model predicts an effective heat clamp that closely links fetal to maternal temperature.

Animals↗
PubMed1988

Fetal breathing and sleep state responses to graded carboxyhemoglobinemia in sheep.

To investigate CO effects on brain oxygenation, graded carboxyhemoglobinemia (HbCO) was produced in nine unanesthetized fetal sheep by infusing CO-laden erythrocytes in exchange for fetal blood. For the 1st h after this procedure, the mean fetal carboxyhemoglobin levels were 16.5 +/- 0.4% [control (C) = 1.4 +/- 0.4%] for mild HbCO, 22.7 +/- 0.6% (C = 1.8 +/- 0.4%) for moderate HbCO, and 27.8 +/- 0.5% (C = 2.1 +/- 0.7%) for severe HbCO. This induction of HbCO significantly reduced mean preductal arterial PO2 values to 4.3 Torr below control for mild HbCO, 4.6 Torr below control for moderate HbCO, and 5.5 Torr below control for severe HbCO. The respective arterial O2 contents were decreased by 17, 21, and 29%. Mean arterial pH was lowered only during severe HbCO, and arterial PCO2 values were unchanged. HbCO produced a fetal tachycardia. Mean arterial blood pressure was only increased during severe HbCO. The incidences of rapid eye movements and breathing activity were decreased by HbCO in a dose-dependent manner. When related to calculated brain tissue PO2, these decreases were similar to those measured during hypoxic hypoxia and anemia, suggesting that carboxyhemoglobin effects result solely from diminished oxygenation. It is concluded that 1) the peripheral arterial chemoreceptors in the fetus apparently have little effect on hypoxic inhibition of breathing and 2) the carboxyhemoglobin concentrations required to inhibit fetal breathing are greater than those likely to be encountered clinically.

Animals↗
PubMed1988

In vivo brown fat response to hypothermia and norepinephrine in the ovine fetus.

The goal of this study was to assess the response of fetal brown fat in vivo to hypothermia and norepinephrine infusion. In 10 unanaesthetized, chronically-prepared fetal sheep (133 +/- 2 days of gestation) cold water was passed through tubing encircling the fetus in utero and plasma glycerol concentration was measured as an indicator of brown fat activity. Following cooling for 60 min, amniotic fluid temperature fell 7.79 degrees C to 31.66 +/- 1.73 degrees C (n = 8, P less than 0.001) and maternal temperature fell 0.63 degree C to 38.63 +/- 0.08 degrees C (n = 9, P less than 0.001). Eight of the fetuses were subjected to a second experiment in which norepinephrine was infused intravenously for 15 min. During infusion fetal arterial temperature fell 0.38 degrees C to 39.05 +/- 0.25 degrees C (n = 7, P less than 0.05). Amniotic fluid temperature (n = 7, NS) and maternal arterial temperature (n = 7, NS) remained constant. Glycerol concentration during the infusion increased from 0.73 to 1.27 mg/dl, a 74% increase over control (n = 8, P less than 0.001). Although clearly detectable, these glycerol responses to hypothermia and norepinephrine stimulation are one-third or less of those achieved after birth, indicating that thermogenesis remains quiescent in the near-term fetal sheep, despite powerful stimuli for activation.

Adipose Tissue, Brown↗
PubMed1987

Nifedipine: effects on fetal and maternal hemodynamics in pregnant sheep.

We investigated the effects of nifedipine, a calcium entry blocker, on the fetal and maternal circulation. Nifedipine was administered intravenously for 30 minutes to chronically instrumented pregnant ewes. Infusion of 5 micrograms.kg-1.min-1 resulted in a 30% to 50% increase in total and regional fetal cerebral blood flow to the brain stem, watershed, and subcortical regions (p less than 0.05), without a significant change in fetal oxygenation or cardiac output. Infusion of 10 micrograms.kg-1.min-1 decreased uterine blood flow by 21% (p less than 0.001) and fetal arterial oxygen content by 15% (p less than 0.01), with no further increase in fetal cerebral blood flow. Maternal arterial pressure decreased and heart rate increased (p less than 0.001) without variation of arterial blood gases. Significant plasma levels of nifedipine were detected in the fetal and maternal circulations. In view of the potential adverse effects on the fetus, further studies are needed before nifedipine is considered for use in human pregnancy.

