| Background Many researches showed thatleukocytes play an important role in myocardial ischemia-reperfusion injury. Blood gets into touch with a lot of man-made substances such as glass, plastic and others during cardiopulmonary bypass. It makes completment activated, leukocyte harmed, oxygen-derived free radical produced, metabolized product of arachidonic acid delivered and micro-polymorphonuclear embolus formed, and causes myocardial cell injury and micro-vascular obstruction. The results above produce myocardial tissue changes in function and structure. Myocardium reperfusion injury will take placeduring the process of aortic cross-clamping and declamping. All of these injuries substances comes from leukocytes.The shortages of crystalloid cardioplegia solution had been recognized. Warm oxygenated blood cardioplegia perfusion had been accepted since 1989. The method of continuous warm oxygenated blood cardioplegia perfusion has achieved great clinical effects on most internal operation patients. Zhuang Shicai, Zhang Daxin and Fa Xian'en et al adopted the method of micro-dose continuous warm oxygenated blood cardioplegia perfusion and had avoided many deficiencies (for instance hyperkalimia , hemodilution ,the increase of erythrocyte damage et al), but some paper reported that warm blood cardioplegia perfusion could cause inflammatory mediators increased ,these mediators relate to leukocyte-infiltration in myocardium.With the development of imunology and blood transfusion technology, It is well known that NHFTR\GVHD\CMV are related to leukocyte.Due to the causes above, explorers try to deplete the leukocyte of oxygenated blood cardioplegia to reduce the extent of myocardial damage after reperfusion. This study is to research the myocardia protected effects of warm oxygenated7leukocyte-depleted blood cardioplegia.Methods We selected 20 patients with heart diseases whose aortic cross-clamping time were more than 40 minutes . They were randomized into two groups: leukocyte-depleted and control groups, 10 patients with each group. Control group received normal warm blood cardioplegia perfusion(leukocyte count 4930 ?790.0/ul)and leukocyte-depleted group(LD) perfused with leukocyte-depleted warm oxygenated blood (leukocyte count 49.0 ± 7. 38/ul). Detected the serum levels of human heart fatty acid-binding protein(HH-FABP) and myeloperoxidase (MPO) of right atrium myocardium on different time port to evaluate their effects of myocardial protection.Results HH-FABP The serum HH-FABP levels of both group increased significantly after aortic declamping, and peaked at 40 minutes after aortic declamping and decreased gradually hereafter. LD Versus control groups, serum levels were 40.57 ± 7.79 vs 56. 17 ± 11. OOug/L, 52.52 ± 11.27 vs 86. 41 ± 17. 56ug/L, 52. 18 ± 11.60 vs 82. 19 ± 21. 41ug/L 40. 79±1015 vs 54. 04±14. 80ug/L at 20min , 40min, GOmin , 90min after aortic declamping respectively.Significant difference (P<0.01 or P<0.05); LD Group HH-FABP concentration, were 3.88±1.03,18.20 ± 2.11, 31. 80 ± 8. 05ug/L at pre-operation, SOminuts after aortic cross-clamping immediately and control group were 3.64 ± 0.817,18.68 ± 2.48, 37.22 ± 7.962ug/L no significantly (P>0. 05). At 60minutes of two groups, HH-FABP were no statistical significance (P>0.05).Results as above suggested that a significant positive serum HH-FABP levels and aortic cross-clamping time(LD group r=0.9624 r'=0.9262 P<0.01 control group r=0. 7031 , r2=0. 4943, P<0. 01 ). Meantime displayed that LD group serum levels remarkable lower than control group and shown that HH-FABP can reflect the severity of myocardial ischemia reperfusion injury .MPO MPO contents of myocardium at pre-operation and aortic cross-clamping 30minutes were no statistical significance between two groups, (P>0.05) After reperfusion Sminutes versus pre-operation. MPO contents of LD group were 2.86 ± 0.81 vs 2.483 ± 0.53, no remarkable in creased P>0.05; control group were 4.355 ± 0.586 vs 2.547 ± 0.456, increased hig...
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