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Biomedical subjects

O D Saugstad

Publications and source records attributed to O D Saugstad.

At least 109 records · Page 6Linked to original sources
PubMed1994

Cerebral blood flow and plasma hypoxanthine in relation to surfactant treatment.

We have previously reported reduction in EEG activity in preterm babies after tracheal instillation of Curosurf. To elucidate the cause of EEG depression, we have examined cerebral blood flow (CFB), amplitude-integrated EEG (aEEG), mean arterial blood pressure (MABP) and plasma hypoxanthine (Hx) concentration in a group of preterm babies before and immediately after administration of surfactant. No change occurred in CBF immediately after surfactant treatment despite a significant decrease in MABP. At 60 min after surfactant administration, a significant reduction in CBF occurred (p < 0.05). However, when CBF values were corrected for changes in PaCO2, no reduction in CBF was observed. Mean plasma Hx concentration was 11.6 (SD 7.3) mumol/l before surfactant therapy, which decreased significantly to 8.1 (5.8) mumol/l (p < 0.05) 15-30 min after treatment. No correlations were found between plasma Hx concentration and FiO2, a/A pO2, PaCO2, SaO2, arterial blood pressure, CBF or the degree of EEG depression. This study indicates that EEG depression observed after surfactant instillation is not caused by cerebral ischemia.

Biological Products↗
PubMed1994

Modulation of the xanthine oxidase/xanthine dehydrogenase ratio by reaction of malondialdehyde with NH2-groups.

The potential of xanthine oxidoreductase to generate oxygen radicals depends on the ratio of xanthine dehydrogenase and xanthine oxidase. Previous studies showed that the lipid peroxidation products, malondialdehyde and 4-hydroxynonenal have different effects on xanthine oxidoreductase activity. These results suggest that the activity of xanthine oxidase, but not xanthine dehydrogenase, is influenced by NH2-group modulation. We therefore investigated the influence of malondialdehyde on xanthine oxidoreductase. Malondialdehyde reacted with NH2-groups to form Schiff bases, and this reaction was associated with inhibition of xanthine oxidase; SH-groups were not affected. Malondialdehyde had no influence on the xanthine dehydrogenase activity. The inhibited xanthine oxidase was converted to an active xanthine dehydrogenase by dithiothreitol treatment. These experiments indicate the importance of NH2-groups for xanthine oxidase but not for xanthine dehydrogenase activity. Beside the well known regulation of the xanthine dehydrogenase/xanthine oxidase ratio by the redox status of SH-groups, substances reacting with NH2-groups of the xanthine oxidoreductase are also able to change the xanthine dehydrogenase/xanthine oxidase activity ratio, thereby influencing the potential to generate oxygen radicals by xanthine oxidoreductase.

Animals↗
PubMed1994

Changes in apnea and autoresuscitation in piglets after intravenous and intrathecal interleukin-1 beta injection.

UNLABELLED: Piglets were given IL-1 beta intravenously (Index I, n = 8) or intrathecally (Index II, n = 9) prior to apnea to test the hypothesis that IL-1 beta may prolong periods of apnea during sleep and infection. Apnea variables and the quality of autoresuscitation were recorded and compared to an apnea control group (Ctr. I, n = 7, apnea without injection of IL-1 beta) and a procedure control group (Ctr. II, n = 6, apnea after intratecally injected sterile water). Hypoxanthine (Hx) and xanthine (X) were analyzed in plasma, CSF and vitreous humor. The duration of apnea was significantly longer in the Index I - mean: 38, intraquartile range: 27-52 sec and Index II-group 26 (24-36) sec than in the Ctr. 1-12 (10-13) sec (p < 0.01) and the Ctr. II-group 14 (6-18) sec (p < 0.01). The number of respirations per 2 min following apnea in the Index I-group mean: 21, intraquartile range: 7-40 and was significantly less than in the Ctr. I-group 109 (39-150) (p < 0.01), while a similar tendency was found in the Index II-group 42 (27-55) (p = 0.06). IN CONCLUSION: Intravenous and intrathecal injection of IL-1 beta prolong the duration of apnea and modifies autoresuscitation.

Animals↗
PubMed1993

[Recommendations of the Council for Nutrition on infant nutrition. Norwegian National Nutrition Council].

