Vojnosanitetski Pregled (Jan 2002)
Changes of cortisol levels and index of lipid peroxidation in cerebrospinal fluid of patients in the acute phase of completed stroke
Abstract
Background. Brain ischemia initiates series of biochemical reactions that could, directly or indirectly, induce and extend processes that damage numerous cellular and subcellular structures. One of the reactions of organism to ischemia is the increased release of glucocorticoid hormones, included in regulation of effects of numerous mediators/modulators that could be released in the acute phase of brain ischemia. Considering that brain infarction induced systemic response of organism to stress, we presumed that it reflected the contents of cortisol in the cerebrospinal fluid (CSF) during the acute phase of the disease, and that cortisol influenced damaging processes of lipid peroxidation in CNS initiated by ischemia. The aim of our investigation was to define temporal dynamics and manner correlation of cortisol concentration and index of lipid peroxidation (ILP) in the CSF patients in the acute phase of completed stroke. Methods. In this investigation we followed changes of cortisol concentration and ILP in the CSF of 53 patients in the acute phase of completed stroke. Control group included 14 age and sex matched patients, subjected to diagnostic lumbar radiculography because of the sudden motor deficiency onset, without disturbances in the CSF passage and without pain and the consequences of anti-pain and anti-inflammatory therapy. From the perspective of the duration of period after an ischemic episode patients were divided into four groups: group A: 0-6 hours (n=12), group B: 7-12 hours (n=14), group C: 13-24 hours (n=14), and group D: 24-48 hours of postischemic period (n=13). Concentration of cortisol in the CSF was measured by quantitative RIA method (Cortisol Bridge kit, Biodata). The ILP was determined according to the spectrophotometric method. Results. Concentration of cortisol in the CSF of patients with completed stroke was of amount 69 ± 6.7 pmol/ml CSF and was significantly increased (p<0.001) compared to the values of the control group (2.49 ± 0.29 pmol/ml CSF). From 0 to 6 hours after the ischemic insults concentration of cortisol in the CSF the amount was 15.9 ± 2.4 pmol/ml CSF (p<0.001), then was progressively increasing and was maximal from 13 to 24 hours after insults (123.2 ± 7.1 pmol/ml CSF), (p<0.001). In patients with completed stroke ILP in the CSF was twice increased in the course of 48 hours compared to controls (0.54 ± 0.08 nmolMDA/ml CSF), (p<0.05). By comparing the observed parameters we found significant negative correlation between this two indicators in period from 7 to 24 hours (r=-0.77), (p<0.001). Conclusion. The main potentially protective effect of the increased CSF cortisol concentration in patients with completed stroke in the acute phase could be the decrease of deleterious effects of lipid peroxidation reactions induced by ischemia. This mechanism could be the attempt of organism to compensate ischemia-disturbed homeostasis.
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