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Biomedical subjects

G G Power

Publications and source records attributed to G G Power.

At least 37 records · Page 2Linked to original sources
PubMed1996

Plasma endothelin-1 levels during asphyxia in the fetal goat.

The changes in fetal carotid arterial plasma levels of endothelin-1, catecholamines, PO2, PCO2 and pH were measured after intermittent repetitive umbilical cord occlusion in late gestation pregnant goats (n = 9). Endothelin-1 levels increased to 3.58 +/- 0.28 pg/ml immediately after the onset of fetal hypoxia, a level significantly higher than the respective values in the control period (p < 0.05). The elevation of fetal plasma endothelin-1 levels correlated inversely with carotid arterial PO2 (r = -0.41, p < 0.05) and pH (r = - 0.43, p < 0.05). The results suggest that increased endothelin-1 levels may contribute to the maintenance of the fetal circulation during fetal asphyxia.

Animals↗
PubMed1995

Role of prostaglandin I2 and prostaglandin E2 in the initiation of nonshivering thermogenesis during the simulation of birth in utero.

Because maximal nonshivering thermogenesis can commence only after occlusion of the umbilical cord, circulating stimulators and inhibitors were hypothesized to alter brown fat activity in the perinatal period. The roles of prostaglandin I2 (PGI2) and PGE2 in the initiation of nonshivering thermogenesis at birth were investigated. Indomethacin (45 mg bolus, 3 mg h-1 thereafter) was infused into 10 near-term fetal sheep to decrease prostanoid synthesis; 6 age-matched fetuses were infused with saline as controls. Sixteen hours later, birth was simulated in utero by sequentially cooling the fetus, ventilating its lungs with oxygen and occluding the umbilical cord. In the control fetuses, the plasma concentrations of PGI2 and PGE2 and free fatty acids, an index of nonshivering thermogenesis, were unaffected by cooling. Ventilation caused the concentration of PGI2 to increase 108% (P < 0.001) and that of PGE2 to decrease 26% (P < 0.05), while fatty acid concentrations increased 100% (P < 0.05). After cord occlusion, PGI2 concentrations remained elevated whereas PGE2 concentrations decreased a further 46% (P < 0.01), and fatty acid concentrations increased a further 100% (P < 0.05). In the indomethacin-treated fetuses, PGI2 and PGE2 concentrations decreased to 20% of the preinfusion values (P < 0.001) and did not change during the experiment. Cooling initiated a 300% increase in fatty acid concentrations (P < 0.05) and ventilation and cord occlusion induced no further significant changes. Thus, prostanoid concentrations follow changes in nonshivering thermogenic activity and support a regulatory role for PGI2 and PGE2 in the initiation of thermogenesis. Before birth, high concentrations of PGE2 favour suppression of thermogenesis, and after birth this inhibition is removed and there is stimulation by PGI2.

Animals↗
PubMed1995

A potential role for adenosine in the inhibition of nonshivering thermogenesis in the fetal sheep.

Adenosine is released by the placenta into the fetal circulation and has potent antilipolytic properties in vitro. Nonshivering thermogenesis cannot be demonstrated by cooling fetal sheep in utero but can be induced by supplemental oxygenation and umbilical cord occlusion; this suggests the presence of inhibitor(s) of placental origin. To test whether circulating adenosine could be such an inhibitor, a series of experiments was carried out in nine fetal sheep at 136-145 d gestation. Birth was simulated in utero by sequentially cooling the fetus 2.49 +/- 0.23 degrees C with no change in the low levels of plasma FFA or glycerol; ventilating with O2 via an exteriorized tracheostomy tube and umbilical cord occlusion. Thermogenic indices rose markedly, and plasma FFA and glycerol concentrations peaked at 725 +/- 88 microEq/L (p < 0.01) and 771 +/- 154 mumol/L, (p < 0.001), respectively, O2 consumption rose to 20 +/- 2 mL/min/kg, and temperature increased 1.99 +/- 0.35 degrees C. The long-acting adenosine analog N6-(L-2-phenylisopropyl)-adenosine (PIA) was then infused (90 micrograms/kg bolus, then 300 micrograms/kg/h for 30 min); plasma FFA and glycerol decreased to 265 +/- 56 microEq/L (p < 0.003) and 477 +/- 102 mumol/L (p < 0.04), respectively; O2 consumption fell rapidly to 4.5 +/- 0.3 mL/min/kg (p < 0.01); temperature decreased 1.89 +/- 0.39 degrees C (p < 0.001); and fetal arterial BP decreased to 38 +/- 5 mm Hg (p < 0.004) in 30 min. A stepped dose-response study was performed in three fetal sheep.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1994

