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Biomedical subjects

G G Power

Publications and source records attributed to G G Power.

At least 19 recordsLinked to original sources
PubMed1998

Brain temperature and metabolic responses during umbilical cord occlusion in fetal sheep.

The purpose of this study was to compare core body and brain temperatures after complete but intermittent occlusions of the umbilical cord. Thermocouple probes were placed in the parasagittal parietal cortex, ascending aorta, and jugular vein of eight near-term fetal sheep and in the maternal descending aorta. Three days later, after an initial control period, the umbilical cord was occluded for 5 min, followed by a 30-min recovery period, and this cycle was repeated 4 times. Temperature changes, blood gases, and plasma glucose, lactate and adenosine were measured. In the first occlusion period, body core temperature increased 0.12 degreesC over control, and then declined to baseline after cord release, and this pattern was repeated with subsequent occlusions. Brain temperature, however, did not increase in response to any of the cord occlusions. Plasma adenosine increased 2.4-fold during the first occlusion, but not during subsequent occlusions, despite a continuing pattern of constant brain temperature, a result which minimizes adenosine's importance as a continuing regulator of cerebral metabolism. We conclude that brain temperature fails to increase because of diminished heat production by the brain and increases in cerebral blood flow, responses which delay complete depletion of adenosine 5'-triphosphate stores in brain tissue.

Acidosis, Respiratory↗
PubMed1998

Evidence for mechanisms of the acute-phase response to endotoxin in late-gestation fetal goats.

OBJECTIVE: The aim of this study was to evaluate the relationship between febrile response to fetal endotoxin administration and fetal plasma endogenous pyrogen, tumor necrosis factor-alpha, the possible putative pyrogen mediator prostaglandin E2, and the endogenous antipyretic arginine vasopressin in late-gestation pregnant goats. STUDY DESIGN: Changes in fetal core temperature, plasma tumor necrosis factor-alpha, prostaglandin E2, and arginine vasopressin levels were measured after administration of Escherichia coli endotoxin (70 microg/kg of fetal weight) to 10 fetal goats in late gestation. RESULTS: Fetal body temperature did not rise after endotoxin administration. Fetal plasma tumor necrosis factor-alpha and arginine vasopressin increased to 87.5 +/- 15.2 pg/mL and 25.1 +/- 4.8 pg/mL, respectively, after 1 to 2 hours (P < .05). Fetal plasma prostaglandin E2 levels did not change significantly throughout the study. CONCLUSION: The absence of a febrile response to endotoxin in late-gestation fetal goats is accompanied by a deficient responses in prostaglandin generation in the periphery and increased activity of the antipyrogen arginine vasopressin.

Acute-Phase Reaction↗
PubMed1997

Plasma adenosine responses during repeated episodes of umbilical cord occlusion.

OBJECTIVE: The purpose of this study was to measure changes in adenosine concentration in fetal arterial blood with use of an animal model of intermittent cord occlusion. Adenosine has been shown to be a potent vasodilator and inhibitor of metabolic processes in the adult, actions that help maintain a balance between oxygen supply and oxygen use. STUDY DESIGN: After a 30-minute control period, five chronically instrumented fetal sheep (125 +/- 2.2 days' gestation) were subjected to a 1-minute cord occlusion, followed by a 2-minute recovery. The occlusion-release cycle was repeated 20 times. Then, after a 1-hour interim, the same 20 cycles of occlusion were repeated. Fetal blood was collected during cord occlusion and 30 seconds after release. RESULTS: The plasma adenosine concentration averaged 0.82 +/- 0.19 mumol/L during the initial control period. The plasma adenosine concentration increased significantly to 1.06 +/- 0.23 mumol/L and 1.19 +/- 0.20 mumol/L during and after the fifth occlusion (p < 0.05 and 0.01, respectively). The plasma adenosine concentration reached a maximal level of 1.31 +/- 0.28 mumol/L after the twentieth cord occlusion. The concentration during the second group of occlusions was also higher than that during the control period (p < 0.05) but not higher than that during the first recovery period. By the conclusion of the study the plasma adenosine concentration had returned to 0.70 +/- 0.16 mumol/L. CONCLUSIONS: Plasma adenosine increases cyclically with intermittent cord occlusion in the near-term fetal sheep, but the response is attenuated or lost after 2 hours. These results together with those of earlier studies are consistent with a hypoxic protective action of adenosine that is largely restricted to early time periods of continuing intermittent hypoxia.

