Artikel
Isoprostane and cerebral metabolism after aneurysmal subarachnoid hemorrhage in humans – A preliminary experience
Isoprostan und der zerebrale Metabolismus nach aneurysmatischer Subarachnoidalblutung des Menschen – vorläufige Ergebnisse
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Autoren
Veröffentlicht: | 23. April 2004 |
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Gliederung
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Objective
8-Epi-Prostaglandin F2α (Isoprostane) is a product of the non-enzymatic radical induced breakdown of arachnoidonic acid. As shown in animal models, it has effects on cerebral metabolism. The purpose of this study has been to test the hypothesis that isoprostane influences cerebral metabolism after subarachnoid hemorrhage (SAH) in humans.
Methods
A total of 21 studies were performed on 5 SAH patients (age 47±5 years, Hunt and Hess 4). Until day 10 Isoprostane was measured in arterial, jugular-venous blood samples and cerebrospinal fluid (CSF). In addition arterio-venous difference for oxygen (avDO2) and glucose (avDGlc) were evaluated. Metabolic ratio (MR=avDO2/avDGlc) was calculated to estimate cerebral metabolism. Relative hyperglycolysis was defined as MR less than 0.6.
Results
On the average, isoprostane concentrations were higher in arterial than in jugular-venous blood and CSF 165.9±142 pg/l, 113.6±69.3 pg/l and 63.6±28 pg/l, respectively. Mean avDO2 and avDGlc was 3.2±1.6 Vol% and 5.6±7.4 mg%. In 71% of studies Isoprostan concentrations were higher in arterial than in jugular-venous blood. There was a statistical trend for arterial isoprostane and avDO2 (p=0.08) Relative hyperglycolysis was seen in 53% of studies where isoprostane was higher than in studies with normal MR.
Conclusions
Isoprostane seems to influence cerebral metabolism. Most interestingly, it is likely to be generated in other organs than the brain.