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O D Saugstad

Publications and source records attributed to O D Saugstad.

At least 127 records · Page 7Linked to original sources
PubMed1992

[D-penicillamine: old drug, new indication? D-penicillamine reduced pulmonary hypertension induced by free radicals].

Pulmonary hypertension is one of the major problems in the neonatal period. Free oxygen radicals play important role in the activation of pulmonary vasoconstriction. Since D-penicillamine has proved to be a strong antioxidant in newborns it was of interest to investigate the effect of the drug in the oxygen radical induced pulmonary hypertension. According to our animal experiments D-penicillamine inhibits the xanthine oxidase induced pulmonary hypertension in piglets. The same inhibitory effect was observed in the prostanoid metabolism. Could D-penicillamine be used in the treatment of pulmonary hypertension in the newborn?

Animals↗
PubMed1992

Sudden infant death syndrome victims show local immunoglobulin M response in tracheal wall and immunoglobulin A response in duodenal mucosa.

Twenty-two sudden infant death syndrome (SIDS) cases and 22 controls were examined immunohistochemically with regard to IgA, IgM, and IgG plasma cells in tracheal wall and duodenal mucosa. Furthermore, the presence of secretory component in tracheal surface and gland epithelium as well as in duodenal crypt and villus epithelium were evaluated. The examined specimens were obtained at autopsies. The control groups consisted of 11 infants who died of noninfectious causes and 11 who died of infections. In the tracheal wall, the SIDS group had higher IgM cell numbers than the control group that died of noninfectious causes (p less than 0.01), whereas the SIDS victims had lower IgA and IgM cell numbers than the infectious control group (p less than 0.01). In the duodenal mucosa, the SIDS group had significantly higher IgA cell numbers than the noninfectious control group (p less than 0.02) but lower IgA cell numbers than the infection group (p less than 0.01). Secretory component was present in the epithelium from all SIDS cases and controls, both in the tracheal wall glands and in the duodenal crypt mucosa. These findings indicate that the mucosal immune system is stimulated in SIDS.

Antibody-Producing Cells↗
PubMed1992

Hypoxemia and reoxygenation with 21% or 100% oxygen in newborn pigs: changes in blood pressure, base deficit, and hypoxanthine and brain morphology.

To study whether room air is as effective as 100% O2 in resuscitation after hypoxia, hypoxemia (PaO2 2.3-4.3 kPa) was induced in newborn pigs (2-5 d old) by ventilation with 8% O2 in nitrogen. When systolic blood pressure had fallen to 20 mm Hg, animals were randomly reoxygenated with either 21% O2 (group 1, n = 9) or 100% O2 (group 2, n = 11) for 20 min followed by 21% O2 in both groups. Controls (group 3, n = 5) were ventilated with 21% O2 throughout the experiment. Base deficit peaked at 31 +/- 5 mmol/L (mean +/- SD) for both hypoxic groups at 5 min of reoxygenation and then normalized over the following 3 h. There were no statistically significant differences between the two groups during reoxygenation concerning blood pressure, heart rate, base deficit, or plasma hypoxanthine. Hypoxanthine peaked at 165 +/- 40 and 143 +/- 42 mumol/L in group 1 and 2 (NS), respectively, and was eliminated monoexponentially in both groups with an initial half-life for excess hypoxanthine of 48 +/- 21 and 51 +/- 27 min (NS), respectively. Blinded pathologic examination of cerebral cortex, cerebellum, and hippocampus after 4 d showed no statistically significant differences with regard to brain damage. We conclude that 21% O2 is as effective as 100% O2 for normalizing blood pressure, heart rate, base deficit, and plasma hypoxanthine after severe neonatal hypoxemia in piglets and that the extent of the hypoxic brain damage is similar in the two groups.

Animals↗
PubMed1992

Activation of the plasma kallikrein-kinin system in respiratory distress syndrome.

Components of the plasma kallikrein-kinin and fibrinolytic systems together with antithrombin III were measured the first days postpartum in 13 premature babies with severe respiratory distress syndrome (RDS). Seven of the patients received a single dose of porcine surfactant (Curosurf) as rescue treatment. Nine premature babies without lung disease or any other complicating disease served as controls. There were no differences in prekallikrein values between surfactant treated and non-treated RDS babies during the first 4 d postpartum. The controls had, however, significantly higher prekallikrein values than the RDS babies already at the first day of age (mean +/- SD 32 +/- 8% in controls versus 22 +/- 6 and 21.5 +/- 5% in the treated and nontreated RDS groups, respectively). Plasma kallikrein activities did not differ between RDS and control patients. Plasma kallikrein inhibition values, which increased steadily in all groups, were lower in the RDS babies treated with surfactant than in controls at d 2 and 4. The degree of degradation of plasma high molecular weight kininogen was measured in RDS patients treated with surfactant and was significantly higher when compared with controls at d 1, demonstrating an increased proteolysis of kininogen to kinin early in RDS. There were no differences in plasminogen and plasmin values between RDS and control babies. This study shows that the plasma kallikrein-kinin system is activated in RDS. This system as well as the fibrinolytic system does not seem to be influenced by rescue instillation of a single dose of porcine surfactant into the lungs of premature babies with RDS.