Because of the high frequency of nursing mothers there is concensus that, in general, the diet of Norwegian newborns is good for the first six months of life. However, several publications have questioned the recommendations concerning the babies' diet from the age of six to 12 months with respect to time of weaning and introduction of cow's milk, and intake of energy, fat-soluble vitamins, iron and essential fatty acids. The Norwegian National Nutrition Council has therefore evaluated the available data, and has adjusted some of the recommendations, including the recommendations for energy intake, energy percent from fat and essential polyunsaturated fatty acids.

Breast Feeding↗
PubMed1993

[Neonatal respiratory distress syndrome treated with a natural surfactant. The Norwegian Curosurf study].

43 Norwegian premature infants with respiratory distress syndrome were randomized to receive either a high dose (initial dose 200 mg/kg) or a low dose (initial dose 100 mg/kg) of natural porcine surfactant (Curosurf). In the high dose group, up to five doses of surfactant could be given compared with three in the low dose group. In the high dose group, oxygen requirement was significantly lower during the first 36 hours after surfactant was administered than the requirement in the low dose group. There was no difference in outcome between the high and low dose groups. Outcome was poor for babies with birthweight < 750 gram or gestational age < 26 weeks, in spite of an initial favourable surfactant response in several of them. We conclude that the initial dose of Curosurf should be 100 mg/kg and two more doses can be given if necessary.

Biological Products↗
PubMed1993

Elevated beta-endorphin immunoreactivity in the cerebrospinal fluid in victims of sudden infant death correlates with hypoxanthine in vitreous humour.

Beta-endorphin (BEND) may induce respiratory depression. Elevated levels of beta-endorphin immunoreactivity (BENDI) in the CSF are found in children with apnoea and in about 50% of sudden infant death (SID) victims. Premortal hypoxia in SID victims has been indicated by elevated hypoxanthine (HX) levels in the vitreous humour (VH). In this study we correlated BENDI in CSF with HX in VH in SID victims (n = 19) and controls (n = 18). BEND in CSF was measured by RIA, and HPLC was used for identification of BENDI. HX in VH was measured by HPLC. All the SID victims had elevated levels of HX in VH. The BENDI in CSF divided the SID victims into two subpopulations (P < 0.01); one with undetectable levels (< 4.3 fmol/ml) (n = 10) and one with high levels (160-400 fmol/ml) (n = 9). In the SID subpopulation with high levels of BENDI in CSF, we found a correlation between BENDI in CSF and HX in VH (r = 0.92). Control infants who died a stressful death, such as during heart operations (n = 2), had high levels of BENDI in CSF and low levels of HX in VH. Controls who died of infections (n = 11) had low levels of BENDI in CSF and elevated levels of HX in VH. Because hypoxia in itself does not increase BENDI in CSF, increased BENDI in CSF is probably not secondary to hypoxia but may be of aetiological significance.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1993

Effect of the hypoxanthine/xanthine oxidase system on dopamine outflow from rat striatal synaptosomes.

The effect of the oxygen radical generating system, hypoxanthine/xanthine oxidase (Hx/XOD), on the spontaneous and potassium-stimulated outflow of the neurotransmitter dopamine (DA) from rat striatal synaptosomes was studied. The efficacy of some radical scavengers was also tested. DA outflow was measured by incubation of [3H]-DA prelabeled synaptosomes (P2) in Krebs-Ringer buffer, containing either normal or depolarizing K+ concentrations. The reactions were terminated by filtration of the synaptosomes through Sartorius filters. Hx/XOD increased the spontaneous DA outflow in a dose and time dependent manner. The reduction found in synaptosomal DA content could be explained by disturbances of DA uptake or reuptake. The K+ stimulated outflow was not altered by the lower doses of Hx/XOD, whereas, when very high doses of Hx/XOD were used, the K+ stimulated DA outflow was decreased. High doses of Hx/XOD may deplete the synaptosomal DA releasable pool, leaving little DA available for extra-stimulated outflow by high concentrations of K+. The K(+)-stimulated outflow of DA is a less sensitive process against radical attack than the spontaneous release of DA. A protective action of catalase, but no effect of superoxide dismutase was demonstrated in these experiments.

