casein-kinase-ii and Myocardial-Ischemia

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.

Topics: Cardioplegic Solutions; Casein Kinase II; Coronary Artery Bypass; Heart Arrest, Induced; Humans; Interleukin-6; Interleukin-8; Leukapheresis; Middle Aged; Myocardial Ischemia; Myocardial Reperfusion Injury; Protein Serine-Threonine Kinases

Prognostic assessment of unstable angina pectoris is a common clinical problem for physicians. Markers of myocardial cell injury, serial electrocardiographic findings and ST segment monitoring are mainly studied for prognosis. We investigated the relation between myocardial injury and the value of cardiac troponin T and QT interval dispersion in hospitalized unstable angina patients. This is a prospective study that includes adult patients admitted to an emergency department with Braunwald class IIIB unstable angina pectoris. Eighty-six patients were enrolled in the study (mean age of 57 +/- 12 years, 63 males and 23 females). Cardiac troponin T was assayed and QT dispersion calculated from surface ECG. Fifty-eight patients with troponin T < 0.1 ng/ml and 28 patients with troponin T levels > or = 0.1 formed group 1 and group 2, respectively. There were no significant differences in sex, age, history of coronary revascularization or ECG findings such as ST depression and T inversions between the two groups. The QT dispersion was significantly greater in patients with elevated cardiac troponin T levels (77 +/- 18 msec vs 38 +/- 13 mse; p < 0.014). Because QT interval dispersion exhibited an association with cardiac troponin T levels, it may be used as a non-invasive marker of ischemic injury in patients with unstable angina.

Topics: Aged; Angina, Unstable; Biomarkers; Casein Kinase II; Electrocardiography; Female; Heart Rate; Humans; Male; Middle Aged; Myocardial Ischemia; Myocardium; Prospective Studies; Protein Serine-Threonine Kinases

Protein kinase C (PKC), p38 MAP kinase, and mitogen-activated protein kinase-activated kinases 2 and 3 (MAPKAPK2 and MAPKAPK3) have been implicated in ischemic preconditioning (PC) of the heart to reduce damage following a myocardial infarct. This study examined whether extracellular signal-regulated kinase (Erk) 1, p70 ribosomal S6 kinase (p70 S6K), casein kinase 2 (CK2), and other hsp27 kinases are also activated by PC, and if they are required for protection in rabbit hearts. CK2 and hsp27 kinase activities declined during global ischemia in control hearts, whereas PC with 5 min ischemia and 10 min reperfusion increased their activities during global ischemia. Resource Q chromatography resolved two distinct peaks of hsp27 phosphotransferase activities; the first peak (at 0.36 M NaCl) appeared to correspond to the 55-kDa MAPKAPK2. Erk1 activity was elevated in both control and PC hearts after post-ischemic reperfusion, but no change was observed in p70 S6K activity. Infarct size (measured by triphenyltetrazolium staining) in isolated rabbit hearts subjected to 30 min regional ischemia and 2 h reperfusion was 31.0+/-2.6% of the risk zone in controls and was 10.3+/-2.2% in PC hearts (p<0.001). Neither the CK2 inhibitor 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) nor the Mek1/2 inhibitor PD98059 infused during ischemia blocked protection by PC. The activation of CK2 and Erk1 in ischemic preconditioned hearts appear to be epiphenomena and not required for the reduction of infarction from myocardial ischemia.

Topics: Animals; Casein Kinase II; Chromatography, Ion Exchange; Enzyme Activation; Female; Immunoblotting; In Vitro Techniques; Intracellular Signaling Peptides and Proteins; Ischemic Preconditioning, Myocardial; Male; Mitogen-Activated Protein Kinase 3; Mitogen-Activated Protein Kinases; Myocardial Infarction; Myocardial Ischemia; Protein Serine-Threonine Kinases; Rabbits; Ribosomal Protein S6 Kinases