Antithrombin III↗
PubMed1992

Raised plasma hypoxanthine levels as a prognostic sign in preterm babies with respiratory distress syndrome treated with natural surfactant.

Plasma hypoxanthine concentration was measured in twelve preterm babies with respiratory distress syndrome (RDS) treated with 200 mg/kg of a porcine surfactant (Curosurf). Five of the babies died within one week and seven survived the neonatal period. Surviving babies had no significant changes in plasma hypoxanthine concentration throughout a one hour study period following the administration of surfactant. By contrast, in nonsurvivors the mean plasma hypoxanthine concentrations increased from 6.8 mumol/l before surfactant administration to 14.2 mumol/l 15 minutes after surfactant treatment. Survivors had a mean maximal increase in plasma hypoxanthine of 1.9 mumol/l 15-30 min factor surfactant treatment compared with 9.4 mumol/l in nonsurvivors (p < 0.05). The babies who developed intracranial hemorrhage had significantly higher maximal plasma hypoxanthine increase (mean 9.6 mumol/l) compared with babies who did not develop intracranial hemorrhage (mean 1.1 mumol/l) (p < 0.01). The combination of high PaO2 and high hypoxanthine concentration could lead to an increased production of oxygen radicals which might be harmful. We conclude that plasma hypoxanthine concentration may serve as an indicator of the prognosis in preterm babies treated with natural surfactant. Further, it seems important to reduce oxygen supplementation as soon as surfactant is given to possibly limit oxygen radical production.

Biomarkers↗
PubMed1991

A new biochemical method for estimation of postmortem time.

Hypoxanthine (Hx) is formed by hypoxic degradation of adenosine monophosphate (AMP) and might be elevated due to antemortem hypoxia. However, it also increases after cessation of the life processes. Until now measurements of potassium in corpus vitreous humor have been used by forensic pathologists to determine postmortem time. In this study the influence of postmortem time and temperature on vitreous humor Hx and potassium levels were compared. Repeated sampling of vitreous humor was performed in 87 subjects with known time of death and diagnosis. The bodies were kept at either 5 degrees C, 10 degrees C, 15 degrees C or 23 degrees C. Hx was measured by means of HPLC and potassium by flame photometry. In 19 subjects from whom samples were obtained within 1.5 h after death, the normal level of Hx could be estimated to be 7.6 mumol/l and that of potassium to be 5.8 mmol/l. The spread of the potassium levels measured shortly after death was much greater than for the corresponding Hx levels. In the four temperature groups the Hx level increased 4.2, 5.1, 6.2 and 8.8 mumol/l per h, respectively, whereas the corresponding figures for potassium were 0.17, 0.20, 0.25 and 0.30 mmol/l per h. The vitreous humor concentration of both Hx and potassium increases fairly linearly after death. The slopes are steeper with increasing temperature. Since the scatter of the levels is greater for potassium than for Hx, the latter parameter seems to be better suited for the determination of time of death in cases without antemortem hypoxia, especially during the first 24 h.

Adolescent↗
PubMed1991

Reactive oxygen metabolites produce pulmonary vasoconstriction in young pigs.

Reactive oxygen metabolites appear to modulate pulmonary vascular changes. To study the effects of free radical formation in vivo, we investigated five groups of young pigs by recording hemodynamic changes after xanthine oxidase infusion alone and after pretreatment with hypoxanthine or possible blocking agents. The pulmonary vascular pressure increased rapidly in the groups without inhibition reaching maximum levels 25 min after the start of the experiment. The pulmonary artery blood flow declined toward minimum values at the same time. Compared to baseline levels, the calculated vascular lung resistance increased by 300% when the pigs were pretreated with hypoxanthine, and by 150% when xanthine oxidase was given alone. These findings suggest enhanced pulmonary vasoconstriction as a result of high initial hypoxanthine levels probably capable of forming larger quantities of oxygen radicals. The vascular reaction was attenuated when the pigs were pretreated with indomethacin (cyclo-oxygenase inhibitor) or allopurinol (xanthine oxidase inhibitor). Furthermore, the presence of catalase (hydrogen peroxide scavenger) reduced the pulmonary vasoconstriction significantly. We observed less decline in arterial oxygen tension and oxygen saturation when the animals had been pretreated with inhibitory agents, compared to the blood gas changes found in the xanthine oxidase group. The systemic pressure recordings in the carotid artery remained at baseline levels in all groups. We conclude that oxygen radicals formed by the hypoxanthine-xanthine oxidase system produce severe pulmonary vascular constriction in young pigs.