Animals↗
PubMed1993

Oxygen radicals stimulate thromboxane and prostacyclin synthesis and induce vasoconstriction in pig lungs.

Reactive oxygen species have earlier been shown to induce vasoactive changes. In the present investigation we hypothesized that active oxygen intermediates would stimulate arachidonic acid metabolism and thereby influence the pulmonary circulation. Four groups of 8-week old pigs were studied after infusion of an oxygen radical generator. Haemodynamic changes were recorded, and thromboxane (TX)B2 (the stable metabolite of TXA2) and 6-keto-prostaglandin (PG)F1 alpha (the stable metabolite of prostacyclin, PGI2) measured by a radioimmunoassay technique after infusion of xanthine oxidase (XO) alone or in combination with pharmacological inhibitors. In the XO group pulmonary vascular resistance increased rapidly compared to baseline levels. Maximum resistance increase was 118.4 +/- 27.5%, 25 min after the XO infusion (p < 0.05 compared to baseline). The vasoconstriction was significantly attenuated after pretreatment with the cyclo-oxygenase inhibitor indomethacin. In this group the pulmonary resistance increase was 21.2 +/- 24.3% at 25 min (p < 0.01 vs. XO group). In a group given allopurinol (xanthine oxidase inhibitor), the resistance increased by 44.3 +/- 28.8% (p < 0.02 vs. XO group), and during catalase infusion (hydrogen peroxide scavenger), the increase was 52.9 +/- 24.2% (p < 0.01 vs. XO group). Along with the pulmonary vascular pressure augmentation, we measured 1.9 fold TXB2 and 2.2 fold 6-keto-PGF1 alpha concentration increases in the XO group. However, both TXB2 and 6-keto-PGF1 alpha formation was significantly inhibited by indomethacin (p < 0.01 respectively vs. XO group), allopurinol (p < 0.01 and p < 0.05 respectively vs. XO group) and catalase (p < 0.01 and p < 0.02 respectively vs. XO group).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Hypoxanthine, xanthine, and uric acid in newborn pigs during hypoxemia followed by resuscitation with room air or 100% oxygen.

OBJECTIVE: To determine if resuscitation with room air is as effective as resuscitation with an FIO2 of 1.0. DESIGN: Prospective, randomized laboratory study. SETTING: Experimental laboratory (neonatal or delivery ward). SUBJECTS: Twenty piglets, 1 to 2 wks of age. INTERVENTIONS: Piglets were randomized into two groups. Both groups underwent hypoxemia for 2 hrs and then underwent reoxygenation for 1 hr (group 1 with an FIO2 of 1.0 and group 2 with an FIO2 of 0.21). MEASUREMENTS AND MAIN RESULTS: Hypoxanthine, xanthine, uric acid, PaO2, oxygen saturation, pH, base excess or deficit, and arterial pressure. During hypoxemia (PaO2 26 to 49 torr [3.5 to 6.5 kPa]), the mean hypoxanthine concentrations increased (p < .02) from 26.1 to 115.4 mumol/L in plasma, from 20.9 to 81.7 mumol/L in cerebrospinal fluid, and from 12.9 to 21.5 mumol/L in vitreous humor. Xanthine concentrations changed in a similar way, whereas uric acid concentrations increased only in plasma. During reoxygenation, hypoxanthine concentrations increased both in cerebrospinal fluid and in the vitreous humor. Final concentrations in these two fluid areas were 81.8 and 39.4 mumol/L, respectively (p < .02). Xanthine concentrations increased similarly. In plasma, hypoxanthine and xanthine concentrations decreased during reoxygenation. The final mean concentration of hypoxanthine was 76.8 mumol/L (p < .02). No change in plasma or cerebrospinal fluid uric acid concentrations were found during reoxygenation. The other measurements varied throughout the experiment, but no differences were found between the groups. CONCLUSIONS: There were no significant differences between the two treatment groups at any stage in the experiments. In this porcine model of hypoxemia, resuscitation with room air was as effective as was resuscitation with an FIO2 of 1.0, when circulating concentrations of oxypurines were used as an end-point.

Air↗
PubMed1993

Erythropoietin, protein, and iron supplementation and the prevention of anaemia of prematurity.