Increase of fetal arterial blood temperature by reduction of umbilical blood flow in chronically instrumented fetal sheep.

The effect of reduced umbilical blood flow rate on fetal core temperature was investigated in five chronically instrumented fetal sheep (gestational age 124 days). On average, fetal-maternal temperature difference increased 0.13 +/- 0.02 degrees C when blood flow rate was decreased to about 1/3 of normal (248 +/- 69 ml min-1) for 30 min. The small temperature rise is the consequence of predominant heat dissipation through the placenta, and of diminished oxygen consumption.

Animals↗
PubMed1994

Relationship between plasma adenosine concentration and breathing movements in growth-retarded fetuses.

OBJECTIVE: The purpose of this study was to investigate the relationship between plasma adenosine concentration and breathing movements in growth-retarded fetuses. STUDY DESIGN: We measured the incidence of fetal breathing movements and breathing rate immediately before cordocentesis in 26 growth-retarded fetuses at 31 to 38 weeks' gestation. Blood retrieved by cordocentesis was then analyzed for umbilical venous plasma adenosine concentration, blood gases, and pH. RESULTS: In growth-retarded fetuses with hypoxia and acidosis plasma adenosine concentration was elevated and the incidence of fetal breathing movements was reduced. The change in plasma adenosine concentration correlated inversely and significantly with the incidence of fetal breathing movements. CONCLUSION: Decreased breathing movements correlate with elevated plasma adenosine concentration in fetuses. We postulate that the enhanced adenosine formation in growth-retarded fetuses may modulate the inhibition of fetal breathing movements.

Adenosine↗
PubMed1994

Role of prostaglandin E2 and prostacyclin in nonshivering thermogenesis during simulated birth in utero.

Prostaglandin E2 (PGE2) inhibits and prostacyclin (PGI2), stimulates lipolysis in vitro. Their role in initiating nonshivering thermogenesis at birth was investigated in 16 fetal sheep at 129-143 days gestation. In 10 fetuses indomethacin, a prostaglandin synthesis inhibitor, was infused; in 6 fetuses saline was administered as a control. 16 h later birth was simulated in utero. The plasma levels of PGE2 and PGI2 were unaffected by cooling. In the control fetuses, ventilation with oxygen caused PGE2 to fall, PGI2 to rise, and initiated moderate thermogenesis, signaled by a twofold increase in plasma free fatty acids (FFA). After umbilical cord occlusion, PGE2 decreased further (PGI2 was unchanged) and thermogenesis accelerated. In indomethacin-treated fetuses, in which the prostanoids had decreased and remained at approximately 20% normal, cooling initiated moderate nonshivering thermogenesis, and ventilation and cord occlusion caused no further changes. Changes in plasma adenosine were similar in control and indomethacin-treated groups. We conclude that declining PGE2 and rising PGI2 contribute to the initiation of thermogenesis at birth, but that other agents possibly of placental origin may play a contributory role.

6-Ketoprostaglandin F1 alpha↗
PubMed1994

Plasma adenosine concentration in appropriate- and small-for-gestational-age fetuses.

