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Biomedical subjects

O D Saugstad

Publications and source records attributed to O D Saugstad.

At least 91 records · Page 5Linked to original sources
PubMed1995

[Screening of newborn infants in Norway for severe metabolic disease].

The objective of neonatal screening for phenylketonuria and congenital hypothyroidism is early diagnosis and initiation of treatment to prevent brain damage and mental retardation. We present the results of the Norwegian national neonatal screening programme for phenylketonuria and congenital hypothyroidism. Screening for phenylketonuria based on serum phenylalanine determinations started in 1967 and covered the whole country in 1978. National screening for congenital hypothyroidism started in 1979. One hundred children with phenylketonuria and 280 children with a strong indication of congenital hypothyroidism have been detected up to 1 October 1994. Screening-related challenges and principles of treatment are discussed.

Congenital Hypothyroidism↗
PubMed1995

[Neonatal screening for metabolic diseases--a task without priority in the Norwegian health policy?].

The Norwegian national screening programme for early diagnosis of phenylketonuria and congenital hypothyroidism was established in 1978-79. The organization and implementation of the programme is based on a marginal cost policy profile and has kept almost the same structure throughout the period of national neonatal screening. We focus on practical measures aimed at increasing the quality of the programme, and suggest a health political reconsideration of public preference and financial support for neonatal screening in Norway.

Congenital Hypothyroidism↗
PubMed1995

Changes in the concentration and distribution of immunoglobulin-producing cells in SIDS palatine tonsils.

Seventeen sudden infant death syndrome (SIDS) cases and 9 controls, were examined immunohistochemically with regard to the presence of IgA-, IgM-, IgD, and IgG, as well as for the subtypes IgG1-, IgG2-, IgG3-, and IgG4-immunocytes. Differences in compartmentalization were also investigated. Differences were demonstrated between SIDS and controls in total number of IgG cells per 0.1 mm2 tissue area (median: 18.3, range: 12.3-30.2 versus median: 6.3, range: 2.0-14.6) (p < 0.01), and for IgA immunocytes (median: 3.9, range: 2.4-5.0 versus median: 1.5, range: 1.1-3.7) (p < 0.05), while no differences were demonstrated for IgM cells (median: 1.8, range: 1.2-3.3 versus median: 1.8, range: 0.7-5.6) or IgD cells (median: 1.9, range: 0.8-2.9 versus median: 1.6, range: 0.7-2.4). Differences were demonstrated between SIDS and control IgG plasma cells in all the four palatine tonsillar compartments; germinal centre (p < 0.01), mantle zone (p < 0.05), interfollicular area (p < 0.01) and reticular epithelium (p < 0.01). Furthermore, the number of IgA cells was higher in SIDS vs. controls in both the germinal centre (median: 1.4, range: 0.6-2.1 versus median: 0.6, range: 0.3-1.3) (p < 0.05) and in the interfollicular area (median: 2.2, range: 1.1-3.1 versus median: 0.5, range: 0.4-2.0) (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Antibody-Producing Cells↗
PubMed1995

SIDS cases have increased levels of interleukin-6 in cerebrospinal fluid.

Cerebrospinal fluid (CSF) from 20 infants who died of sudden infant death syndrome (SIDS), 7 cases of infectious death and 5 cases of violent death were examined with respect to concentrations of interleukin-6 (IL-6). The measurements were performed by ELISA. IL-6 levels in SIDS were significantly lower than in infectious death (p < 0.02), but significantly higher than in violent death (p < 0.02). Since IL-6 plays an important role in immune responses and may induce fever, the findings may suggest that immune activation plays a role in SIDS. The presence of cytokines in the central nervous system (CNS) may cause respiratory depression, especially in vulnerable infants.

Enzyme-Linked Immunosorbent Assay↗
PubMed1995

Release of xanthine oxidase to the systemic circulation during resuscitation from severe hypoxemia in newborn pigs.

Xanthine oxidase may contribute to oxygen free radical formation during reoxygenation after hypoxia, but in humans the enzyme is present in substantial amounts only in the liver and intestine. We developed a sensitive assay for xanthine oxidase using 14C-xanthine as substrate and investigated whether xanthine oxidase was released into the systemic circulation when 19 newborn pigs were resuscitated after severe hypoxemia. In five piglets plasma xanthine oxidase concentrations increased from undetectable levels to a median value of 8 (range 4-18) microU/ml after 30 min of reoxygenation. In these pigs serum aspartate aminotransferase increased from 45 to 148 U/l, while alanine aminotransferase was unchanged (28-31 U/l). The release of xanthine oxidase did not seem to correlate with the severity of the histological brain damage after 4 days. We conclude that only low levels of xanthine oxidase are released to the systemic circulation after severe hypoxemia in newborn pigs.