The effectiveness of recombinant human erythropoietin (r-HuEpo) in raising haemoglobin concentrations in very low birthweight infants was examined in a randomised multicentre study. Twenty nine 'healthy' appropriate for gestational age infants with birth weights 900-1400 g entered the study at 3 weeks of age. All infants received breast milk supplemented with 9 g/l human breast milk protein from 3 to 8 weeks of age. Eighteen mg iron was given daily from week 3 and was doubled if serum iron concentration fell below 16.0 mumol/l. Fourteen infants were randomised to receive 100 U/kg r-HuEpo subcutaneously three times a week from week 3 to week 7; 15 infants served as controls. After one week reticulocyte and haemoglobin concentrations were significantly higher in the r-HuEpo treated group and the haemoglobin values remained significantly higher throughout r-HuEpo treatment and at the concentrations observed in full term infants. No adverse effects were associated with the treatment. In stable very low birthweight infants with optimal iron and protein intakes, moderate dose r-HuEpo can produce significant gains in red cell production that may be clinically useful.

Anemia, Neonatal↗
PubMed1993

Cerebral blood flow and evoked potentials during reoxygenation with 21 or 100% O2 in newborn pigs.

The effects of resuscitation with 21 or 100% O2 on cerebral blood flow (CBF) and somatosensory evoked potentials (SEPs) were studied in 19 newborn pigs anesthetized with pentobarbital sodium. They were ventilated with 8% O2 until base excess reached -20 mmol/l and then were randomly reoxygenated with 21% O2 (n = 10) or 100% O2 (n = 9) for 25 min followed by 21% O2. Mean duration of hypoxemia in the two groups was 57 +/- 6 (SE) and 59 +/- 6 min, respectively. CBF determined by radioactive microspheres was significantly increased in all areas in both groups after 5 and 20 min of reoxygenation. At 5 min of reoxygenation forebrain O2 uptake (CMRo2) had increased significantly compared with baseline values in the 21% O2 group (2.5 +/- 0.1 to 3.2 +/- 0.2 ml.100 g-1.min-1) but not in the 100% O2 group. There were, however, no significant differences between the two groups in CBF or CMRo2 at any time, and by 60 min of reoxygenation both had returned to baseline levels. SEPs were not significantly different in the two groups. We conclude that, as judged by CBF, CMRo2, and SEP, 21% O2 is not inferior to 100% O2 when hypoxemic newborn pigs are reoxygenated.

Animals↗
PubMed1993

Hypoxanthine, xanthine, and uric acid concentrations in plasma, cerebrospinal fluid, vitreous humor, and urine in piglets subjected to intermittent versus continuous hypoxemia.

Infants with sudden infant death syndrome have higher hypoxanthine (Hx) concentrations in their vitreous humor than infants with respiratory distress syndrome and other infant control populations. However, previous research on piglets and pigs applying continuous hypoxemia has not been able to reproduce the concentrations observed in infants with sudden infant death syndrome. To test whether intermittent hypoxemia could, in part, explain this observed difference, Hx, xanthine (X), and uric acid were measured in vitreous humor, urine, plasma, and cerebrospinal fluid in newborn piglets during intermittent hypoxemia (IH) or continuous hypoxemia (CH) of equal degree and duration. Urinary Hx excretion was significantly higher (p < 0.04) in the IH group after 60 min of hypoxemia. The vitreous humor Hx increase was significantly higher in the IH group (from 21.0 +/- 7.8 to 44.1 +/- 25.5 mumol/L, p < 0.01 versus baseline) than in the CH group (from 16.4 +/- 4.2 to 23.2 +/- 7.3 mumol/L, p < 0.05 versus baseline) (p < 0.05 IH versus CH). X increased significantly more (p < 0.05) in vitreous humor in the IH group than in the CH group. No differences between the two groups were found in plasma and cerebrospinal fluid for either Hx, X, or uric acid. We conclude that vitreous humor Hx and X increases more during IH than during CH.

Animals↗
PubMed1993

Resuscitation of asphyxic newborn infants with room air or 100% oxygen.