Adenosine↗
PubMed1997

Engine and radiator: fetal and placental interactions for heat dissipation.

The 'engine' of fetal metabolism generates heat (3-4 W kg-1 in fetal sheep) which has to be dissipated to the maternal organism. Fetal heat may move through the amniotic/allantoic fluids to the uterine wall (conductive pathway; total conductance, 1.1 W degrees C-1 kg-1) and with the umbilical arterial blood flow (convective pathway) to the placenta. Because resistance to heat flow is larger than zero fetal temperature exceeds maternal temperature by about 0.5 degree C (0.3-1 degree C). Probably 85% of fetal heat is lost to the maternal organism through the placenta, which thus serves as the main 'radiator'. Placental heat conductivity appears to be extremely high and this may lead to impaired heat exchange (guinea-pig placenta). A computer simulation demonstrates that fetal temperature is essentially clamped to maternal temperature, and that fetal thermoregulatory efforts to gain thermal independence would be futile. Indeed, when the late gestational fetus in utero is challenged by cold stress, direct and indirect indicators of (non-shivering) thermogenesis (oxygen consumption, increase of plasma glycerol and free fatty acid levels) change only moderately. In prematurely delivered lambs, however, cold stress provokes summit metabolism and maximum heat production. Only when birth is imitated in utero (by cord clamping, external artificial lung ventilation and cooling) do thermogenic efforts approach levels typical of extra-uterine life. This suggests the presence of inhibitors of thermogenesis of placental origin, e.g. prostaglandins and adenosine. When the synthesis of prostaglandins is blocked by pretreatment with indomethacin, sheep fetuses react to intra-uterine cooling with vigorous thermogenic responses, which can be subdued by infusion of prostaglandin E2 (PGE2). Since the sheep placenta is known to produce sufficient amounts of PGE2, it seems that the placenta controls fetal thermogenic responses to some extent. This transforms the fetus into an ectothermic organism, and yet allows the newborn the full exploitation of thermoregulatory responses typical of endothermic animals.

Animals↗
PubMed1997

Improved method for single-bolus kinetic measurements using a noncleared reference indicator.

After intravenous injection of a tracer as a single bolus, its concentration decreases as it mixes with the plasma, disperses throughout the circulation, and enters body pools. Kinetic values that are dependent on early concentrations may be in considerable error because mixing is not instantaneous throughout the circulation, and this problem is particularly acute in the mammalian fetus, with its distinctive circulatory pattern. To minimize this error, a method was developed in which the noncleared reference tracer 125I-labeled albumin was injected together with a representative, rapidly cleared metabolite 14C-labeled palmitic acid, and the former was used to correct for mixing delay. A total of 19 disappearance curves were studied after intravenous injection into seven near-term fetal sheep. Kinetic values were calculated with and without correction for mixing delay. Taking account of mixing delay increased the calculated volume of distribution 41% [from 44 +/- 4 (SE) to 62 +/- 3 ml/kg, P < 0.001], increased plasma clearance rate 13% (from 41 +/- 2 to 47 +/- 1 ml-min-1.kg-1, P < 0.002), decreased the rate constant for irreversible loss 26% (from 1.05 +/- 0.07 to 0.78 +/- 0.04 min-1, P < 0.001), and increased the calculated effective half-life 26% (0.71 +/- 0.06 to 0.90 +/- 0.05 min, P < 0.001). Thus use of the additional reference marker significantly altered calculated results and provided values believed to more accurately describe rapid disappearance from the central mixing compartment into metabolic pools.

Animals↗
PubMed1997

Fetal plasma hypoxanthine level in growth-retarded fetuses before labor.

Hypoxanthine is one of the purine nucleotides and is presumed to accumulate during hypoxia and acidemia. It remains uncertain, however, whether plasma hypoxanthine concentration is a useful indicator of fetal asphyxia; and its relationship to other markers of fetal physiologic state is not clearly defined. The aim of this study was to evaluate whether the level of fetal plasma hypoxanthine is correlated with fetal hypoxia and acidosis in growth-retarded fetuses before the onset of labor. Cordocentesis was performed in 34 growth-retarded fetuses at 31-35 weeks' gestation for the measurement of umbilical venous plasma concentrations of hypoxanthine, hemoglobin and lactate concentrations, blood gases, and base deficit. Umbilical venous plasma hypoxanthine concentration was found to be increased significantly, in parallel with the degree of acidosis (r = -0.74, P < 0.05) and base deficit (r = -0.41, P < 0.05), but not to bear a significant relationship to the degree of hypoxemia or other measured variables. We conclude that increases in the plasma concentration of hypoxanthine may reflect an impaired physiological state in growth-retarded fetuses before labor.