OBJECTIVE: Our purpose in this study was to investigate the relationship between fetal plasma adenosine concentration and catecholamine concentration, blood gases, and pH in appropriate- and small-for-gestational-age fetuses. STUDY DESIGN: Cordocentesis was performed in 23 appropriate- and 14 small-for-gestational-age fetuses at 30 to 37 weeks' gestation for the measurement of umbilical venous blood plasma adenosine and catecholamine concentrations, blood gases, and pH. RESULTS: In small-for-gestational-age fetuses plasma adenosine concentration was higher, umbilical venous PO2 and pH were lower, and PCO2 was significantly higher than in appropriate-for-gestational-age fetuses. The elevation of plasma adenosine concentration was inversely related to umbilical venous PO2 and pH. CONCLUSION: Some small-for-gestational-age fetuses are exposed to diminished oxygen tension and acidotic blood gas values in utero. We postulate that the accompanying elevation of plasma adenosine may elicit protective adaptation during fetal asphyxia as a stress response.

Adenosine↗
PubMed1993

Disappearance of palmitic acid from plasma of fetal and newborn sheep.

These studies were undertaken to measure the kinetic constants that characterize the disappearance of a representative free fatty acid (FFA) from the plasma of fetal and newborn sheep. A bolus of albumin-complexed [14C]palmitic acid was infused intravenously, and during the next 8 min, 24 arterial samples were collected to characterize the disappearance curve. Palmitic acid disappearance from plasma was well described by a double-exponential model. When birth was simulated in utero, kinetic values were not changed by cooling. However, after intrauterine ventilation with O2, the volume of distribution of the FFA increased 29%, its plasma clearance rate decreased 26%, and its apparent half-life in the plasma lengthened from 0.8 to 1.2 min (all P < 0.01, n = 8). After umbilical cord occlusion, plasma clearance rate decreased a further 19% and half-life lengthened to 1.4 min. About 60% of the increase in FFA concentration during simulated birth is explained by increased release from adipose stores, and 40% is explained by decreased clearance. Further experiments tested the influence of FFA concentrations themselves. After infusion of unlabeled FFA, clearance of the tracer decreased 23% (P < 0.05, n = 5), a result consistent with a saturable membrane transporter of FFAs.

Animals↗
PubMed1992

Modulation of growth hormone secretion by thermogenically derived free fatty acids in the perinatal lamb.

To evaluate the hypothesis that the rapid fall in circulating GH concentrations at birth is secondary to the initiation of nonshivering thermogenesis and the consequent rise in FFA levels, a series of experiments was performed in late-gestation fetal sheep. By sequentially cooling the fetus by means of a coil placed around the fetal thorax, ventilating with oxygen via an exteriorized tracheostomy tube, and separating the fetus from the placenta by occluding the umbilical cord, nonshivering thermogenesis could be induced in utero. In the first protocol (n = 6) cooling alone had no effect on fetal plasma FFA levels, oxygenation elevated FFAs slightly from 64 +/- 7 mu Eq/liter to 183 +/- 29 mu Eq/liter, and cord occlusion caused a further marked rise (P less than 0.005) to 635 +/- 69 mu Eq/liter. Neither cooling nor ventilation affected fetal plasma GH concentrations which fell (P less than 0.001) from 160 +/- 17 ng/ml to 65 +/- 13 ng/ml upon cord occlusion. When the cord occluder was removed FFA levels fell (P less than 0.001) and GH concentrations rose (P less than 0.001) once more, and when the cord was again occluded FFA levels rose (P less than 0.001) and GH concentrations fell (P less than 0.001). In a second protocol nine fetuses were cooled, ventilated, and the umbilical cord occluded. Once more, plasma FFA levels rose (P less than 0.001) and GH concentrations fell (P less than 0.001); when thermogenesis was inhibited by the infusion of the adenosine agonist N6-(L-2-phenyl isopropyl)-adenosine, FFA levels fell from 725 +/- 88 mu Eq/liter to 265 +/- 56 mu Eq/liter and GH concentrations rose from 54 +/- 13 ng/ml to 323 +/- 73 ng/ml. In two further protocols the possibility that PIA was acting directly on GH secretion was excluded in six fetuses with low plasma FFA levels and in three fetuses with elevated plasma FFA levels secondary to a fatty acid emulsion infusion. These studies provide direct evidence that the pattern of change in plasma GH concentrations at birth in the sheep is determined in part by the rise in plasma FFAs of thermogenic origin.

