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Biomedical subjects

O D Saugstad

Publications and source records attributed to O D Saugstad.

At least 145 records · Page 8Linked to original sources
PubMed1990

[Treatment considerations for children during terminal care].

There should be a special obligation to shield children with a terminal illness from pain and from the psychological suffering when death is approaching. In spite of this, the child has the right to be informed about the prognosis and decisions taken concerning treatment. We discuss the difficult question of informed consent in pediatrics. Who can make an informed consent on behalf of a minor? At which age should a child make its own decisions concerning medical treatment? In pediatrics there are certain circumstances where withdrawal of intensive medical care is justified. Examples are given from oncological and neuromuscular diseases, as well as from the neonatal period. We discuss how termination of intensive care could take place. The medical team should make the decision alone, but should never go against the parents' will. It is underlined that termination of intensive care in the above-mentioned circumstances is completely different from active euthanasia, which we strongly oppose.

Adolescent↗
PubMed1990

Spinal muscular atrophy type I combined with atrial septal defect in three sibs.

All three children of an unrelated Norwegian couple were born with spinal muscular atrophy (SMA I) as confirmed by autopsy in two of them. Two of the children died at birth, whereas one lived for 7 weeks on support systems that included artificial ventilation. All three children had large atrial septal defects (ASD). One had valvular aortic stenosis. Another had arrhinencephaly and transient pleural effusion which was evacuated during pregnancy. The findings may reflect concurrence of unrelated disorders caused by genetic or environmental factors, segregation of linked genes, pleiotropism or the existence of a previously unknown disease.

Abnormalities, Multiple↗
PubMed1990

Oxygen toxicity in the neonatal period.

Oxygen is toxic because it produces oxygen radicals. One important oxygen radical generating system is hypoxanthine-xanthine oxidase. Hypoxic newborn babies who have elevated concentrations of hypoxanthine in tissues and body fluids and simultaneously are treated with supplementary oxygen, may therefore produce oxygen radicals in excess overwhelming the body's natural defence systems against free radicals. Further, the capacity of many of these defence systems are probably reduced in the preterm baby. A series of conditions in neonates may, at least partly, be caused by oxygen radicals, e.g. bronchopulmonary dysplasia, retinopathy of prematurity, necrotising enterocolitis and patent ductus arteriosus. These conditions may be different facets of one disease; the "Oxygen radical disease in neonatology". It is speculated that oxygen radicals play a role in regulating the perinatal circulation. This new insight concerning the role of oxygen radicals may have fundamental consequences for treatment and handling of sick newborn babies.

Animals↗
PubMed1990

Hypoxanthine, xanthine, and uric acid concentrations in the cerebrospinal fluid, plasma, and urine of hypoxemic pigs.

The concentrations of hypoxanthine, xanthine, and uric acid in plasma and cerebrospinal fluid (CSF), as well as the urinary output of hypoxanthine and xanthine, were measured in four groups of pigs (three groups with different degrees of hypoxemia and one control group). During hypoxemia with arterial O2 tension between 2.1 and 3.0 kPa [group 1, fractional inspired oxygen (FiO2) = 0.08], hypoxanthine increased in CSF from a mean basal value of 18.1 to 39.3 mumol/L at death (p less than 0.02), in plasma from 25.4 to 103.6 mumol/L (p less than 0.05), and in urine from 21.3 to 87.1 nmol/kg/min (p less than 0.02). Xanthine changed in a similar way: in CSF from 4.0 to 10.6 mumol/L (p less than 0.02), in plasma from 0.7 to 48.1 mumol/L (p less than 0.02), and in urine from 4.0 to 12.6 nmol/kg/min (p less than 0.05). Uric acid increased in CSF from 2.7 to 11.6 mumol/L (p less than 0.05), and in plasma from 15.4 to 125.0 mumol/L (p less than 0.02). During hypoxemia with arterial O2 tension between 3.0 and 4.0 kPa (group 2, FiO2 = 0.11), hypoxanthine increased in the CSF from 14.7 to 42.9 mumol/L (p less than 0.02). Plasma hypoxanthine increased from 20.3 to a maximum of 44.1 mumol/L (p less than 0.02), but decreased to initial values by the time of death. The urinary excretion of hypoxanthine increased from 13 to 54 nmol/kg/min (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Changes in oxypurine concentrations in vitreous humor of pigs during hypoxemia and post-mortem.

