| 1. |
- Basu, Samar, et al.
(författare)
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Development of a novel biomarker of free radical damage in reperfusion injury after cardiac arrest
- 2000
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Ingår i: FEBS Letters. - 0014-5793 .- 1873-3468. ; 470:1, s. 1-6
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Tidskriftsartikel (refereegranskat)abstract
- In a porcine model of cardiopulmonary resuscitation (CPR), we investigated changes in the plasma levels of 8-iso-PGF(2alpha), a marker for oxidative injury, and 15-keto-dihydro-PGF(2alpha), an inflammatory response indicator during the post-resuscitation period after cardiac arrest. Twelve piglets were subjected to either 2 or 5 min (VF2 and VF5 group) of ventricular fibrillation (VF) followed by 5 min of closed-chest CPR. Six piglets without cardiac arrest were used as controls. In VF5 group, 8-iso-PGF(2alpha) in the jugular bulb plasma (draining the brain) increased four-fold. Jugular bulb 8-iso-PGF(2alpha) in the control group remained unchanged. The 15-keto-dihydro-PGF(2alpha) also increased four-fold in the VF5 group. Thus, 8-iso-PGF(2alpha) and 15-keto-dihydro-PGF(2alpha) measurements in jugular bulb plasma may be used as biomarkers for quantification of free radical catalyzed oxidative brain injury and inflammatory response in reperfusion injury
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| 2. |
- Basu, Samar, et al.
(författare)
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Evidence for Time-dependent Maximum Increase ofFree Radical Damage and Eicosanoid Formation in theBrain as Related to Duration of Cardiac Arrest andCardio-pulmonary Resuscitation
- 2003
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Ingår i: Free radical research. - : Informa UK Limited. - 1071-5762 .- 1029-2470. ; 37:3, s. 251-256
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Tidskriftsartikel (refereegranskat)abstract
- Recovery of neurological function in patients following cardiac arrest and cardiopulmonary resuscitation (CPR) is a complex event. Free radical induced oxidative stress is supposed to be involved in this process. We studied levels of 8-iso-PGF2alpha (indicating oxidative injury) and 15-keto-dihydro-PGF2alpha (indicating inflammatory response) in venous plasma obtained from the jugular bulb in a porcine model of experimental cardiopulmonary resuscitation (CPR) where 2, 5, 8, 10 or 12 min of ventricular fibrillation (VF) was followed by 5 or 8 min of closed-chest CPR. A significant increase of 8-iso-PGF2alpha was observed immediately following restoration of spontaneous circulation in all experiments of various duration of VF and CPR. No such increase was seen in a control group. When compared between the groups there was a duration-dependent maximum increase of 8-iso-PGF2alpha which was greatest in animals subjected to the longest period (VF12 min + CPR8 min) of no or low blood flow. In contrast, the greatest increase of 15-keto-dihydro-PGF2alpha was observed in the 13 min group (VF8 min + CPR5 min). Thus, a time-dependent cerebral oxidative injury occurs in conjunction which cardiac arrest and CPR.
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| 3. |
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| 5. |
- Friberg, Hans, et al.
(författare)
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Terapeutisk hypotermi efter hjärtstopp : ny länk i kedjan som kan rädda liv
- 2004
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Ingår i: Läkartidningen. - 0023-7205 .- 1652-7518. ; 101:30-31, s. 2412-6
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Tidskriftsartikel (refereegranskat)abstract
- Sudden, unexpected cardiac arrest is a common cause of death. Among patients who are successfully resuscitated, a majority dies without regaining consciousness. Therapeutic hypothermia has recently been shown to improve neurological outcome in two randomized studies and to improve survival in one of them. Based on the two studies, international evidence-based recommendations have been proposed and published (ILCOR). In this review we discuss the theoretical background of hypothermic neuroprotection and therapeutic implications. We propose that victims of cardiac arrest with return of spontaneous circulation and persistent unconsciousness are considered for hypothermia treatment and that data from treated patients are collected in a common website database (see: www.scctg.org) to allow further evaluation of the use of ICU resources, efficacy of hypothermia treatment and potential risks.