Alanine Transaminase↗
PubMed1995

Effects of oxygen radicals on cysteinyl leukotriene metabolism and pulmonary circulation in young pigs.

The effects of oxygen radicals, generated by the hypoxanthine-xanthine oxidase (XO) system, on pulmonary circulation and release of cysteinyl-containing leukotrienes (LTs) were studied in pigs after XO infusion into the right atrium. A 2.3-fold increase in pulmonary vascular resistance (PVR) (p < 0.05 vs. baseline) and a 2.1-fold increase in LT release (p < 0.05 vs. baseline) was observed. Pretreatment with indomethacin and allopurinol attenauted the vascular response (p < 0.01 and p < 0.05 vs. XO), and the LT release was inhibited by allopurinol and catalase (p < 0.01 and p < 0.02 vs. XO). We conclude that oxygen radicals stimulate lipoxygenase metabolism. This coincides with the observed increase in PVR, however, no causal relationship can be derived from the data presented.

Animals↗
PubMed1995

Beta-endorphin may be a mediator of apnea induced by the laryngeal chemoreflex in piglets.

To determine whether beta-endorphin is involved in the laryngeal chemoreflex, we initially injected 0.01-1 mg of beta-endorphin into the cisterna magna (i.c.m.) and registered the respiratory and cardiovascular patterns in 5-10-d-old piglets. From 0.1 to 1 mg of beta-endorphin i.c.m. induced a decrease in the minute volume, heart rate, and blood pressure within 15 min. Within the next 30 min respiratory pauses accompanied by blood pressure increases and reductions in heart rate developed, similar to the respiratory and cardiovascular pattern of the induced laryngeal chemoreflex. Based on these initial data, we decided to induce a laryngeal chemoreflex in piglets pretreated with 0.1 mg of beta-endorphin i.c.m (n = 6), 0.2 mg of beta-endorphin i.c.m. (n = 6), 0.1 mg of beta-endorphin i.c.m. and 100 micrograms/kg naloxone i.v. (n = 6), 100 micrograms/kg naloxone i.v. (n = 6), or water i.c.m. (n = 6). Because elevated levels of hypoxanthine in the vitreous humor may indicate hypoxia before death, we therefore measured the postmortem hypoxanthine levels in the vitreous humor. The laryngeal chemoreflex-induced apnea was shortened in the piglet group pretreated with water i.c.m and naloxone i.v. (p < 0.01) and in the piglet group pretreated with 0.1 mg of beta-endorphin i.c.m and naloxone i.v. (p < 0.05), but not significantly prolonged in the piglet groups pretreated with 0.1 or 0.2 mg of beta-endorphin i.c.m. when compared with the piglets pretreated with water i.c.m.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1995

D-penicillamine inhibits the action of reactive oxygen species in the pig pulmonary circulation.

Oxygen radicals produced by the hypoxanthine-xanthine oxidase (Hyp-XO) system potently constrict the pulmonary circulation of pigs. D-penicillamine (DPA) is thought to be a free radical scavenger. In the present work we have studied if DPA may influence the vasoactive action of Hyp-XO in pig lungs. Further, we have measured how this drug influences the output of cyclooxygenase and lipoxygenase products from the left atrium in pigs infused with XO into the pulmonary circulation. Twelve young pigs were divided into two groups. Group 1, the XO group, was infused 1 U/kg XO into right atrium. Group 2, the DPA group, was pretreated with DPA, 100 mg/kg intravenously before XO infusion as in group 1. Pulmonary artery pressure, left atrial pressure, pulmonary artery blood flow and systemic blood flow and pressure were recorded continuously. Plasma tromboxane B2 and prostaglandin (6-keto-PGF1 alpha) were determined with a radioimmunoassay method. Cysteinyl containing leukotrienes LTC4, LTD4, and LTE4, were measured together by RIA analyses of plasma samples, using a monoclonal antibody. There was a significant parallel decrease in paO2 and saO2 during the 130 minutes duration of the experiments in both groups without differences between the groups. Pulmonary vascular pressure and resistance increased sharply with a peak found after 25 minutes in the XO group. DPA attenuated the hemodynamic response. DPA inhibited the XO induced pulmonary blood pressure changes with 80% and inhibited the increase in pulmonary vascular resistance 68%. Plasma TXB2 increased two folds in the XO group reaching a maximum after 40 minutes, this effect was completely inhibited by DPA (92% inhibition). DPA also inhibited the XO induced increase in 6-keto-PGF1 alpha, however, not as efficient as with TXB2 (40% inhibition). Plasma cysteinyl leukotrienes increased after XO infusion reaching a peak at 20 minutes. DPA completely abolished this effect (100% inhibition). The study demonstrates that DPA attenuates or even abolishes the hemodynamic effects of XO on the pulmonary circulation in pigs. It seems that DPA inhibits the production of both lipoxygenase and cyclooxygenase products per se, and it is tempting to speculate that the observed DPA effect is caused by its action as an oxygen radical scavenger. It is further speculated that the vasoconstricting effect of XO is due to the fact that oxygen radicals may inactivate nitric oxide (NO), and that DPA stabilizes NO so it more efficiently possess its vasorelaxant activity. We conclude that DPA is an extremely potent inhibitor of XO induced pulmonary vascular effects. The mechanism of action is not fully understood, although its action as an oxygen radical scavenger may explain part of it.

