The Study Of Protective Effect And Mechanism Of NXKKFY On Experimental Myocardial Ischemia In Rats

CAHD is the abbreviation of coronary atherosclerotic heart disease, theaeteria coronaria hardening and then leading to ischemic and hypoxia myocardialdisease. It is common and frequent in the aged people. The reason of myocardialischemia (MI) is the injury of oxyradical, the dysfunction of blood vesselendothelium, the infiltrating of the neutrophil etc. In the past, people think that thereperfusing of the blood were the measure of preventing cell damage, but for thepast few years the thinking is changed that the reperfusing of the blood can alsoaggravate the damage of the cell. Then the inchoate prevention and cure to thisdisease is fundamental and important more. The department of traditional Chinesemedicine in JI LIN university is engaged in the task and creating NXKKFY. It is autility prescription of treatment on CAHD which belong to blood stagnancy due todeficiency of QI. It can cure the disease and lessen the distress of the patient. Thepurpose of the experiment is to make clear of the effect and the reason of thehealing of NXKKFY and then to direct the clinical application. Rats were randomly divided into 6 groups, that is the normal, the group ofmodel of MI, the control group of DSDW, low-dose group of NXKKFY,midst-dose group of NXKKFY and high dose group of NXKKFY. After 20 days'treatment of the medicine we inject ISO to the rats and make the model of MI,then monitoring them with ECG. After making sure the model is right, weanesthetize the rats, sliver the abdomen and get the blood. Then testing thechanging of the content of CK, AST, LDH, NO, NOS, GSH-PX and H₂O₂ in theblood-serum. Observing the impairment of tissue of the cardiac muscle. The resultof the experiment is the 90% rats in the model group show the appearance ofmyocardial ischemia, compared with normal group the difference is significant(P<0.05). But in the groups of the NXKKFY, the rates cut down significantly andthe degreement of myocardial ischemia lessen. NXKKFY can also lessen thecontent of CK, AST, LDH and protect and improve the impairment of tissue of thecardiac muscle. On the whole we can conclude that NXKKFY can protect thedisease rats by stabilizing the electrophysiology of the cadiocyte, protecting theintegrity of cadiocyte cell membrane and improving the damage of myocardialischemia. In a word, NXKKFY have the effect of the protection to the rats ofmyocardial ischemia damage.NO come from the generating of NOS. NO can protect the vascularendothelial cell. It cause the vasodilatation, inhibiting substance of the bloodadhere to the vessel wall and preventing the hyperplasy of vessel wall cell. NOcan resist oxidation, inhibit aggregation, adhesion and activation of PMN andthrombocyte in the part of ischemia. NO decrease the secretion of PMM, inhibitthe activity of peroxydase and clean the oxyradical. Ablove all we can concludethat NO can protect the impaired myocardial cell. By the experiement weconclude that during process of myocardial ischemia the contents of NO andactivity of NOS decrease, but the groups of NXKKFY, the contents of NO andactivity of NOS are all advanced, and effect of midst-dose group and high dosegroup is more significant (P<0.01). Compared with the control group thedifference is quiet (P>0.05). NXKKFY can make the activity of NOS to enhanceand lead to increase the protection to the myocardial cell.During the course of myocardial ischemia, it can generate OFR in differentways in the body. At the same time, the system of antioxygenizing desorys. OFRcan be cleaned by SOD, but beyond the capability of the SOD, OFR then changeinto H2O2. And the H2O2 then may be cleaned by GSH-PX mainly. In short timeof MI, it can generate a lot of H2O2, and many GSH-PX be expended, thecapability of the GSH-PX in the blood serum decline quickly, the system ofantioxygenizing in the body desorys soon. In this experiment, the contents ofH2O2 increase and activity of GSH-PX decrease, but NXKKFY can decrease thecontents of H2O2 and increase the activity of GSH-PX, and effect of high dosegroup is more significant (P<0.01). Compared with the control group thedifference is quiet (P>0.05). NXKKFY can make the activity of GSH-PX toenhance and lead to decrease the damage to the myocardial cell.CAHD belongs to blood stagnancy due to deficiency of QI in Chinesetraditional medicine. Deficiency of QI is the radical reason and blood stagnancy isthe consequence which lead to the ischemic and hypoxia myocardial diseasetogether. Then principal of cure is to supply the QI and promoting blood flow.NXKKFY is developed from the tradition famous prescription of BYHWT. It is autility prescription of treatment on CAHD. Now in the reach of pharmacology,many sorts of medicinal herbs in this compound preparation all can protect thedamage of MI cell, it can increase the contents of NO and improve the activity ofGSH-PX.NXKKFY have the efficiency of antioxygenizing, vasodilatating andprotecting the function of blood vessel endothelium and so on.In the summary, in this experentment we can conclude that NXKKFY canproctect the cell membrane and prevent the overflowing of the myocardiumenzyme to damage the cell, stabilize the myocardial cell electrophysiology anddecrease the damage of myocardial cell shape. Reason of the protection due tothat NXKKFY can increase the activity of NOS and lead to strengthen theprotection to the myocardial cell and make the activity of GSH-PX to enhance anddecrease the damage of the H2O2 to the myocardial cell.