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| 6. |
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| 7. |
- Gedeborg, Rolf, et al.
(författare)
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Adverse effects of high-dose epinephrine on cerebral blood flow during experimental cardiopulmonary resuscitation
- 2000
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Ingår i: Critical Care Medicine. - 0090-3493 .- 1530-0293. ; 28:5, s. 1423-1430
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE:To study the effects of high-dose epinephrine, compared with standard-dose epinephrine, on the dynamics of superficial cortical cerebral blood flow as well as global cerebral oxygenation during experimental cardiopulmonary resuscitation. We hypothesized that high-dose epinephrine might be unable to improve cerebral blood flow during cardiopulmonary resuscitation as compared with standard-dose epinephrine.DESIGN:Randomized controlled study.SETTING:University hospital research laboratory.SUBJECTS:A total of 20 male anesthetized piglets.INTERVENTIONS:Ventricular fibrillation was induced. A nonintervention interval of 8 mins was followed by open-chest cardiopulmonary resuscitation. The animals were randomized to receive repeated bolus injections of either 20 microg/kg (standard-dose group, n = 10) or 200 microg/kg (high-dose group, n = 10) of epinephrine.MEASUREMENTS AND MAIN RESULTS:Focal cortical cerebral blood flow was measured continuously by using laser Doppler flowmetry. The duration of blood flow increase was significantly shorter in the high-dose group after the second dose of epinephrine. In the high-dose group there was also a consistent tendency for lower peak levels and shorter duration of flow increase in response to repeated bolus doses of epinephrine. Cerebral oxygen extraction ratio was significantly lower in the high-dose group after administration of epinephrine.CONCLUSIONS:Repeated bolus doses of epinephrine 200 microg/kg, as compared with 20 microg/kg, do not improve superficial cortical cerebral blood flow during experimental open-chest cardiopulmonary resuscitation. High-dose epinephrine appears to induce vasoconstriction of cortical cerebral blood vessels resulting in redistribution of blood flow from superficial cortex. This might be one explanation for the failure of high-dose epinephrine to improve overall outcome in clinical trials.
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| 9. |
- Gedeborg, Rolf, et al.
(författare)
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Cerebral ischaemia in experimental cardiopulmonary resuscitation--comparison of epinephrine and aortic occlusion.
- 2001
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Ingår i: Resuscitation. - 0300-9572 .- 1873-1570. ; 50:3, s. 319-29
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Tidskriftsartikel (refereegranskat)abstract
- The apparent inability of epinephrine to improve outcome after cardiopulmonary resuscitation (CPR) could be caused by direct negative effects on the cerebral circulation. Constant aortic occlusion with a balloon catheter could be an alternative way to improve coronary and cerebral perfusion during CPR. The objective of the present study was to compare the effects of standard-dose epinephrine with balloon occlusion of the descending aorta on cortical cerebral blood flow augmentation during CPR. Ventricular fibrillation was induced in 24 anaesthetised piglets. A non-intervention interval of 9 min was followed by open-chest CPR. The animals were randomised to receive repeated intravenous bolus doses of epinephrine 20 microg/kg or balloon occlusion of the descending aorta. Focal cortical cerebral blood flow was measured continuously using laser-Doppler flowmetry. Balloon occlusion of the aorta resulted in a significantly higher mean cortical cerebral blood flow and a lower cerebral oxygen extraction ratio than epinephrine during CPR. After restoration of spontaneous circulation the cerebral perfusion appeared compromised to the same extent in both groups, with lower blood flow compared to baseline, high cerebral oxygen extraction and cerebral tissue acidosis. No difference in cerebral cortical vascular resistance between the two groups could be detected. It is concluded that aortic balloon occlusion was superior to epinephrine in cerebral blood flow augmentation during resuscitation and did not generate adverse effects on cerebral blood flow, oxygenation or tissue pH after restoration of spontaneous circulation. No evidence of cerebral vasoconstriction induced by standard-dose epinephrine was found.
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