Animals↗
PubMed1992

Plasma adenosine and cardiovascular responses to dipyridamole in fetal sheep.

The effects of dipyridamole infusion on fetal arterial plasma adenosine level, [ADO], and the systemic cardiovascular system were studied in 10 fetal sheep at 130-135 days gestational age. Dipyridamole (0.25 mg/kg) was infused into the fetuses intravenously during normoxia and hypoxia. Plasma [ADO] was measured using high-performance liquid chromatography, (HPLC), and fetal heart rate and arterial blood pressure were monitored throughout the study. These studies were performed in the absence and presence of theophylline, an adenosine receptor antagonist. During normoxia (PO2, 23.8 +/- 2.0 Torr), dipyridamole infusion increased fetal plasma [ADO] from 0.82 +/- 0.10 microM to 1.41 +/- 0.16 microM within 1 min (P < 0.01) and fetal heart rate from 157 +/- 6 bpm to 174 +/- 7 bpm (P < 0.01), but did not change mean blood pressure. Fetal plasma [ADO] and fetal heart rate returned to basal levels quickly. Treatment with theophylline did not alter the elevation of plasma [ADO] after dipyridamole infusion, but abolished responses of fetal heart rate to dipyridamole infusion. After 15 min of hypoxia with an average arterial PO2 of 15.4 +/- 1.1 Torr, fetal plasma [ADO] increased to 1.15 +/- 0.14 microM (P < 0.01). Dipyridamole infusion then further raised fetal plasma [ADO] to 1.67 +/- 0.27 microM (P < 0.01). The duration of the increase of fetal plasma [ADO] after dipyridamole infusion was no longer in hypoxia than in normoxia, however there was no significant change in the pattern of transient fetal bradycardia and persistent hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1991

Factors influencing the initiation of nonshivering thermogenesis.

The aim of this study was to observe the sequential effects of oxygenation, umbilical cord occlusion, and finally cooling on circulating catecholamines and nonshivering thermogenesis in fetal sheep. We studied five fetal sheep at 132 +/- 3 days' gestation. The fetuses were first ventilated with oxygen; PaO2 levels were maintained above 150 mm Hg, and by 60 minutes there was a significant rise in both plasma glycerol and free fatty acid levels. After umbilical cord occlusion there was a peak in plasma catecholamine and triiodothyronine levels but no significant increase in lipolysis. Cooling, by circulating cold water through a coil around the fetus, induced maximum lipolysis and temperature difference between brown fat and body core, when plasma catecholamine levels were falling. During this study the changes in plasma catecholamine levels did not correlate with the onset of nonshivering thermogenesis. Cutaneous cooling, which causes neurally mediated sympathetic stimulation of brown adipose tissue, is the major signal for the initiation of nonshivering thermogenesis and thus neonatal adaptation.

Animals↗
PubMed1991

Endometrial transport generates the maternal-fetal electrical potential difference in guinea pigs.

These studies examined the transport characteristics of the uterine endometrium with respect to the origin and mechanism of generation of the maternal-fetal electrical potential difference (PD) in pregnant guinea pigs. Late-gestation animals were used in two experimental preparations. In vivo, a sealed uterine pouch that preserved blood flow to the endometrium was prepared by removal of the fetus, placenta, and fetal membranes from the uterus and replacement with Earle's solution, a balanced electrolyte solution. In vitro, sections of uterine wall comprised of myometrium and endometrium without fetal membranes were mounted in Ussing chambers. Transuterine PDs (fetal side negative) were indistinguishable in vivo and in vitro, averaging 29.6 +/- 4.5 and 32.6 +/- 6.1 (95% confidence interval) mV in the respective preparations. Both values are within the range of maternal-fetal PD measured in intact guinea pigs, indicating that the fetoplacental unit is not essential in generating an intrauterine PD. The maternal-fetal PD, therefore, is likely a passive result of the fetus and placenta being immersed in fluids at the intrauterine potential. In vitro, both PD and short-circuit current (Isc) were completely inhibited by ouabain (10(-3) M) at the serosal (maternal) side of the uterine wall but unaffected by the inhibitor from the luminal (fetal) side. Amiloride (10(-5) M) and valinomycin (10(-5) M) caused decreases in the PD when added to the luminal side, both in vivo and in vitro, and were both ineffective from the serosal side in vitro. Isc was reduced 83% from 315 +/- 24 to 53 +/- 6 (SE) microA/cm2 after luminal amiloride (5 x 10(-4) M), indicating that Na+ is the predominant ion actively transported.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1991

