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- 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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- Liu, X. L., et al.
(författare)
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Differences in cerebral reperfusion and oxidative injury after cardiac arrest in pigs
- 2003
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Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 47:8, s. 958-967
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: An investigation of the free radical scavenger sodium 2-sulfophenyl-N-tert-butyl nitrone (S-PBN) and the weak vasodilatator Tris buffer mixture (TBM) on cerebral cortical blood flow (CCBF) and the jugular bulb concentration of two eicosanoids, indicators of oxidative stress and inflammation, was undertaken in 30 anaesthetized piglets during cardiopulmonary resuscitation (CPR) and after restoration of spontaneous circulation (ROSC).METHODS: Thirty animals were subjected to 8 min of untreated circulatory arrest followed by 8 min of closed-chest CPR. During CPR, the animals were randomized to receive 60 mg/kg S-PBN, 1 mmol/kg TBM or 2 ml/kg normal saline (n = 10 in each group). Systemic haemodynamic variables, CCBF and jugular bulb plasma concentrations of 8-iso-PGF2alpha and 15-keto-dihydro-PGF2alpha were measured.RESULTS: The CCBF during reperfusion after ROSC was greater in the TBM group than in the S-PBN group, the regression coefficient between CCBF and mean arterial blood pressure being lower in the S-PBN group than in the TBM group. The jugular bulb plasma concentration of 8-iso-PGF2alpha during the first 30 min after ROSC was greater in the TBM group than in the S-PBN group. Administration of TBM after vasopressin did not attenuate the pressor effect of vasopressin.CONCLUSION: Administration of S-PBN during CPR results in less cerebral oxidative stress, possibly by promoting normal distribution of cerebral blood flow.
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- Liu, X. L., et al.
(författare)
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Neurological outcome after experimental cardiopulmonary resuscitation : a result of delayed and potentially treatable neuronal injury?
- 2002
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Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 46:5, s. 537-546
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: In experimental cardiopulmonary resuscitation (CPR) aortic balloon occlusion, vasopressin, and hypertonic saline dextran administration improve cerebral blood flow. Free radical scavenger alpha-phenyl-N-tert-butyl-nitrone (PBN) and cyclosporine-A (CsA) alleviate neuronal damage after global ischemia. Combining these treatments, we investigated neurological outcome after experimental cardiac arrest.METHODS: Thirty anesthetized piglets, randomly allocated into three groups, were subjected to 8 min of ventricular fibrillation followed by 5 min of closed-chest CPR. The combined treatment (CT) group received all the above-mentioned modalities; group B was treated with balloon occlusion and epinephrine; and group C had sham balloon occlusion with epinephrine. Indicators of oxidative stress (8-iso-PGF(2 alpha)), inflammation (15-keto-dihydro-PGF(2 alpha)), energy crisis (hypoxanthine and xanthine), and anoxia/hypoxia (lactate) were monitored in jugular bulb venous blood. Neurological outcome was evaluated 24 h after CPR.RESULTS: Restoration of spontaneous circulation (ROSC) was more rapidly achieved and neurological outcome was significantly better in the CT group, although there was no difference in coronary perfusion pressure between groups. The jugular venous PCO2 and cerebral oxygen extraction ratio were lower in the CT group at 5-15 min after ROSC. Jugular venous 8-iso-PGF(2 alpha) and hypoxanthine after ROSC were correlated to 24 h neurological outcomeCONCLUSIONS: A combination of cerebral blood flow promoting measures and administration of alpha-phenyl-N-tert-butyl-nitrone and cyclosporine-A improved 24 h neurological outcome after 8 min of experimental normothermic cardiac arrest, indicating an ongoing neuronal injury in the reperfusion phase.
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- Nozari, A, et al.
(författare)
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Differences in the pharmacodynamics of epinephrine and vasopressin during and after experimental cardiopulmonary resuscitation.
- 2001
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Ingår i: Resuscitation. - 0300-9572 .- 1873-1570. ; 49:1, s. 59-72
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Tidskriftsartikel (refereegranskat)abstract
- Vasopressin has been investigated as a possible alternative to epinephrine during cardiopulmonary resuscitation (CPR). We tested the hypothesis that vasopressin, in comparison with epinephrine, would improve cerebral blood flow and metabolism during CPR as well as after restoration of spontaneous circulation (ROSC). A total of 22 anaesthetised piglets were subjected to 5 min of ventricular fibrillation followed by 8 min of closed-chest CPR. The piglets were randomly allocated to receive repeated boluses of either 45 microg/kg epinephrine or 0.4 U/kg vasopressin IV. Haemodynamic parameters, cerebral cortical blood flow and cerebral tissue pH and PCO(2) were continuously monitored during CPR and up to 4 h after ROSC. Cerebral oxygen extraction ratio was calculated. Cerebral cortical blood flow increased transiently after each bolus of epinephrine, while only the first bolus of vasopressin resulted in a sustained increase. The peak in cerebral cortical blood flow was reached approximately 30 s later with vasopressin. During the initial 5 min following ROSC, cerebral cortical blood flow was greater in the vasopressin group. In conclusion, there is a difference between epinephrine and vasopressin in the time from injection to maximal clinical response and the duration of their effect, but their overall effects on blood pressures and cerebral perfusion do not differ significantly during CPR. In contrast, vasopressin results in a greater cerebral cortical blood flow during a transient period after ROSC.
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