Allopurinol↗
PubMed1991

Increased plasma hypoxanthine values in humans during exposure to simulated altitude of 7,620 meters (25,000 feet).

In this study we have determined the effect of severe and moderate hypoxemia on plasma hypoxanthine and lactate values. Hypoxemia was induced in healthy humans in a low pressure chamber. The test subjects breathed atmospheric air at barometric pressures of 279 mm Hg and 385 mm Hg, representing a simulated altitude of about 7,620 and 5,334 m (25,000 and 17,500 ft), respectively. Exposure to 279 mm Hg represents a severe hypoxemia and all subjects exposed to this simulated altitude for 2 min showed symptoms related to hypoxia. After this exposure, plasma hypoxanthine increased by an average of 2.4 times compared to preexposure values. Exposure to 385 mm Hg represents a moderate hypoxemia and the persons tested at this simulated altitude for 45 min showed no or minor symptoms related to hypoxia and there was no change in plasma hypoxanthine values. In contrast to the unchanged plasma hypoxanthine values there was a 50% increase in plasma lactate values after 30 min exposure. We conclude that plasma hypoxanthine is a reliable marker for severe cellular hypoxia in humans and that enhanced plasma hypoxanthine levels are a rapid response to cellular hypoxia.

Adolescent↗
PubMed1991

Hypoxanthine levels in vitreous humor: evidence of hypoxia in most infants who died of sudden infant death syndrome.

Postmortem changes of the hypoxanthine in vitreous humor in humans were investigated. Hypoxanthine is formed from hypoxic degradation of adenosine monophosphate. Repeated sampling was performed in 13 deceased adults. Keeping the bodies at +6 degrees C, the increase of the hypoxanthine levels was estimated to 3.5 mumol/L per hour when sampling was started more than 12 hours after death (range 2.8 to 5.6 mumol/L per hour). Results of hypoxanthine measurements from vitreous humor in 73 infants with sudden infant death syndrome, 17 infants and children who died sudden violent deaths, and 6 neonates who died suddenly without hypoxemia prior to death were corrected according to the expected postmortem hypoxanthine increase. The time between death and autopsy was similar in the three groups studied. The corrected median hypoxanthine level in the group with sudden infant death syndrome was 227 mumol/L, which is significantly higher than in the other groups; 22 mumol/L in the group who had violent deaths (P less than .01), and 0 mumol/L in the neonate group (P less than .01). The findings seem to confirm that sudden infant death is preceded by a relatively long period of tissue hypoxia in most cases.

Aged↗
PubMed1991

The influence of intratracheal saline upon the dynamic lung-thorax compliance of premature newborn rabbits.

A modern therapy for the respiratory distress syndrome in neonates is the substitution of alveolar surfactant. Supplementary surfactant has to be applied to the lung via an aqueous emulsion. To estimate the effects of fluids instilled into the lungs a total of 144 premature newborn rabbits were used. They were delivered by hysterotomy after 27, 28 or 29 gestational days (term = 31 +/- 1 days; mean +/- SD), anaesthetized (0.5 mg ethylurethane/kg b.w.), paralyzed (1 mg pancuronium bromide/kg b.w.) and ventilated by positive pressure (P = 25 hPa; f = 40/min; I:E = 1:1) with 100% oxygen. By means of body-plethysmography the tidal volume (VT) was recorded before and regularly during 90 min after the application of 0 (controls), 5, 10 or 20 ml saline (0.9% NaCl solution) per kg b.w. intratracheally. Dynamic lung-thorax compliance (Crs) was calculated as VT/P and related to the body weight. The initial Crs values (mean +/- SD) were 0.06 +/- 0.02 (27 days), 0.62 +/- 0.52 (28 days) and 1.08 +/- 0.21 (29 days) ml/hPa/kg, respectively (p less than 0.001). Intratracheal saline application had no detectable effect on Crs in rabbit neonates on day 27 of gestation. On day 28 or 29 of gestation there was a transient (approximately 15 min) Crs reduction, increasing with the volume of applied liquid. At a given saline quantity the severity of Crs reduction depended more on the magnitude of the initial Crs values than on the gestational day.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[Surfactant treatment of premature infants with respiratory distress syndrome].

The present status of surfactant treatment of preterm babies suffering from respiratory distress syndrome is reviewed, with special emphasis on data from the European Collaborative Multicenter Study Group which used porcine surfactant (Curosurf). Treatment with this surfactant reduced neonatal mortality by 40%. In the treated group the percentage of survivors with no bronchopulmonary dysplasia was more than twice the percentage in the control group. The authors also report experience from the first eight patients treated with surfactant (Curosurf) in Norway. The Norwegian results, although collected from a small study group, conform well with the results reported from the Collaborative European Multicenter Study Group.

Drug Evaluation↗