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Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899
Online ISSN 1827-1839
Tachtsi M. D., Pitoulias G. A., Kostoglou C., Papadimitriou D. K.
Aristoteleion University of Thessaloniki, School Medicine, 2nd Department of Surgery-Division of Vascular Surgery “G. Gennimatas” Hospital, Thessaloniki, Greece
AIM: The aim of the study was to determine the quantity of produced mediators of inflammation (cytokines and eicosanoids), during carotid endarterectomy (CEA), which are factors of ischemic damage of the brain.
METHODS: Two groups (A and B) of 15 patients each, with internal carotid backpressure >30 mmHg were operated in our institution. We did not use a shunt in Group A during CEA and group B was operated upon with a shunt.
Plasma concentrations of Interleukin-1b (IL-1b), Thromboxane B2 (TXB2), Prostaglandin E2 (PGE2) and tumor necrosis factor-a (TNFa) were measured by enzyme-linked immunosorbent assay (ELISA) technique.
RESULTS:We measured gradual increase of levels of IL-1b and TXB2 during cross-clamping and during reperfusion in group A (P<0.05). The levels of TNFa increased only during reperfusion (P<0.05). The concentration of IL-1b and TNFa remained almost stable in group B, whereas the concentration of TXB2 reduced but not significantly (P>0.05). The levels of PGE2 remained stable in both groups.
CONCLUSION: We should consider the increase of proinflammatory mediators during carotid cross-clamping when no shunt is used. The critical concentration of these mediators that threaten the brain’s vitality is not yet detected. However, the clinical significance of this is unclear, since there were no perioperative strokes.