| Background and objective: With the use of cardiopulmonary bypass (CPB) and high concentration potassium cardioplegia, cardiac surgery developed quickly. However, dysfunction of myocardium following CPB is the main reason of postoperative complication and death. One of the reason of postoperative myocardial dysfunction is the primary heart disease, but ischemic reperfusion injury during CPB is the most important reason. Due to the exposure of blood to nonphysiologic surface and the release of endoloxin, open-heart surgery induces a systemic inflammatory response in a human heart. There is clinical and experimental evidence indicating that polymorphonuclear neutrophils (PMNs) and endothelial cells (ECs) play a prominent role in the inflammatory component of post- ischemic injury. With the activation of PMNs and ECs, adhesion molecules were released. PMNs and ECs initiates a specific cascade of cell-cell interactions leading first to adhesion of PMNs to vascular endothelium, then to coronary capillary plugging (no-flow) and reduction in coronary blood How, resulting eventually in myocardial infarction and apoptosis. Moreover, activated PMNs are a rich source of free oxygen radicals and proteolytic enzymes capable of damaging myocardial cell membranes. The systemic inflammatory response, in uncomplicated case, is a temporary event representing a physiologicalreaction to tissue injury. When the systemic inflammatory response is exaggerated, the postoperative course may be complicated by organ dysfunction, including respiratory failure, renal dysfunction, bleeding disorders, altered liver function, and ultimately, multiple system organ failure (MSOF).Usually, the history of rheumatoid heart disease is long, and dysfunction of myocardium is severe. Inhibition of inflammatory response and reduction of adhesion molecules release are main methods to prevent patients from organ failure, postoperative complications and death. At present, getting rid of neutrophils with filtration, complement and adhesion molecule monoclonal anti-body were used to inhibit inflammatory response. It was reported that the type of cardioplegic solution may affect the inflammatory reactions and the release of adhesion molecules during repcrfusion. No clear difference has been observed in patients with rheumatoid heart disease outcome between the both group in this study.The concentration of myocardial enzymes and intracellular adhesion molecule-1 were measured. This study attempt to determine the effect of cold blood cardioplegia on cardiac function and adhesion molecule during CPB in patients with rheumatoid heart disease.Methods: Twenty patients with rheumatoid heart disease and without liverand renal dysfunction were randomly divided into cold blood cardioplegia group (group CBC) and cold crystalloid cardioplegia group (group CCC). Blood samples were taken from center vein before operation (T1), at the end of CPB (T2), lh(T3), 24h(T4) and 72h after CPB(T5) to measure activity of aspartate transaminase (AST), lactic dehydrogenase (LDH), crealine kinasc (CK), creatine kinase isoenzyme (CK-MB), hydroxybutyric dehydrogenase (HBDH) and level of soluble intracellular molccule-1 (sICAM-1).Results: (1) Ail patients survived the surgery and were discharged in goodcondition. No complication was observed. There were no statistical significance in patients characteristics between cold blood cardioplegia group and cold crystalloid cardioplegia group. (2) There was no difference in the levels of AST baseline valuebetween group CBC and group CCC before operation (P0.05). The levels of AST increased significantly from the end of CPB to 72h after CPB (F<0.01), and reach peak levels 24h after CPB (P<0.01). The levels of AST decreased at 72h after CPB (P<0.01). The levels of AST in group CBC lower than in group CCC significantly from the end of CPB to 72h after CPB (P<0.05). There was no difference in the levels of LDH baseline value between group CBC and group CCC before operation (P0.05). The levels of LDH increased significantly from the end... |
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