Acid-Base Equilibrium↗
PubMed1996

The relationship between uterine artery Doppler velocimetry and umbilical venous adenosine levels in pregnancies complicated by preeclampsia.

OBJECTIVE: The aim of this study was to evaluate the relationship between uteroplacental circulatory insufficiency and the fetoplacental release of adenosine in pregnancies complicated by preeclampsia. STUDY DESIGN: We performed uterine artery Doppler velocimetry and calculated the pulsatility index of the uterine artery, to detect uteroplacental circulatory insufficiency, immediately before cordocentesis in 39 pregnant women complicated by preeclampsia. Umbilical venous blood obtained by cordocentesis was then analyzed for blood gases, pH, and plasma adenosine levels. Increased plasma adenosine was taken to signal its increased release from the placenta and fetus relative to its rate of disappearance. RESULTS: The mean umbilical venous plasma adenosine level in the abnormal pulsatility index group was 1.78 +/- 0.17 mumol/L (mean +/- SEM, n = 25), significantly higher than in the normal pulsatility index group 0.58 +/- 0.14 mumol/L (n = 14, p < 0.001). Furthermore, in the abnormal pulsatility index group the elevation of plasma adenosine levels in the umbilical vein was found even in normoxic fetuses. CONCLUSION: Fetal plasma adenosine increases before uteroplacental circulatory insufficiency becomes severe enough to cause generalized fetal hypoxemia. We postulate that enhanced adenosine formation in the fetus, umbilical cord vessels, and particularly the placenta may, at least in part, contribute to control and maintenance of placental blood flow.

Adenosine↗
PubMed1996

Maternal theophylline administration and breathing movements in late-gestation human fetuses.

OBJECTIVE: To investigate the relation between maternal administration of theophylline and breathing movements during late gestation in human fetuses. METHODS: After a 1-hour control period, 17 women with normally grown fetuses at 33-38 weeks' gestation were given 400 mg of sustained-release theophylline orally. Maternal plasma theophylline and glucose concentrations were measured every hour, and the incidence of fetal breathing movements and breathing rates were measured continuously during the next 8 hours. Results were compared with those of a similar control group that did not receive theophylline. RESULTS: The maternal plasma theophylline concentration increased to detectable levels after 1 hour, reached therapeutic levels of 6.9 +/- 0.4 micrograms/mL (standard error of the mean) after 6 hours, and thereafter averaged 8.3 +/- 0.3 micrograms/mL, significantly higher than initial control values (P < .05). The mean glucose concentration was unchanged during the first 6 hours (79.2 +/- 1.1 mg/dL) and then decreased somewhat, averaging 75.8 +/- 1.1 mg/dL in the 7-8 hour period. The incidence of fetal breathing increased 26.4 +/- 1.9% after 5 hours and remained elevated during the next 3 hours at levels significantly higher than in the initial control period (P < .05) and higher than in the control group that did not receive theophylline. The mean hourly breathing rate averaged 40.9 +/- 1.3 breaths per minute after ingestion of theophylline, a nonsignificant change. CONCLUSIONS: Ingestion of theophylline by pregnant women in late gestation is associated with an increase in fetal breathing movements. Theophylline has been used widely in the management of asthma in pregnancy, and the assessment of fetal breathing movements is used routinely for evaluation of fetal status. Therefore, account must be taken of changes in breathing movements caused by maternal theophylline administration.

Adult↗
PubMed1996

Autoradiographic analysis of expanded skeletal muscle in rats.

The use of tissue expanders in reconstructive surgery is now common. However, the physiologic mechanisms by which expansion is achieved are not well understood. A recent study demonstrated that rapid expansion of skeletal muscle is accompanied by an increase in the number of sarcomeres within a muscle fiber. This is in contrast to previous animal studies whose results suggested that synthesis of sarcomere units was limited to the perinatal period. To further investigate potential increases in sarcomeres and attempt to localize the active sites of sarcomere synthesis, labeled adenosine (3H) was injected into rats during the expansion of skeletal muscle. Adenosine was taken up by the muscle fibers and incorporated in the newly formed actin as part of light chains. An autoradiographic analysis of histologic sections of the expanded muscle demonstrated a statistically significant increase in radioactivity within the expanded muscle. The distribution of the radioactivity followed a proximal-to-distal gradient, with the proximal sections exhibiting more than 50 percent greater activity than the distal aspects. These data suggest a preference for sarcomere synthesis in the proximal portion of the expanding skeletal muscle. The significance of this finding is uncertain. However, we suspect that sarcomere synthesis is tension-dependent and likely to be related to local tension applied to a portion of the muscle fibers rather than to an anatomic site of preference.