Animals↗
PubMed1987

Fetal breathing, sleep state, and cardiovascular responses to graded hypoxia in sheep.

Graded isocapnic hypoxemia was produced in unanesthetized fetal sheep by varying the inspired O2 concentration (21, 12, 10.5, and 9%) of the ewe. This produced corresponding mean preductal arterial O2 tension (PaO2) values of 25.2 +/- 1.1 (control), 20.1 +/- 1.0 (mild hypoxia), 17.8 +/- 0.9 (moderate hypoxia), and 16.8 +/- 1.4 Torr (severe hypoxia). These were associated with mean arterial O2 contents (CaO2) of 7.18 +/- 0.44, 5.19 +/- 0.34, 4.24 +/- 0.33, and 3.27 +/- 0.20 ml/dl, respectively. The most severe hypoxia was associated with metabolic acidosis and fetal bradycardia. Hypoxia did not reduce significantly the incidence of low-voltage electrocortical activity. The incidence of breathing and rapid eye movements was not affected by mild hypoxia; however, the incidence of both was significantly reduced during moderate and severe hypoxia. It is concluded that 1) acute reductions in the mean PaO2 of 5.9 +/- 0.6 Torr and CaO2 of 2.00 +/- 0.23 ml/dl are critical in that greater reductions inhibit fetal eye and breathing activity and 2) hypoxia probably inhibits eye and breathing movements by altering sleep state.

Animals↗
PubMed1987

Fetal breathing, sleep state, and cardiovascular responses to graded anemia in sheep.

Graded anemia was produced for 2 h in 10 unanesthetized fetal sheep by infusing plasma in exchange for fetal blood. This reduced the mean fetal hematocrits during the 1st h of anemia to 19.7 +/- 0.5% [control (C) = 28.2 +/- 1.1%] for mild anemia, 17.4 +/- 0.9% (C = 30.0 +/- 1.1%) for moderate anemia, and 15.1 +/- 1.0% (C = 29.2 +/- 1.3%) for severe anemia. The respective mean arterial O2 contents (CaO2) were 4.46 +/- 0.20, 3.89 +/- 0.24, and 3.22 +/- 0.19 ml/dl. Mean arterial PO2 was reduced significantly (by 2 Torr) only during moderate anemia, and mean arterial pH was decreased only during severe anemia. No significant changes occurred in arterial PCO2. Fetal tachycardia occurred during anemia. Mean arterial pressure was reduced by 2-3 mmHg during mild anemia; however, no significant blood pressure changes were observed for moderate or severe anemia. The incidence of rapid-eye movements and breathing activity was not affected by mild anemia, but the incidence of both was reduced significantly during moderate and severe anemia. It is concluded that 1) a reduction in CaO2 of greater than 2.48 +/- 0.22 ml/dl by hemodilution inhibits rapid-eye movements and breathing activity, and 2) the PO2 signal for inhibition does not come from arterial blood but from lower PO2 in tissue.

Anemia↗
PubMed1987

Oxygen supply and the placenta limit thermogenic responses in fetal sheep.

