title: Leukocyte-depleted continuous blood cardioplegia for coronary artery bypass grafting.
abstract: Many cardiac surgeries are performed with blood cardioplegia. However, some studies suggest that activated neutrophils form blood cardioplegia can cause reperfusion injury. In this study we assessed myocardial protection using a leukocyte-depleted cardioplegic solution. Patients undergoing elective coronary artery bypass grafting (CABG) with continuous blood cardioplegia were divided into two groups: the LD group, which received leukocyte-depleted blood cardioplegia (n = 11); and the control group, which received nonfiltered blood cardioplegia (n = 11). IL-6, IL-8, CK-MB, and troponin T were measured in the coronary sinus blood immediately after the release of the aortic cross-clamp. Cytokine concentrations were also measured upon the patient's return to the ICU. The total dopamine and dobutamine doses, hemodynamic measurements after surgery, and the leukocyte filtration rate were also measured. During antegrade cardioplegia infusion, leukocytes were almost completely removed (filtration rate: 85.8+/-4.0%). However, during terminal warm cardioplegia, leukocyte removal decreased (filtration rate: 39.9+/-7.8%). Immediately after the release of the aortic cross-clamp, plasma CK-MB and troponin T concentrations were significantly lower in the LD group (17.7+/-1.9 U/l and 0.017+/-0.002 ng/ml, respectively) than in the control group (30.3+/-3.6 U/l and 0.072+/-0.029 ng/ml, respectively). The IL-6 and IL-8 concentrations were similar in the LD group and the control group. After the return to the ICU, the CK-MB and troponin T concentrations were similar in the two groups. No significant differences were found in the total doses of dopamine or dobutamine after surgery in the two groups (99+/-77 vs 101+/-128 microg/kg/min). No significant differences were found in the hemodynamic parameters after surgery in the two groups. In patients undergoing CABG with continuous blood cardioplegia, leukocyte-depleted blood cardioplegic solution may attenuate reperfusion injury.
authors.affiliation: Department of Cardiovascular and Thoracic Surgery, Dokkyo University Koshigaya Hospital, Saitama, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Murai
authors.forename: T
authors.initials: T
authors.lastname: Imazeki
authors.forename: S
authors.initials: S
authors.lastname: Shioguchi
authors.forename: M
authors.initials: M
authors.lastname: Saitou
authors.forename: S
authors.initials: S
authors.lastname: Gon
authors.forename: H
authors.initials: H
authors.lastname: Yoshida
authors.forename: I
authors.initials: I
authors.lastname: Hata
mesh_terms: D002314:Cardioplegic Solutions; D047390:Casein Kinase II; D001026:Coronary Artery Bypass / Q000379:methods*; D006324:Heart Arrest, Induced / Q000379:methods*; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D007937:Leukapheresis; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000601:surgery; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control; D017346:Protein Serine-Threonine Kinases
chemical_list: D002314:Cardioplegic Solutions; D015850:Interleukin-6; D016209:Interleukin-8; D047390:Casein Kinase II; D017346:Protein Serine-Threonine Kinases