In the vitreous humor from three hypoxemic and one control group of pigs, hypoxanthine, xanthine, and uric acid concentrations were measured. The purine concentrations were measured before the hypoxemia, at the time of death, and 24 h post-mortem. During hypoxemia with arterial O2 tension between 2.1 and 3.0 kPa [fractional inspired oxygen (FiO2) = 0.08], hypoxanthine concentrations increased from a mean basal value of 11.7 +/- 5.6 mumol/L to 16.3 +/- 2.4 mumol/L at the time of death (NS). Xanthine concentrations changed from a basal value of 0.3 +/- 0.1 mumol/L to 0.6 +/- 0.2 mumol/L (p less than 0.02), and uric acid changed from 3.4 +/- 1.1 mumol/L to 5.0 +/- 4.5 mumol/L (NS). During hypoxemia with arterial O2 tension between 3.0 and 4.0 kPa (FiO2 = 0.11), hypoxanthine increased in the vitreous humor from a mean basal value of 9.1 mumol/L to 20.3 mumol/L at the time of death (p less than 0.02). Xanthine concentrations increased from 0.3 mumol/L to 1.3 mumol/L (p less than 0.05), whereas there was no change in uric acid concentration (basal 5.0 +/- 0.8 mumol/L and final 4.5 +/- 1.0 mumol/L). During milder hypoxemia with arterial O2 tension between 4.3 and 5.6 kPa (FiO2 = 0.14), or in the control group (FiO2 = 0.21), neither of the metabolites changed significantly. The vitreous humor was not stable post-mortem, inasmuch as the mean concentration of hypoxanthine increased from 18.2 +/- 7.7 mumol/L to 121.6 +/- 57.4 mumol/L 24 h post-mortem (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[Hypoxic pulmonary vasoconstriction following lung damage by xanthine oxidase--studies in rats].

The main reason for an insufficient oxygenation of the arterial blood during acute lung injury should be an increased shunt fraction. The aim of this study was to check if in this connection the magnitude of hypoxic pulmonary vasoconstriction is reduced--a fact, which could be causal involved in the arising of increased shunt fraction. 21 male rats were anaesthetized (pentobarbitone) and ventilated artificially (F1O2 = 0.6). In 10-minute-intervals hypoxia (F1O2 = 0.06) was applied. After the first hypoxic exposure the animals were divided into 4 groups according to the application of 3 U xanthine oxidase (XO) or 0.5 ml physiological saline (NaCl) intratracheally (i.t.) or intravascularly (i.v.)--group A: XO i.t.; group B: XO i.v.; group C.: NaCl i.t.; group D: NaCl i.v. At the end of each hypoxic or hyperoxic period (steady state) mean blood pressure in the right ventricle (Prv) and in the A. carotis communis (Psa) were measured. Then blood samples (100 microliters each) were drawn from the artery and the right ventricle and pH, PO2, PCO2, SO2 and hemoglobin concentration were determined. During hyperoxic conditions from the latter values we calculated the shunt fraction. Additional the lung-thorax compliance before and after the application was measured body plethysmographically. As an indirect measure of the reagibility of the pulmonary vasculature the increase of Prv during hypoxic exposure was considered. In the groups B, C and D no significant changes between the measured parameters before and after the application procedure could be observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Reactive oxygen metabolites relax the lamb ductus arteriosus by stimulating prostaglandin production.

To determine whether oxygen metabolites can cause ductus relaxation, we used rings of fetal ductus obtained from 36 near-term lambs and measured the effects of the oxygen metabolites generated by the combination of hypoxanthine and xanthine oxidase. The oxygen metabolites produced by hypoxanthine plus xanthine oxidase caused relaxation of the ductus that was inhibited by catalase (hydrogen peroxide scavenger) but not by superoxide dismutase (superoxide anion scavenger). In addition, hypoxanthine plus xanthine oxidase produced a 14-fold increase in prostaglandin (PG) E2 production with only twofold increase in 6-keto-PGF1 alpha (the stable metabolite of PGI2). PGE2 is the most potent relaxant of the ductus arteriosus. The presence of either catalase or indomethacin blocked both the increase in prostaglandin production and the relaxation. We conclude that reactive oxygen metabolites relax the ductus arteriosus and oppose the normal constriction that occurs after birth. However, the vasoactive effects of reactive oxygen metabolites in the ductus appear to be mediated exclusively through the generation of PGE2.

Animals↗
PubMed1989

Circulatory effects of oxygen radicals.

Oxygen radicals have vasoactive properties. The hypoxanthine-xanthine oxidase system generates oxygen radicals. This system relaxes isolated constricted ductus rings from fetal lambs and constricts the pulmonary circulation of adult pigs. Since catalase, and not superoxide dismutase, inhibits the effect of the hypoxanthine-xanthine oxidase system, we believe the effect is caused by the hydroxyl radical. The hydroxyl radical stimulates prostaglandin synthesis in the vessel wall and high concentrations of prostanoids can be measured after hypoxanthine-xanthine oxidase exposure. Indomethacin inhibits the vasoactive effects of the hypoxanthine-xanthine oxidase system. We believe the hypoxanthine-xanthine oxidase system plays an important role in regulating the normal circulation.

Animals↗
PubMed1988

High activities of erythrocyte glutathione peroxidase in patients with the Lesch-Nyhan syndrome.