Animals↗
PubMed1994

Is partial deletion of the complement C4 genes associated with sudden infant death?

The two C4 loci C4A and C4B in 61 cases of sudden infant death (SID), 93 living controls and 7 cases of infectious death were studied. In the SID group 13.1% showed deletion of the C4A gene, while 2.5% of the cases showed deletion of the C4B gene. This was not significantly different from neither the controls nor the infectious death group. We were not able to confirm that deletion of the C4B gene is associated with SID. However, in the SID group deletion of either the C4A or the C4B gene was associated with signs of infections prior to death (P = 0.035). This observation may indicate that a proportion of SID victims are more vulnerable to infections than other infants.

Adult↗
PubMed1994

Beta-endorphin immunoreactivity in spinal fluid and hypoxanthine in vitreous humour related to brain stem gliosis in sudden infant death victims.

Beta-endorphin may induce respiratory depression and bradycardia. Elevated levels of hypoxanthine (HX) in vitreous humour (VH) may possibly indicate hypoxia before death. Furthermore, gliosis in the brain stem may reflect a previous hypoxic/ischaemic injury in the brain. In the present study we relate beta-endorphin immunoreactivity (BENDI) in the CSF to the presence or absence of reactive astrocytosis in the nucleus olivae inferior (NOI). The relationship between the HX concentration in VH and the number of reactive astrocytes in sudden infant death (SID) cases (n = 17) and controls (n = 23) was also studied. The number of reactive astrocytes was examined in the NOI by immunohistochemical demonstration of glial fibrillary acidic protein (GFAP). The BENDI in CSF and the number of reactive astrocytes in the NOI divided the SID victims into two subpopulations (P < 0.01). One had a median of < 4 fmol/ml BENDI in CSF (range < 4) and 2 reactive astrocytes (range 0-15), and was similar to the controls that died from infections. The other subpopulation had a median of 260 fmol/ml BENDI in CSF (range 160-400) and 13 reactive astrocytes (range 7-33), similar to the control infants with previous hypoxia. In this latter SID subpopulation the number of reactive astrocytes correlated positively with BENDI in CSF (r = 0.7, P < 0.05). All the SID victims had elevated levels of HX in VH. In the SID subpopulation with high level of BENDI in CSF and increased number of activated astrocytes, the correlation factor between HX in VH and activated astrocytes was r = 0.7 (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Astrocytes↗
PubMed1994

Vitreous humor hypoxanthine levels in SIDS and infectious death.

Hypoxanthine concentrations in vitreous humor were determined in 107 cases of sudden infant death syndrome (SIDS) and compared with levels in 4 cases of borderline SIDS, 26 cases of infectious death and 16 cases of sudden violent death. The hypoxanthine measurements were made using a high-performance liquid chromatography method. The hypoxanthine levels were significantly (p < 0.01) higher in SIDS than in violent deaths, while no significant difference was found between SIDS and infectious deaths. The present report demonstrates a similar distribution pattern of hypoxanthine levels in vitreous humor in SIDS and infectious death. We have previously described signs of immune stimulation both in peripheral organs and in the central nervous system in these conditions. This indicates that the death mechanism in SIDS has some similarities with infectious death.

Age Factors↗