Animals↗
PubMed1996

Exogenous infusion of adenosine depresses whole body O2 use in fetal/neonatal sheep.

To examine a possible metabolic regulatory role for adenosine, infusions of adenosine and adenosine deaminase were given to 11 near-term fetal sheep during the simulation of birth in utero. Fetal arterial blood gases, the concentration of a number of metabolites, insulin, and whole body O2 consumption (VO2) were measured. After intrauterine ventilation and cord occlusion, fetal/neonatal VO2, measured by closed-circuit respirometry, averaged 11.0 +/- 1.1 (SE) ml (STPD).min-1.kg fetal wt-1 and plasma adenosine concentration ([Ado]) was 1.29 +/- 0.21 microM. Infusion of adenosine (1.5 mumol.min-1.kg-1) during the next 30-min interval increased [Ado] to 1.57 +/- 0.28 microM (not significant) and decreased VO2 to 7.7 +/- 0.5 ml.min-1.kg-1 (P < 0.05). The infusion reduced systolic blood pressure by 19% (P < 0.01) and diastolic blood pressure by 25% (P < 0.01) and increased heart rate by 19% (P < 0.01). At the highest rate of adenosine infusion studied (6 mumol.min-1.kg-1), [Ado] increased to 4.27 +/- 0.46 microM (P < 0.001) and VO2 did not measurably decline further, although there were further decreases in blood pressure and increases in heart rate. After administration of adenosine deaminase, [Ado] decreased to 0.58 +/- 0.13 microM (P < 0.05), whereas VO2 increased to 11.2 +/- 0.8 ml.min-1.kg-1 (P < 0.05); blood pressure and heart rate returned to basal levels. The dependence of VO2 on [Ado] is described by the relationship VO2 = 6.14 + 4.89 exp(-0.45[Ado]) (n = 144; r = 0.34; P < 0.001). Throughout the experiment, arterial O2 content and plasma glucose, lactate, glycerol, and fatty acid concentrations were normal or elevated, and, therefore, O2 lack and substrate deficiency were unlikely to have caused the reduction in VO2. We conclude that plasma adenosine may act as a messenger of energy status for the ovine fetus/neonate and may contribute thereby to a maintenance of a balance between O2 supply and O2 demand.

Adenosine↗
PubMed1996

Suppressive action of endogenous adenosine on ovine fetal nonshivering thermogenesis.

Nonshivering thermogenesis is not initiated when the fetal sheep is cooled in utero but appears to require the removal of an inhibitor of placental origin at birth. To test whether adenosine is such an inhibitor, we examined the effect of the adenosine antagonist theophylline on the initiation of nonshivering thermogenesis during sequential cooling, ventilation, and umbilical cord occlusion in utero. Theophylline (18 mg/kg bolus and 0.6 mg.kg-1.min-1 thereafter) was infused for 90 min before and 90 min after cord occlusion. Theophylline enhanced the nonshivering thermogenic free fatty acid (FFA) and glycerol responses before cord occlusion, raising FFA concentrations 99% to 415 +/- 60 mueq/l (P < 0.01) and glycerol levels 87% to 526 +/- 135 mumol/l (P < 0.05). These FFA (P < 0.001) and glycerol (P < 0.05) concentrations were significantly greater than the corresponding period during the birth-simulation control. Umbilical cord occlusion did not alter FFA levels but induced a 41% rise in glycerol concentrations to 774 +/- 203 mumol/l (P < 0.05). The increases in nonshivering thermogenic indexes after the administration of the adenosine-receptor antagonist suggest that the quiescent state of ovine fetal brown adipose tissue may result, in part, from the tonic inhibitory actions of adenosine and that a decrease in adenosine concentrations enhances nonshivering thermogenesis. However, the further rise after umbilical cord occlusion suggests that at least one other inhibitor of placental origin inhibits nonshivering thermogenesis before birth.

Adenosine↗
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↗