Changes in plasma adenosine during simulated birth of fetal sheep.

Adenosine is known to inhibit nonshivering thermogenesis in adult brown fat. These experiments were undertaken to test whether fetal adenosine, normally present in high concentrations, suppresses lipolysis in utero and then falls after birth, permitting thermogenesis to begin. To test this hypothesis, we measured fetal plasma adenosine concentration [ADO] using high-performance liquid chromatography in 11 fetal sheep at 135-140 days gestation during simulated birth. During an initial control period, fetal [ADO] averaged 1.9 +/- 0.3 microM, about four times maternal [ADO] (0.4 +/- 0.1 microM, P less than 0.001). The fetus was then cooled by circulating cold water through a plastic coil encircled about the fetal torso. One hour later, when fetal core temperature had decreased 2.3 degrees C, fetal [ADO] averaged 2.8 +/- 0.5 microM, a 50% increase (P less than 0.05), while thermogenesis remained inactive. Next the fetal lungs were ventilated with O2 to raise arterial Po2 to greater than or equal to 150 Torr. Fetal [ADO] decreased only slightly, and thermogenic responses were modest. Finally, the umbilical cord was occluded. Fetal [ADO] decreased rapidly and 60 min later averaged 1.1 +/- 0.2 microM, 40% below initial control (P less than 0.05) and 57% below the previous period (P less than 0.001). As [ADO] fell, strong thermogenic responses became apparent, as indicated by seven- to eightfold increases in plasma glycerol (P less than 0.001) and a doubling in fetal O2 consumption (P less than 0.001). These results are consistent with the hypothesis that high fetal [ADO] inhibits thermogenesis before birth but then decreases after cord occlusion, allowing thermogenesis to begin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1990

Transuterine ion movement and electrical potential difference in pregnant guinea pigs.

An investigation of the site and mechanism responsible for the maternal-fetal electrical potential difference (PD) was done in 11 anesthetized guinea pigs at 54-56 days gestation. We removed the most distal fetus and placenta from one uterine horn and secured a catheter, thermistor, and Ag-AgCl electrode in the resulting pouch. The pouch was filled with Earle's solution. We placed another thermistor and electrode in the maternal abdomen. The PD between electrodes was monitored continuously; periodic samples of maternal blood and intrauterine fluid were taken. Thirty minutes after the uterus was filled, the PD (uterine cavity negative) averaged 29.6 +/- 4.5 (95% confidence interval of the mean) mV. Over 4 h, intrauterine K+ concentration [( K+]) decreased from 4.9 to 2.6 +/- 0.5 meq/l, against a chemical and electrical gradient. In eight animals, we measured bidirectional Na+ flux using 22Na and 24Na. The flux ratio was not distinguishable from unity despite a significant PD. Our data indicate that the maternal-fetal PD is probably generated by the endometrial epithelium and that Na+ and K+ both move across the epithelium by active transport or cotransport rather than simple diffusion.

Animals↗
PubMed1990

Rate of disappearance of glycerol from plasma of fetal and newborn sheep.

