摘要:

A transfontanellar range-gated ultrasound Doppler technique for recording blood flow velocity in an artery on the base of the skull was validated in eight anesthetized newborn lambs during hypo-, normo-, and hypercarbia. Blood flow velocity was linearly related to PaCO2from 20 to 80 mm Hg; mean blood flow velocity (Vmean) (r= 0.86,p< 0.001), peak systolic blood flow velocity (r0.83,p< 0.001), and end-diastolic blood flow velocity (r0.87,p< 0.001). Vmean changed 2.0% per mm Hg of PaCO2. A linear relationship was demonstrated between brain blood flow (BBF), as determined by the microsphere method, and PaCO2(r= 0.91,p< 0.001), with BBF changing 3.6%/mm Hg of PaCO2. Blood flow velocity was linearly related to BBF in the PaCO2range studied; Vmean (r= 0.89,p< 0.001), peak systolic blood flow velocity (r= 0.87,p< 0.001), and end-diastolic blood flow velocity (r= 0.87,p< 0.001). However, Vmean predicted only approximately 55% of the change in BBF, which suggests a concomitant change in the cross-sectional area of the artery being studied. Despite this limitation, these data suggest that blood flow velocity, recorded by a transfontanellar range-gated Doppler technique from one of the two main arteries perfusing the brain, provides qualitative information on changes in BBF. (Pediatr Res24:423–426, 1988)

ISSN:0031-3998    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Pancreatic acini of control and reserpine-treated rats were incubated with the isotopic tracer36Cl to compare Cl accumulation in the absence and presence of secretagogues and transport inhibitors. Two phases of Cl accumulation were ascertained in resting control cells: an initial rate (0–5 min) and a steady state level (10–30 min) of accumulation. Both phases were enhanced by acetylcholine (1 μM) and caerulein (10 nM), but not by 10 nM vasointestinal peptide or 10 μM forskolin. Exposure to 1 mM DIDS (4,4‘-diisothiocyano-2,2’-stilbene disulfonic acid) inhibited both phases of Cl accumulation, whereas exposure to 1 mM amiloride had a delayed effect on the initial rate and reduced the steady state phase in both resting (unstimulated) or acetylcholine-stimulated cells. Furosemide (1 mM) had no effect on Cl accumulation when added to the cells just before tracer, but reduced it when added 10 min before. Neither the initial phase nor the steady state level of Cl accumulation were enhanced by acetylcholine in acini of reserpine-treated rats and the effect of DIDS on the initial phase was smaller than in control cells. Continued exposure to this inhibitor resulted, furthermore, in a significantly larger steady state Cl content. The inhibitory effects of amiloride and of a 10-min preincubation with furosemide were similar to those observed in control cells. These results sanest that Cl accumulates in rat pancreatic acini by way of DIDS-sensitive mechanisms that are activated by Ca2+-mediated, but not by cAMP-mediated, secretagogues. These mechanisms are altered in acini of reserpine-treated rats. Those responsible for the early (initial) phase are made insensitive to secretagogues but retain some sensitivity to DIDS. Mechanisms responsible for the maintenance of the steady state level are also altered as suggested by the paradoxical effect of DIDS. As this inhibitor blocks Cl conductances and Cl/HCO3exchange, either or both of these transport mechanisms may be altered after chronic reserpine. This alteration can explain the reduced in vivo pancreatic fluid secretion observed in the treated animals, as pancreatic fluid secretion is Cl-dependent in the rat. The reserpine-treated rat is an experimental model of cystic fibrosis and a similar defect in Cl transport may also underlie the reduced pancreatic fluid secretion observed in this disease. A generalized defect in Cl transport may be present in exocrine cells of CF patients and of the animal model, involving alterations in the interaction of membrane transport mechanisms with regulatory molecules activated by tissue-specific second messengers. (Pediatr Res24: 427–432, 1988)

