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Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,632
Online ISSN 1827-191X
Göl M. K., Nisanoglu V., Iscan Z., Balci M., Kandemir Ö., Tasdemir O.
Cardiovascular Surgery Clinic Türkiye Yüksek I˚htisas Hospital Ankara, Turkey
Background. A nitric oxide donor, sodium nitroprusside has been reported to reduce the inflammatory response during cardiopulmonary bypass (CPB). To investigate this, a double-blind and prospective study was conducted.
Methods. Twenty patients with multi vessel coronary disease were randomly chosen to form study (SNP) and control groups. In the SNP group, 0.5 μg/kg/min sodium nitroprusside were administered for 20 min right after the release of the aortic crossclamp. Mac-1 (CD11b/CD18) leukocyte adhesion molecule expressions, interleukin-6 levels were measured from radial artery blood as well as leukocyte and platelet counts in both groups at 6 different time points: a) before anesthesia, b) after heparin administration, c) after aortic crossclamp release, d) after protamine administration, e) 3 hours after the termination of CPB, f) 24 hours after the termination of CPB.
Results. The increase in Mac-1 expressions were not different between the two groups at any time point except the measurements after the administration of protamine. At this time point, Mac-1 expressions were not different between the groups (99.8±30.7 vs 134.6±95.1%, p=0.076), but higher when compared with the preinduction levels. IL-6 levels for SNP and control groups was 89±43 and 215±131 pg/dL, respectively (p=0.016) 3 hours after the termination of CPB. Twenty-four hours after the termination of CPB, IL-6 levels were still significantly higher in the control group (47±27 vs 111±68 pg/dL, p=0.039). Leukocyte and platelet counts were not different at any time point between the groups.
Conclusions. Systemic inflammatory response in patients undergoing CPB can be reduced to a certain level with sodium nitroprusside, especially the activation of vascular endothelial cells can be inhibited, but activation of lekocytes still takes place.