| Myocardial ischemia injury (MII) is a serious harmful diseaseof mankind. But the myocardial ischemia reperfusion injury isgenerally a main interference in the therapy for acute myocardialischemia. That brings a new question for discussion of clinicaltherapy. In the current study, the rats of myocardial ischemia inducedby isoproterenol as used as models to investigate the effects ofNXKKFY on myocardial ischemia injury and their possiblemechanisms. NXKKFY is developed from the tradition famous prescriptionof BYHWT. It is a utility prescription of treatment on mycocardialischemia injury which belong to blood stagnancy due to deficiencyof QI in our department (The department of traditional Chinesemedicine in JI LIN university). In clinical, it can be authenticatedthat NXKKFY could improve myocardial ischemia conditionobviously and soften clinical symptom. At the same time, we findNXKKFY can decrease myocardial ischemia injury. By setting upthe myocardial ischemia injury model of rat and producing relativeexperimental evidences, we observe the effect of myocardialischemia injury in rats after treated by NXKKFY. We approach themechanism of NXKKFY and provide an experimental basis forfurther investigating and clinical use. Rats were randomly divided into normal control group, negativecontrol group, compound DanShen pilular group, low-dose group ofNXKKFY, midst-dose group of NXKKFY and high-dose group ofNXKKFY. The rats were treated by NXKKFY or compoundDanShen pilular with intragastric administration for 20 days.Myocardial lesion model was induced by 5 mg/kg of isoproterenol scin rat. This resulted in J point of ECG moving upward, the activitiesof CK, LDH and AST in serum enhancing, the activities ofNa+-K+-ATPase,Ca2+-ATPase in myocardium depressing and thecontent of Ca2+ enhancing, as well as severe pathological injury.From the experiment, the following conclusions can be gain:1,The changes in ECG:The ECG results showed that NXKKFY markedly diminishedthe rise of J point↑which was used to illustrate the severity ofmyocardial ischemia.2,The changes of biochemical parameters:The changes of biochemical parameters exhibited thatNXKKFY could restrain the increase of CK,LDH and AST activities.There was a significant defference in respect of their effects on CK,LDH and AST between the groups of NXKKFY and the negativecontrol group. It suggests that the ischemia injury of myocardiumwas ameliorated by NXKKFY.3,The changes of content of Ca2+:Compared with normal controlled group, content of Ca2+ inmyocardium increased significantly in negative control group. It isproved that the calcium overload is the important pathogenesis ofmyocardial ischemia injury. The low-dose, midst-dose and high-dosegroup of NXKKFY all can decrease the content of Ca2+, which havevery significant differences by compared with negative control group.The high-dose group of NXKKFY has better capability to decreasethe content of Ca2+ than other dose groups of NXKKFY, which hassignificant difference of statistics. The midst-dose and high-dosegroup of NXKKFY have no significant differences of statistics bycompared with compound DanShen pilular group, but compoundDanShen pilular group has better capability to decrease the contentof Ca2+ than the low-dose group of NXKKFY. All that proved thelow-dose group of NXKKFY, midst-dose group of NXKKFY andhigh-dose group of NXKKFY all can decrease the content of Ca2+ atthe same time. So NXKKFY can play a good role in decrease theinjury of ischemia.4,The changes of Na+-K+-ATPase,Ca2+-ATPase:Compared with normal controlled group, the activities ofNa+-K+-ATPase and Ca2+-ATPase in myocardium decreasedsignificantly in negative control group. It is proved that the excessivedecrease of the activities of Na+-K+-ATPase and Ca2+-ATPase are theimportant pathogenesis of myocardial ischemia injury. The low-dose,midst-dose and high-dose group of NXKKFY all can increase the theactivities of Na+-K+-ATPase and Ca2+-ATPase, which have verysignificant differences by compared with negative control group. Thehigh-dose group of NXKKFY has better capability to increase theactivities of Na+-K+-ATPase and Ca2+-ATPase than other dose groupsof NXKKFY, which has significant difference of statistics. Thehigh-dose group of NXKKFY has no significant difference ofstatistics by compared with compound DanShen pilular group, butcompound DanShen pilular group has better capability to increasethe activities of Na+-K+-ATPase and Ca2+-ATPase than themidst-dose and low-dose group of NXKKFY. All that provedNXKKFY can increase the ability of accelerating the activities ofNa+-K+-ATPase and Ca2+-ATPase. So NXKKFY can play a good rolein protecting the cardiac tissue.5,Pathological change:As pathology results show, the myocardial ultrastructures of ratsof normal control group was normal, while those of negative controlgroup were the worst damaged among six groups. The damage ofhigh-dose group of NXKKFY was less than other dose groups ofNXKKFY. All that proved the degree of injury of cardiac cells islighter than negative control group. It can prove that NXKKFY candecrease the myocardial ischemia injury of rats.In conclusion, In animal models with myocardial damageinduced by isoproterenol in rat, and from the view-point of ECG andsome biochemical changes, the study showed that NXKKFY hasprotective effect on myocardium against ischemia injury and itsmechanism was partly concerned with its effects of inhibition of theproducing of calcium overload and accommodation of energymetabolism.
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