To test the hypothesis that room air is superior to 100% oxygen when asphyxiated newborns are resuscitated, 84 neonates (birth weight > 999 g) with heart rate < 80 and/or apnea at birth were allocated to be resuscitated with either room air (n = 42) or 100% oxygen (n = 42). Serial, unblinded observations of heart rates at 1, 3, 5, and 10 min and Apgar scores at 1 min revealed no significant differences between the two groups. At 5 min, median (25th and 75th percentile) Apgar scores were higher in the room air than in the oxygen group [8 (7-9) versus 7 (6-8), p = 0.03]. After the initial resuscitation, arterial partial pressure of oxygen, pH, and base excess were comparable in the two groups. Assisted ventilation was necessary for 2.4 (1.5-3.4) min in the room air group and 3.0 (2.0-4.0) min in the oxygen group (p = 0.14). The median time to first breath was 1.5 (1.0-2.0) min in both the room air and oxygen groups (p = 0.59), and the time to first cry was 3.0 (2.0-4.0) min and 3.5 (2.5-5.5) min in the room air and oxygen groups, respectively (p = 0.19). Three neonates in the room air group and four in the oxygen group died in the neonatal period. At 28 d, 72 of the 77 surviving neonates were available for follow-up (36 in each group), and none had any neurologic sequelae.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1993

Post-mortem concentrations of hypoxanthine in the vitreous humor--a comparison between babies with severe respiratory failure, congenital abnormalities of the heart, and victims of sudden infant death syndrome.

Post-mortem hypoxanthine concentrations in the vitreous humor of human infants were investigated. Hypoxanthine is formed from hypoxic degradation of adenosine monophosphate. The concentrations in the vitreous humor can give information about antemortem hypoxia. The post-mortem levels were corrected for the time elapsing between death and the autopsy. Four groups of infants were compared: 17 babies who died of respiratory distress syndrome (RDS), 72 infants who died of sudden infant death syndrome (SIDS), 23 children dying of congenital heart disease (both cyanotic and acyanotic), and 15 children dying acutely in accidents without any known significant time of hypoxia before death. The corrected, median hypoxanthine levels in victims of SIDS (200 mumol/L) was significantly higher (p < 0.01) than in the accident group (0 mumol/L), but no clear difference was found between the SIDS group and the RDS group (101 mumol/L), or the heart group (54 mumol/L). A number of children with "normal" hypoxanthine levels (0 to 38 mumol/L) were found in all four groups, but the numbers were significantly lower (p < 0.005) in the RDS, SIDS and heart groups than in the accident group. It is concluded that SIDS is probably not a sudden event, but may be preceded by relatively long, or repeated intermittent periods of hypoxia (of unknown etiology).

Heart Defects, Congenital↗
PubMed1993

Transport of hypoxanthine from plasma to cerebrospinal fluid and vitreous humor in newborn pigs.

To determine whether an elevated level of hypoxanthine in cerebrospinal fluid or vitreous humor might reflect a high plasma hypoxanthine concentration, or whether it necessarily represents local tissue hypoxia, we infused hypoxanthine intravenously to normoxemic and normotensive piglets (n = 6). Hypoxanthine was measured in different body fluids using HPLC. During the 8 hours of infusion hypoxanthine increased in plasma (from 30 +/- 6 mumol/l (mean +/- SD) before the infusion to 68 +/- 20 mumol/l at the end of the infusion, p < 0.01), cerebrospinal fluid (CSF) (19 +/- 8 to 43 +/- 9 mumol/l, p < 0.05) and vitreous humor (15 +/- 5 to 30 +/- 6 mumol/l, p < 0.05). After infusion, hypoxanthine values in all three fluids were similar to those seen in pigs after severe hypoxia. Hypoxanthine in vitreous humor and plasma were significantly correlated (r = 0.80, 95% confidence interval 0.47-0.93, p < 0.001). Urinary excretion of hypoxanthine increased almost 40 times from 0.12 +/- 0.14 to 4.6 +/- 2.9 mumol/kg/h indicating that renal excretion of hypoxanthine is not achieved just by passive filtration. We conclude that in newborn piglets hypoxanthine can pass from plasma to CSF and vitreous humor. Thus an increased CSF hypoxanthine concentration is not definite proof that significant cerebral hypoxia has occurred.

Animals↗