ISSN:0031-3998    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Membrane lipid fluidity was reexamined in red blood cells and ghosts from adults and newborns. Fluorescence anisotropies of the hydrophobic probes 1,6-diphenyl-1,3,5-hexatriene (DPH) and perylene were significantly and substantially greater in fresh intact red cells from newborns than from adults; however, no significant difference was detected with the polar fluorophores, 12-(9-anthroyl) stearic acid and retinol. These results suggest that probes in the hydrophobic core of the membrane have less motional freedom in red cells from newborns than from adults, whereas probe motional freedom in the polar lipid headgroup regions of the membranes is similar for both cell types. DPH fluorescence anisotropy increased upon making white ghosts or upon storage of blood. Temperature studies indicated that DPH fluorescence anisotropy in fresh intact neonatal red cells is increased by an amount corresponding to that produced by cooling adult red cells by 22° C. Elevated intracellular calcium decreased red cell filterability without affecting DPH fluorescence anisotropy of ghost membranes. This result suggests that the effect of calcium in reducing filterability is independent of alterations in membrane lipid motional freedom. It is unlikely that the decreased lipid motional freedom of red cells from newborns contributes significantly to their decreased filterability. (Pediatr Res24: 433–437, 1988)

ISSN:0031-3998    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Previous studies show an inability of the skeletal muscle cell and red blood cell to maintain sodium, potassium, and calcium homeostasis during hemorrhagic shock in adults. However, there is no information on the cellular effects of shock in the neonate. This study examined the effects of hemorrhagic shock on red cell membrane function in a newborn canine model. Changes in sodium, potassium, calcium, and magnesium concentrations in red blood cells and plasma were correlated with changes in intracellular and plasma ATP levels. Newborn dogs (n= 36), 10 to 14 days of age and weighing 501 to 707 g, were studied. After baseline studies (blood pressure, heart rate, temperature), electrolyte and ATP concentrations in red blood cells and plasma were measured. The dogs were then bled 40% of their estimated blood volumes. All parameters were measured after 1 h of shock. This shock model produced hypotension, bradycardia, and acidosis. The red blood cell sodium, calcium, water, and ATP content increased in shock, whereas intracellular magnesium fell. Red blood cell potassium levels, plasma sodium, and calcium concentrations were not significantly altered in shock, although plasma potassium and magnesium levels rose. Our data show that shock in the newborn disrupts cell membrane integrity. Intracellular accumulation of sodium and calcium occurred despite cellular ATP uptake, suggesting that high energy deficits are not the primary mechanism contributing to electrolyte imbalance in newborn shock. (Pediatr Res24: 438–441, 1988)

ISSN:0031-3998    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Membrane properties associated with chemoattractant-mediated cellular responsiveness of neonatal polymorphonuclear leukocytes (PMN) were analyzed using n-formylmethionyl-leucyl-phenylalanine. Inasmuch as aliphatic alcohols as a membrane fluidizer can enhance the chemoattractant binding and affect subsequent cellular responsiveness in adult PMN, neonatal PMN were studied for such properties by their treatment with iso-propyl alcohol, an aliphatic alcohol. The alcohol (p< 0.01). Although the aliphatic alcohol enhanced the membrane fluidity of adult PMN, it did not affect the membrane fluidity of neonatal PMN. We conclude that there is abnormal membrane fluidity as a cause of impaired functional dynamics of the chemoattractant receptors, which appears to underlie the defective modulation of cell functions by the membrane fluidizer in neonatal PMN. (Pediatr Res24: 442–446, 1988)

ISSN:0031-3998    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

This study was undertaken to estimate the extent of molecular defects in the mitochondrial electron-transfer chain of a patient with mitochondrial myopathy. Biochemical and immunochemical studies were performed on the skeletal muscle mitochondria. Spectrophotometry and enzyme activity measurements localized a definite defect at the segment of cytochromecoxidase (complex IV) of the electron-transfer chain. Immunoblotting and immunoprecipitation studies using the anti-complex IV antibody revealed that the contents of subunits 1, 4, 5, 6, and 7 of complex IV were markedly diminished and that subunit 2 was almost absent. Inummohistochemistry of the muscle tissue revealed a considerable accumulation of immunoreactive materials of complex IV in the ragged-red fibers. The immunoblots using the anti-NADH-ubiquinone oxidoreductase antibody demonstrated that the contents of NADH-ubiquinone oxidoreductase subunits were 47% of control and that the contents of three subunits were considerably decreased. The contents of ubiquinol-cytochromecoxidoreductase subunits were also somewhat low (77% of control) and one of the minor contaminants detected in the control was completely absent. High-resolution one-dimensional sodium dodecyl sulfate-urea-gel electrophoresis disclosed that six additional unidentified polypeptides in the control were markedly diminished or completely missing. These results demonstrate that the molecular defects in the mitochondrial electron-transfer chain are more extensive than would be expected from either spectral analysis or enzyme activity measurements alone, and involve not only complex IV but also NADH-ubiquinone oxidoreductase and ubiquinol-cytochromecoxidoreductase and several unidentified mitochondrial proteins. (Pediatr Res24: 447–454, 1988)