The aim of this study was to assess the individual effects of cooling, increased oxygenation, and umbilical cord occlusion on nonshivering thermogenesis in utero. A cooling coil was placed around eight fetal sheep of 132-145 days gestation; thermistors were placed in the fetal esophagus and maternal iliac artery, vascular catheters and a tracheal catheter were inserted, and a snare was placed loosely around the umbilical cord. The next day cold water was circulated through the coil for 5 h. During the 1st h of cooling alone, fetal core temperature fell 2.79 degrees C, but indexes of brown fat activity increased only slightly. After ventilation with O2, plasma free fatty acid concentration (FFA) rose 7.4-fold to 244 +/- 42 mu eq/l, glycerol concentration rose fourfold to 376 +/- 85 microM, and the difference between brown fat and core temperature widened to 0.60 +/- 0.10 degrees C. Ventilation with N2-enriched air did not evoke similar responses. After snaring the umbilical cord while ventilation was continued, FFA rose to 554 +/- 95 mu eq/l, glycerol rose to 684 +/- 76 microM, and the temperature difference widened to 0.77 +/- 0.13 degrees C. Whole-body O2 consumption peaked at 19.6 ml.min-1.kg-1 of fetal tissue. We conclude that fetal thermogenic responses are limited in part by O2 delivery to brown fat and are augmented by occlusion of the umbilical cord.

Adipose Tissue, Brown↗
PubMed1987

Predict fetal brain PO2 during hypoxaemia and anemia in sheep.

The mean brain PO2 of fetal sheep was calculated using equations based on the Krogh cylinder model of O2 diffusion. This analysis took into account the effect of red cell spacing on capillary PO2. Uncompensated changes in arterial O2 tension, the radius of the Krogh cylinder, and metabolic rate of brain tissue were predicted to affect mean brain PO2 more than uncompensated changes in brain blood flow or haemoglobin concentration. Under normal conditions (CaO2 = 7.42 ml/dl), the mean PO2 of the fetal brain was calculated to be about 12 mmHg. Hypoxaemia decreased the predicted mean O2 tension to 7.6 mmHg (CaO2 = 5.19 ml/dl), 5.0 mmHg (CaO2 = 4.11 ml/dl), and 4.3 ml/dl (CaO2 = 3.50 ml/dl). Isovolaemic anaemia reduced mean brain PO2 to 8.7 mmHg (CaO2 = 4.40 ml/dl), 8.3 mmHg (CaO2 = 3.94 ml/dl), and 7.3 mmHg (CaO2 = 3.19 ml/dl). During anaemia the increased distance between red cells was calculated to contribute significantly to brain hypoxaemia. A summary equation is presented which enables the investigator to estimate easily the mean PO2 of the fetal brain when several factors are changed from standard values.

Anemia↗
PubMed1986

Role of arginine vasopressin in fetal renal response to hypertonicity.

We studied the effects of hyperosmolality on fetal renal function and the role of arginine vasopressin (AVP) in these responses. NaCl (9%) was injected intravenously into chronically catheterized ewes and their fetuses, followed by a continuous infusion of 9% NaCl into the ewes. The fetuses were either normal, infused with AVP, or infused with an AVP antagonist. In normal fetuses NaCl injection caused fetal and maternal blood osmolalities to be elevated by 10-15 mosmol/kg for 4 h with no change in fetal blood volume; fetal plasma AVP rose 42%. Fetal arterial pressures rose transiently by 2-10 mmHg. Fetal urine flow rose transiently by 73% after NaCl injection and then averaged 27% below control after 1 h, whereas fetal urine osmolality increased from 188 +/- 31 to 282 +/- 33 mosmol/kg. In a second group of fetuses AVP infusion alone caused fetal urine osmolality to increase by 123 +/- 39 mosmol/kg and urine flow to fall 31%, whereas in a third group the antagonist alone had no effect on urine flow or osmolality. After hypertonic injection into fetuses infused with AVP or the antagonist, the transient changes were similar to those in normal fetuses. However, the sustained increase in urine osmolality and decrease in flow after hypertonic injection were abolished in AVP-infused and antagonist-infused fetuses. Thus it appears that the transient changes in fetal renal function after hypertonic injection are not AVP-induced and may be due to transient increases in arterial pressure, whereas the prolonged changes in urine flow and osmolality appear to be mediated by increases in fetal plasma AVP levels.

Animals↗
PubMed1986

Fetal and uteroplacental heat production in sheep.