The disappearance of glycerol from plasma was studied after a single intravenous injection to estimate its volume of distribution (Vdist), plasma clearance rate, and rate constant for irreversible loss (kd). Studies were repeated before and after birth of the lamb to test whether loss of the placenta could account for rapidly increasing plasma concentrations in the newborn. The disappearance of glycerol was closely described by a double-exponential model in each instance. In fetal sheep Vdist averaged 0.41 +/- 0.15 (SD) 1/kg fetal wt (n = 15). This volume decreased to 0.33 +/- 0.11 l/kg (n = 8) soon after functionally removing the placenta (by snaring the umbilical cord and maintaining the fetus with intrauterine ventilation), but the change was not significant. In newborn lambs 1-3 days of age, Vdist averaged 0.45 +/- 0.11 l/kg (n = 5, NS). Plasma clearance rate also did not change significantly, averaging 7.9 +/- 2.9, 7.9 +/- 3.8, and 9.0 +/- 5.9 ml.min-1.kg-1 in the fetus, after simulated birth, and in the newborn lamb, respectively, kd also was not altered measurably and averaged 0.020 +/- 0.006, 0.024 +/- 0.007, and 0.019 +/- 0.007 min-1 during the same time periods. Similar results were obtained by using three widely different amounts of infused glycerol. The results indicate that removal of glycerol does not depend on placental function to an appreciable extent. It is concluded that plasma glycerol concentration reflects principally glycerol turnover and, hence, lipolysis before and after birth.

Animals↗
PubMed1990

Fetal breathing and cardiovascular responses to graded methemoglobinemia in sheep.

Graded methemoglobinemia (MetHb) was produced in unanesthetized fetal sheep to determine the effects on brain oxygenation. MetHb was induced by infusing methemoglobin-containing erythrocytes in exchange for fetal blood. During the hour after MetHb was established, fetal methemoglobin concentrations averaged 1.23 +/- 0.12 (mild MetHb), 1.71 +/- 0.13 (moderate MetHb), and 2.27 +/- 0.17 g/dl (severe MetHb). MetHb reduced mean arterial O2 content by approximately 19 (mild MetHb), 29 (moderate MetHb), and 39% (severe MetHb). The average preductal arterial PO2 fell by 1.6 (-7%), 2.8 (-11%), and 4.0 Torr (-16%) for mild, moderate, and severe MetHb, respectively. Fetal heart rate increased significantly during mild and moderate MetHb, and mean arterial pressure fell slightly during moderate and severe MetHb. The incidences of fetal breathing and eye movements were reduced in a dose-dependent manner when the calculated brain end-capillary PO2 was less than 14 Torr. We conclude that: 1) the effective capillary PO2 in the fetal brain can be significantly reduced by increasing the distance between non-methemoglobin-laden erythrocytes in capillaries and 2) hypoxic inhibition of fetal breathing probably arises from discrete areas of the brain having a PO2 less than 3 Torr.

Animals↗
PubMed1990

Interdependence of arterial PO2 and O2 consumption in the fetal sheep.

These experiments were undertaken to measure the effects of changing arterial oxygen tension (PaO2) on oxygen use by the fetal body (VO2). Six fetal sheep at 130-140 days gestation were prepared with an endotracheal tube, carotid artery catheter, body-core thermistor, cooling coil and loosely-applied umbilical cord snare. The next day the cord was occluded and the fetal lungs were ventilated with gas mixtures containing different concentrations of oxygen. While fetal core temperature was kept constant, fetal arterial PO2 was cycled between high and low values (span = 7 to 359 mmHg, n = 103) and O2 consumption was measured by the rate of O2 uptake from a closed-rebreathing circuit. VO2 changed directly with changes in PO2 from 10 to 40 mmHg but became insensitive to changes in PO2 above about 50 mmHg. The results were well described over the entire range by the equation: VO2 (ml/min per kg fetal wt) = -9.62 + 6.99 ln PO2(mmHg)-0.66 ln2 PO2. Thus the oxygen consumption of the near-term fetal sheep varies with changes in arterial PO2 in the physiologic range. This finding is distinctly different than the adult at rest but resembles adult tissues such as exercising muscle at VO2max. This finding is consistent with differences in fetal metabolic controls, limited cardiac reserve, and limited tissue diffusion rates in actively metabolizing tissues.

Animals↗