| PrefaceTo date myocardial protection theory has been constantly evolved in clinical, subcellular and molecular level since Melrose used cardioplegic solution in 1955. The myocardial protection includes many aspects in cardiac surgery. In brief, we should improve cardiac function, increase myocardial energy store before operation, reduce myocardial oxygen consumption, prevent myocardial ischemia reperfusion injury during operation, and ensure the coronary artery blood provides, control the heart carries, promote the recovery of the myocardial con-formance after operation. Clinical myocardial protection research is emphasized in improvement of cardioplegic composition and delivery method. Although myocardium is protected in ischemic phase, it is found that restoration of blood flow may carry along an injurious component, which counteract the beneficial effects of reperfusion. This reperfusion attact phenomenon may manifest as myocardial edema, decreased utilization ability of oxygen or matrix, depletion of high energy phosphate and glycogen, intracellular deposition of calcium salt, mitochon-drial injury, myocardial contractile dysfunction and change of ventricular com-plience. Since this phenomenon is appeared few minutes after restoration of blood flow,it is termed myocardial ischemic reperfusion injury(MIRI).Now there are many evidences that neutrophil and oxygen radical are important factors which lead to MIRI. Coronary vascular endothelium is a major target attacted by neutrophil and oxygen radical. And it is found that coronary vascular endothelium is an original source of oxygen radical. Therefore, it is as same important to protect coronary vascular endothelium as protect myocardium. Along with development of modern molecular biology, expression and regulation of genein I/R myocardium were focused on nuclear transcription factor - kappa B (NF-kB) and inhibitorykB( I-kB) . NF-kB belongs to a rel/NF-icB protein family and found primarily in immune, inflammation and cellar defenses, which played very important roles in regulating multiple immediate early gene expressions. The reasons were probably related to impact on the process of inflammatory reaction, cellular apoptosis and necrosis, ischemic preconditioning and ventricular remodeling , etc, especially involving in positive and negative feedback, and cross regulation in NF-kB activation. However,the exact mechanism was unclear,thus,it is necessary to further explore the molecular mechanisms of NF-kB activation in myocardial I/R injury.In 1987 it was first time proved that the major active component of endothe-lial derived relaxing factor was nitric oxide (NO). In the vascular system, NO accounts for vascular relaxion as well as inhibition of platelet and neutrophil ad-hension, aggregation and activation. In this knowledge, contemporary cardiopro-tective strategies to prevent perioperative ischemia reperfustion injury have focused on L-arginine nitric oxide pathway. Tetrahydrobiopterin (BH4) is an essential cofactor required for nitric oxide synthase ( NOS) , and hence NO production is critically dependent on the presence of adequate amounts of BH4. Diminished levels of BH4 might lead to an uncoupling of NOS, with the resultant production of reactive oxygen species instead of NO. MIRI may result in diminished bioavailability of BH4, which might lead to endothelial and myocyte dys-fuction.The main tasks of this research are: ( 1) To estabilish isolated rat mature and immature heart ischemia reperfusion animal model in vivo. (2) We detected the dynamic change of NOS activity, NO content, myocardial content of malon-aldehyde(MDA) , superoxide dismutase ( SOD ) and myocardial mitochondrial ATPase, and the dynamic change of cornory flow ( CF) , lactic dehydrogenase ( LDH) , creatin kinase ( CK) at different point during myocardial ischemia and reperfusion in order to judge the effects of BH4 on isolated rat mature and immature hearts after MIRI; ( 3 ) We examined the express level change of myocardial TNF-a,NF - KB and ICAM-1 at different time...
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