ISSN:0031-3998    

出版商:OVID    

年代:1988

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

The oxidation of [U-14C]succinic semialdehyde to14CO2has been investigated in cultured lymphoblasts to develop a whole cell assay for succinic semialdehyde dehydrogenase. We have previously demonstrated deficiency of this enzyme in extracts of white cells derived from 13 patients with 4-hydroxybutyric aciduria. Major goals were the demonstration of greater residual succinic semialdehyde dehydrogenase activity in patient cell lines and the better representation of physiologyin vivo.In 18 control lymphoblast lines, the conversion of [U-14C]succinic semialdehyde to14CO2was 1579 ± 310 dpm. The mean value in lymphoblasts derived from 11 patients with deficiency of succinic semialdehyde dehydrogenase was 112 ± 36 dpm approximating 7% of the mean control value. Analysis of organic acids produced from [U-14C]succinic semialdehyde in control lymphoblasts indicated that14CO2emanated from the tricarboxylic acid cycle; the major metabolic products were succinic and lactic acids. In the presence of 5mM malonic and 2-propylpentanoic (valproic) acids,14CO2production in a control lymphoblast fine was decreased by 68 and 45%, respectively. The whole cell assay is less laborious than our previously described assay employing cell extracts, and the general trend was the demonstration of higher residual levels of activity for lymphoblasts derived from patients. (Pediatr Res24: 455–460, 1988)

ISSN:0031-3998    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

The peak amplitude of pulsatile cerebral electrical impedance (ΔZ) was compared with simultaneous133xenon clearance estimations of cerebral blood flow (CBF) on 28 occasions in nine infants receiving assisted ventilation who had changes in PaCO2and thereby presumably in cerebral blood flow. Percentage changes from one measurement to the next in each infant were compared. Using linear regression the relationship was ΔZ = 0.5 CBF – 1.5 withr= 0.67. The 95% confidence interval for the regression coefficient was 0.2–0.8 and the mean residual was 28%. Changes in cerebral blood flow in these clinical conditions were similarly detected by the two methods but ΔZ underestimated the magnitude of the change in comparison with CBF and its accuracy was insufficient to allow conclusions about the magnitude of small changes in cerebral blood flow in individual infants. (Pediatr Res24:461–464, 1998)

ISSN:0031-3998    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

The use of glucocorticoids in the management of neonatal respiratory distress syndrome may be associated with abnormalities of growth and neurologic development. In our study, pregnant rats received either 2 or 0.2 mg/kg of dexamethasone on gestational days 17, 18, and 19 and tissues of the offspring were examined for ornithine decarboxylase activity, a marker enzyme for perturbations of cellular maturation. Acutely, the higher dose of dexamethasone suppressed ornithine decarboxylase activity in all tissues except lung, where a short-term stimulation was obtained. Repeated administration of 2 mg/kg resulted in an ornithine decarboxylase pattern consistent with delayed cellular development in all tissues (suppressed activity followed by prolonged postnatal elevations), accompanied by impaired viability and general growth. Lowering the dose of dexamethasone to 0.2 mg/kg eliminated all the adverse effects on viability but still produced perturbations of tissue ornithine decarboxylase, most notably a prolonged suppression of activity across all brain regions. These data suggest that administration of glucocorticoids even at the threshold for effects on respiratory function, may compromise neural development. (Pediatr Res24: 465–469, 1988)

ISSN:0031-3998    

出版商:OVID    

年代:1988

数据来源: OVID