Natural course of iron delocalization and lipid peroxidation during the first eight hours following a 15-minute cardiac arrest in dogs

Krause, Gary S.; Nayini, Narsimha R; White, Blaine C.; Hoenher, Thomas J; Garritano, Ann Marie; O’Neil, Brian J.; Aust, Steven D.

doi:10.1016/s0196-0644(87)80224-x

Cited by 43 publications

(10 citation statements)

References 29 publications

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“…The increase in oxidized brain lipids observed after global cerebral ischemia and reperfusion in this study is consistent with the results of other studies with other animal models [1][2][3][5][6][7][8][9][10][11]16 and consistent with our previous results with the canine model in which cerebral cortex protein oxidation was demonstrated. 21 In contrast to our observations for protein oxidation, the level of oxidized lipids did not increase with increasing periods of reperfusion (Figure 2).…”

Section: Discussionsupporting

confidence: 93%

Normoxic Ventilation After Cardiac Arrest Reduces Oxidation of Brain Lipids and Improves Neurological Outcome

Liu

Rosenthal

Haywood

et al. 1998

Stroke

188

111

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Background and Purpose-Increasing evidence that oxidative stress contributes to delayed neuronal death after global cerebral ischemia has led to reconsideration of the prolonged use of 100% ventilatory O 2 following resuscitation from cardiac arrest. This study determined the temporal course of oxidation of brain fatty acyl groups in a clinically relevant canine model of cardiac arrest and resuscitation and tested the hypothesis that postischemic ventilation with 21% inspired O 2, rather than 100% O 2, results in reduced levels of oxidized brain lipids and decreased neurological impairment. Methods-Neurological deficit scoring and high performance liquid chromatography measurement of fatty acyl lipid oxidation were used in an established canine model using 10 minutes of cardiac arrest followed by resuscitation with different ventilatory oxygenation protocols and restoration of spontaneous circulation for 30 minutes to 24 hours. Results-Significant increases in frontal cortex lipid oxidation occurred after 10 minutes of cardiac arrest alone with no reperfusion and after reperfusion for 30 minutes, 2 hours, and 24 hours (relative total 235-nm absorbing peak areasϭ7.1Ϯ0.7 SE, 17.3Ϯ2.7, 14.2Ϯ3.2, 16.1Ϯ1.0, and 14.0Ϯ0.8, respectively; nϭ4, PϽ0.05). The predominant oxidized lipids were identified by gas chromatography/mass spectrometry as 13-and 9-hydroxyoctadecadienoic acids (13-and 9-HODE). Animals ventilated on 21% to 30% O 2 versus 100% O 2 for the first hour after resuscitation exhibited significantly lower levels of total and specific oxidized lipids in the frontal cortex (1.7Ϯ0.1 versus 3.12Ϯ0.78 g 13-HODE/g wet wt cortex., nϭ4 to 6, PϽ0.05) and lower neurological deficit scores (45.1Ϯ3.6 versus 58.3Ϯ3.8, nϭ9, PϽ0.05). Conclusions-With a clinically relevant canine model of 10 minutes of cardiac arrest, resuscitation with 21% versus 100% inspired O 2 resulted in lower levels of oxidized brain lipids and improved neurological outcome measured after 24 hours of reperfusion. This study casts further doubt on the appropriateness of present guidelines that recommend the indiscriminate use of 100% ventilatory O 2 for undefined periods during and after resuscitation from cardiac arrest.

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Section: Discussionsupporting

confidence: 93%

Normoxic Ventilation After Cardiac Arrest Reduces Oxidation of Brain Lipids and Improves Neurological Outcome

Liu

Rosenthal

Haywood

et al. 1998

Stroke

188

111

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“…10,24 Plasma concentrations of NPBI were further increased in the HIE group when compared to controls. Such finding is consistent with a number of studies that demonstrate iron delocalization in the setting of hypoxia, 25 ischemia reperfusion 26,27 and cardiac arrest. 28 The protein-bound iron is considered a safe vehicle for iron transport and storage because it is not capable of inducing a free radical reaction.…”

Section: Discussionsupporting

confidence: 92%

Iron metabolism and lipid peroxidation products in infants with hypoxic ischemic encephalopathy

