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Perfusion, Vol. 18, No. 1, 3-8 (2003)
DOI: 10.1191/0267659103pf622oa

Correlation between inflammatory response and markers of neuronal damage in coronary revascularization with and without cardiopulmonary bypass

Annamaria Mazzone

C.N.R. Institute of Clinical Physiology, Ospedale G. Pasquinucci, Massa, Italy, mazzone{at}ifc_cnr.pi.it

Jacopo Gianetti

C.N.R. Institute of Clinical Physiology, Ospedale G. Pasquinucci, Massa, Italy

Eugenio Picano

C.N.R. Institute of Clinical Physiology, Ospedale G. Pasquinucci, Pisa, Italy

Stefano Bevilacqua

C.N.R. Institute of Clinical Physiology, Ospedale G. Pasquinucci, Massa, Italy

Giancarlo Zucchelli

C.N.R. Institute of Clinical Physiology, Ospedale G. Pasquinucci, Pisa, Italy

Andrea Biagini

C.N.R. Institute of Clinical Physiology, Ospedale G. Pasquinucci, Pisa, Italy

Mattia Glauber

C.N.R. Institute of Clinical Physiology, Ospedale G. Pasquinucci, Massa, Italy

Off-pump coronary artery bypass graft (CABG) surgery may reduce the inflammatory response and the neuronal damage associated with conventional CABG on cardio-pulmonary bypass. The purpose of this study was to explore the protective effect of off-pump surgery by assessing plasma inflammatory and neuronal injury markers. Forty-one patients with coronary artery disease undergoing elective CABG were examined: 21 on-pump (Group I) and 20 off-pump (Group II). The perioperative release of interleukin-2 receptor (IL-2r), IL-6, tumor necrosis factor-alpha, S-100 protein (S-100) and neuron-specific enolase (NSE) were measured. Postoperative peak values of NSE (p B /0.001) and S-100 (p B /0.05) were significantly lower in Group II. IL-6 showed significantly lower values in off-pump patients (p B /0.001). A significant correlation was found between NSE and IL-6 (p B /0.001). In conclusion, off-pump surgery reduces the inflammatory response as well as the perioperative release of neuronal damage markers. Correlation between inflammatory activation and neuronal markers may suggest a link between inflammation and release of markers of neuronal clinical and subclinical injury.


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