Abstract

The aim of this study was to define concentration changes of soluble adhesion molecules (sICAM-1, sVCAM-1 and sE-Selectin) in cerebrospinal fluid and plasma, as well as, number of peripheral blood leukocytes and the albumin coefficient in the patients with the acute brain infarction. We also, analyzed the correlation between the measured levels, the infarct volume and the degree of neurological and the functional deficit. The study included 50 patients with the acute cerebral infarction and the control group consisted of 16 patients, age and sex matched. Obtained results showed significant increase in number of leukocytes, the albumin coefficient and the level of soluble adhesion molecules within the first seven days in patients. The highest values of measured parameters were noted within the third and the fourth day after the insult, which is the suggested period of maximal intensity of inflammatory reactions. Significant correlation was found between measured parameters and the infarct volume, the degree of neurological and the functional deficit. The results suggest that investigated parameters in CSF and blood represent a dynamic index of inflammatory events as one of the fundametal mechanisms responsible for neuron damage during acute phase of brain infarction.

Highlights

  • Inflammatory mechanisms play an important role in the risk of stroke and during the acute phase of brain ischemia, which contributes to functional outcome of patients

  • Concentrations of soluble adhesion molecules sICAM-1, sVCAM-1 and sE-Selectin were determined in plasma and cerebrospinal fluid (CSF) by ELISA-tests (R&D Systems Europe, Abingdon, UK)

  • Plasma samples were diluted with commercial diluents for detecting sICAM-1 in ratio 1:80, for s-vascular cell adhesion molecule 1 (VCAM-1) and sE-Selectin in ratio 1:50 and all CSF samples in ratio 1:1

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Summary

Introduction

Inflammatory mechanisms play an important role in the risk of stroke and during the acute phase of brain ischemia, which contributes to functional outcome of patients. Several inflammatory molecules are implicated during the acute phase of ischemic stroke, such as cytokines and adhesion cell molecules. Experimental studies showed that peripheral blood leukocytes migrate into the brain parenchyma within the first hours after ischemia [1,11,13,17]. Leukocytes contribute to the development of ischemic brain injury by causing capillary plugging, reducing cerebromicrovascular blood flow, increasing microvascular permeability, and secreting a different toxical mediators including reactive oxygen species, leukotrienes, cytokines, chemokines and cytotoxical enzymes which expanded the existing damage to surrounding tissue [16,27,33,40]

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