2008

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Background: Iron delocalization or misregulation of iron metabolism may play a critical role in the pathology of hypoxic ischemic encephalopathy (HIE).Objective: To study iron metabolism and lipid peroxidation in newborn infants and to correlate non-protein-bound iron (NPBI) concentration with the severity of the post-asphyxial injury and subsequent short-term outcomes.Study Design: Concentrations of NPBI and malondialdehyde (MDA) in the serum and in the cerebrospinal fluid (CSF) were measured in eight healthy newborn infants and nine newborn infants suffering from moderately severe HIE. Short-term outcomes (death, survival with or without neurological abnormality) were noted at hospital discharge.Result: Serum and CSF concentrations of both NPBI and MDA were significantly increased in HIE infants when compared to controls. Serum iron was significantly increased and total iron binding capacity was significantly decreased in HIE infants compared to controls. Out of the nine HIE infants, four infants died and two infants survived with abnormal neurological findings at hospital discharge. These six infants with clinical sequels had significantly increased concentrations of NPBI in the serum and in the CSF; and increased concentrations of MDA in the CSF when compared to the other three who survived without short-term abnormalities. Conclusion:We conclude that hypoxia ischemia alters iron metabolism and lipid peroxidation in newborn infants; and that NPBI and MDA in the CSF are increased in infants with HIE. This study supports a role for iron in oxidative injury to the central nervous system after hypoxic ischemic insults.

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“…The increased detectable rate of plasma non-protein-bound iron in asphyxiated infants could be a result of iron delocalization. A number of studies have demonstrated that iron delocalization could be induced by hypoxia (Buonocore et al 1998), ischemia, and/or reperfusion (Holt et al 1986, Krause et al 1987, Chiao et al 1994, and cardiac arrest (Komara et al 1986). Under normal conditions, iron is mainly bound to its transport protein transferrin and storage protein ferritin (Qian and Tang 1995).…”

Section: Discussionmentioning

confidence: 99%

Effect of asphyxia on non‐protein‐bound iron and lipid peroxidation in newborn infants

Kui

Ming

2003

Develop Med Child Neuro

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The effect of asphyxia on iron metabolism and lipid peroxidation in newborn infants with hypoxic‐ischemic encephalopathy (HIE) was investigated. Non‐protein‐bound iron (NPBI) and lipid peroxidation (thiobarbituric‐acid‐reactive species; TBARS) in plasma and hematological iron indices were measured in 15 healthy newborn infants (mean gestational age 39 04 weeks, SD 1); 15 asphyxiated infants without neurological abnormalities (AS‐HIE; mean gestational age 38.8 weeks, SD 0.9); and 15 asphyxiated infants with neurological abnormalities (AS+HIE; mean gestational age 39.75 weeks, SD 1.4). Follow‐up was performed at the age of 5 months. It was found that the detectable rates of NPBI in 10 of 15 of the AS‐HIE group and 13 of 15 of the AS+HIE group were significantly higher than that of the control group (5 of 15; both p0.01). Plasma levels of TBARS in the control (9.20μmol/L, SD 1.9) and AS‐HIE infants (10.13μmol/L, SD 2.7) were significantly lower than those of the AS+HIE group (13.42μmol/L, SD 2.8). Serum iron, total iron binding capacity, and transferrin saturation in the AS+HIE group was higher than the corresponding values of the control and AS‐HIE groups, although no statistical difference was found among them. At 5 months of age, all control and AS‐HIE infants were neurologically normal, whether or not their NPBI was detectable. Of the 12 AS+HIE infants, four (all of whom had detectable NPBI) were neurologically impaired. The average Gross Development Quotient of AS+HIE infants was significantly lower than that of the control or AS‐HIE groups (p<0.01). Results showed that asphyxia could affect iron metabolism and lead to a significant increase in NPBI and lipid peroxidation in newborn infants with HIE, indicating that iron delocalization induced by asphyxia plays a role in the brain injury of asphyxiated infants.

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Natural course of iron delocalization and lipid peroxidation during the first eight hours following a 15-minute cardiac arrest in dogs

Cited by 43 publications

References 29 publications

Normoxic Ventilation After Cardiac Arrest Reduces Oxidation of Brain Lipids and Improves Neurological Outcome

Normoxic Ventilation After Cardiac Arrest Reduces Oxidation of Brain Lipids and Improves Neurological Outcome

Iron metabolism and lipid peroxidation products in infants with hypoxic ischemic encephalopathy

Effect of asphyxia on non‐protein‐bound iron and lipid peroxidation in newborn infants

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