| PrefaceCoronary artery disease is one of the three major diseases which threaten the health status of the elderly. Once the coronary blood flow stopped, ischemia and anoxia will happen in the myocardial cells of that area. In the recent years, many studies have been developed in the field of how to use the anti - injury mechanism of organism itself. Much attention have been focused upon ischemic preconditioning (IPC).Repeated episodes of ischemia and reperfusion dramatically limit infarct size of myocardium caused by subsequent prolonged period of ischemia. This phenomenon is called " ischemic preconditioning". There are two phases of IPC. One is induced immediately after pretreatment and last about one to three hours, which is called " classic ischemic preconditioning". The other is delayed phase which is induced about twelve to seventy - two hours after pretreatment and is called " second window of protection ( SWOP ) " .IPC has come to be acknowledged as the most consistently powerful and reproducible method of delayed the development of ischemic injury known to date. Therefore, it is a hot - spot to study the mechanism of IPC and use them to serve clinical research. However, the accurate mechanism of IPC which induce anti -injury of ischemia has not been concluded till now. As knowledge of IPC accumulated, it became apparent that several signal transduction pathways may participate.In this paper, we aim to further study the mechanism of IPC and research three signal transduction pathways of IPC, they are the b-adrenergic signal transduction, nitric oxide ( NO) - cGMP signal transduction and protein tyrosine kinase(PTK) pathways. As we know to date, there are only a few studies haveconcentrated these three pathways.Materials1. Animals: Female SD rats ( supplied by Animal Laboratory Center of China Medical University) weighing 270 to 320g were used.2. Drugs: Triphenyltetrazolium chloride (TTC) , 3H - DMA, cAMP RIA kit, [r-32P]ATP, PKA antibody (the first part) ; NO kit, NOS kit, cGMP RIA kit , eNOS immunohistochemistry kit ( the second part) ; [r-32P] ATP, gluten - casein polymer, Whatman P81 ion - exchange filter paper ( the third part).3. Equipment: Animal respirator, Nihon Konden electrocardiograph, stereoscopic microscope, liquid scintillation counter, electrophoresis bath, 721 spectropho to meter, paraffin imbedding full - automatic apparatus, microtome.MethodsIn every part, a rat model of myocardial ischemia/reperfusion injury in vivo was used for these studies. Rats were anesthetized with 3% sodium pentobarbital (60mg/Kg) , intubated, and mechanically ventilated with a respirator with room air. ECG was monitored by bipolar limb leads. Left anterolateral thoracotomy was performed from the second to the fourth intercostals space, and the pericardium was opened. A 3 - 0 silk thread was then passed around the proximal of the left major coronary artery with a small curved needle, and its ends were threaded through a small polyethylene tube. Rats were allowed 5 minutes after surgical preparation to reach a steady state. Coronary occlusion was produced by pulling the snare and clamping it with a mosquito hemostat. Reperfusion was produced by releasing the clamp. Myocardial ischemia was confirmed by ST segment elevation of the ECG as well as observation of regional cyanosis over the myocardial surface.Part OneThe rats were divided into four groups: Ischemic preconditioning group (IPgroup, n = 12) , rats were subjected three cycles of five minutes of ischemia followed by five minutes of reperfusion and then subjected to 30 minutes of ischemia followed by 90 minutes of reperfusion. Ischemia/reperfusion group (I/R group, n = 12) , After surgery, rats were balanced for 35 minutes and then subjected to 30 minutes of ischemia followed by 90 minutes of reperfusion. Control group (CON group, n =6) : After surgery, no procedures were made. After 155 minutes finish the experiment. Preconditioning procedure group ( PC group, n = 36): In this group, rats w...
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