To separate heat production of the fetus from that of the placenta, endometrium, and uterine muscle, we measured total uterine heat production first with the fetus intact and then after the umbilical cord was snared and the fetus killed. Heat production was measured with the Fick principle using thermistors chronically implanted in a maternal artery and major uterine vein and a flowmeter placed on the common internal iliac artery. In nine ewes, carrying lambs weighing 4.46 +/- 0.42 (SE) kg, total uterine heat production fell from 10.6 to 2.9 W after fetal death. Uterine blood flow fell progressively to 90% of control levels during the first hour after death. The caloric equivalent for O2 averaged 4.1 cal/ml O2 for the uterus, 2.2 for the uteroplacenta, and 4.6 for the fetus per se. It was not possible to explain these results using a simple model of maternal-fetal heat transfer. Rather, it was necessary to assume an additional pathway for heat transfer between small uterine veins on the surface of the uterus and cooler structures in the maternal abdomen, presumably the ventral abdominal wall.

Animals↗
PubMed1986

Fetal breathing movement, sleep state and cardiovascular responses to an inhibitor of mitochondrial ATPase in sheep.

Hypoxia abolishes breathing movements in fetal sheep, perhaps by reducing ATP synthesis within regulatory brain cells. This possibility was examined by administering to 13 chronically catheterized fetal sheep oligomycin B, a mitochondrial ATPase inhibitor. Injections into the left external carotid artery of oligomycin B (170 +/- 19 micrograms/kg in 9 fetuses) reduced significantly (P less than 0.01) the incidence of fetal breathing movements from a control mean of 52 +/- 6.3% to 6 +/- 2.2 and 9 +/- 4.4% during the first and second hours after drug injection. Oligomycin did not decrease significantly the incidence of low voltage electrocortical activity or reduce the average duration of a cycle of low and high voltage electrocortical states. Nor did it decrease significantly the incidence of rapid eye movements. Fetal heart rate and mean arterial pressure were not significantly affected, and the arterial blood gases and pH did not significantly differ from control values. However, a large dose of the drug (700 micrograms/kg) produced an isoelectric electrocorticogram, hypertension, and bradycardia associated with a rise in arterial PO2 and a severe metabolic acidosis. In 3 fetal sheep oligomycin also inhibited continuous breathing induced by indomethacin. Injection of the vehicle (ethanol) alone did not alter the incidence of breathing movements, electrocortical activity, eye movements or blood gases. These results suggest that reduced mitochondrial production of ATP may be a mechanism by which hypoxia abolishes fetal breathing activity.

Adenosine Triphosphatases↗
PubMed1986

Effect of cooling and heating on the regional distribution of blood flow in fetal sheep.

This is a study on the effect of cooling and heating amniotic fluid on blood flow to fetal tissues and organs. In 8 unanaesthetized, chronically-catheterised fetal sheep (129-137 days gestation) cold or warm water was passed through tubing encircling the fetus in utero and blood flow was measured using the radionuclide-labelled 15 mu spheres. Following cooling for 30 min, amniotic fluid temperature fell 9.6 degrees C to 29.9 +/- 2.1 degrees C (SEM) fetal arterial temperature fell 2.37 degrees C to 37.30 +/- 0.36, and maternal arterial temperature fell 0.53 degrees C to 38.58 +/- 0.16. Blood flow through the fetal skin fell 60% (P less than 0.01) to 13.6 ml/min per 100 g tissue. Blood flow to the brown fat increased 186% (P less than 0.05) to 99.6 ml/min per 100 g. Following warming for 20 min, fetal temperature rose to 40.43 +/- 0.19 degrees C, and skin blood flow did not change significantly relative to initial control period but rose 200% above that during cooling (P less than 0.01). During both cooling and heating, blood flow to the adrenals rose significantly (P less than 0.05) whereas flow to the carcass, brain, kidneys, and placenta was not altered detectably. Continuous sampling of blood from the inferior vena cava during microsphere injection failed to detect any evidence of arterio-venous shunting through the skin at any temperature studied. Overall, the blood flow responses are consistent with a thermoregulatory role for the skin and brown fat in the near-term fetal sheep.

Amniotic Fluid↗