Antioxidant levels were determined in five patients with the Lesch-Nyhan syndrome. The erythrocyte glutathione peroxidase activity was in average 1.8 times higher in Lesch-Nyhan patients than in controls (1.68 +/- 0.36 versus 0.92 +/- 0.17 mu kat/g hemoglobin, p less than 0.001). Plasma CuZn-superoxide dismutase activity was two times higher (p less than 0.001) and Mn-superoxide dismutase activity was 1.5 times higher (p less than 0.05) than in controls, whilst erythrocyte CuZn-superoxide dismutase, plasma extracellular-superoxide dismutase and lymphocyte superoxide dismutase did not differ between Lesch-Nyhan patients and healthy controls. These data might indicate that Lesch-Nyhan patients are exposed to a higher oxidative load than healthy control persons.

Adolescent↗
PubMed1988

Respiratory failure caused by intratracheal saline: additive effect of xanthine oxidase.

Administration of physiological saline or drugs together with saline into the airways is becoming common clinical practice. However, there are few studies on possible side effects. We have studied the effects of saline, saline plus xanthine oxidase, and saline plus xanthine oxidase plus superoxidase dismutase on lung-thorax compliance and on arterial blood gases in anesthetized, paralyzed guinea pigs, ventilated for 2.5 h. Saline bolus (2-3 ml isotonic saline/kg body weight) into the airways reduced the compliance within 20 min to a mean of 39% of the pretreatment levels, and necessitated as increase in the respirator pressure. Saline plus xanthine oxidase decreased the compliance to 16% of the pretreatment levels. The xanthine oxidase-induced (but not saline-induced) decrease in lung compliance was relieved by superoxide dismutase. According to the present results xanthine oxidase induces a lung injury possible by production of free oxygen radicals. Superoxide dismutase can be valuable in prevention of free oxygen radical-mediated lung damage. Saline alone can be harmful when applied to the airways. This should be considered in clinical trials and in clinical practice.

Animals↗
PubMed1988

Elevated levels of hypoxanthine in vitreous humor indicate prolonged cerebral hypoxia in victims of sudden infant death syndrome.

Hypoxanthine levels in vitreous humor from 32 infants who died of sudden infant death syndrome (SIDS) were determined and compared with levels found in eight children who died of trauma, drowning, or hanging and with levels from seven neonates dying suddenly without long-standing antemortem hypoxia. Determination of hypoxanthine level was done with either a PO2 electrode method or high-performance liquid chromatography. The results obtained by both methods were significantly correlated; therefore they were pooled. The median hypoxanthine level in victims of SIDS (380 mumol/L) was significantly higher (P less than .001) than in the children who died violently (118 mumol/L). Moreover, the levels from the SIDS victims were significantly higher (P less than .001) than those from the neonates who died without long-standing hypoxia (53 mumol/L). It is concluded that SIDS is probably not a sudden event but may be preceded by a relatively long period of respiratory failure and hypoxia.

Female↗
PubMed1988

High postmortem levels of hypoxanthine in the vitreous humor of premature babies with respiratory distress syndrome.

To test whether or not premature babies at risk for retinopathy of prematurity have elevated hypoxanthine levels in the eye, the vitreous humor of 13 premature babies who died of severe respiratory distress syndrome and lung failure, was analyzed for hypoxanthine. Their hypoxanthine level was 459 +/- 171 mumol/L (mean +/- SD) compared with 54 +/- 71 mumol/L in seven newborn babies who died suddenly (P less than .001). In 53 adults who died suddenly, the hypoxanthine concentration was 136 +/- 119 mumol/L (P less than .001 when compared with babies with respiratory distress syndrome). Babies with respiratory distress syndrome underwent a significantly longer period with arterial PO2 levels less than 40 mm Hg (5.3 kPa) and they required supplementation with 100% oxygen significantly longer than control babies. The hypoxanthine concentration was correlated with the time during which the arterial PO2 was lower than 40 mm Hg (5.3 kPa) before death, and a significant positive correlation was found (R = .59, P less than .12). The study shows that high levels of hypoxanthine are found in vitreous humor of premature babies with respiratory distress syndrome. Because hypoxanthine is a potential oxygen radical generator and premature babies might have lower levels of antioxidants than full-term babies, it is suggested that the hypoxanthine accumulation in the eyes of premature babies with respiratory distress syndrome could play a pathogenetic role in the development of retinopathy of prematurity.

Aqueous Humor↗
PubMed1987

Acute and chronic effects of xanthine oxidase on lung thorax-compliance in guinea pigs.

Xanthine oxidase was given intratracheally in a single dose to guinea pigs. Lung compliance was measured after 4 h and 14 days respectively. Lung-thorax compliance was significantly lower compared with saline-treated controls both 4 h and 14 days after application of fluid. At 14 days there was a dose-related response between lung-thorax compliance and xanthine oxidase administered in the range 0-1.0 U. Superoxide dismutase (SOD) had a protective effect on xanthine oxidase action at 4 h, but not after 14 days. We suggest that the decreased lung-thorax compliance was caused by superoxide radicals, produced by the hypoxanthine-xanthine oxidase system, damaging lung tissue. We speculate that free oxygen radicals produced by the hypoxanthine-xanthine oxidase system could be an important contributory pathogenetic factor in producing both acute and chronic lung damage in, for instance, premature babies or adults, with respiratory distress syndrome.

Animals↗