| Machanism of cardioprotective effect in ischemic preconditioning is in all the kinds of animals in cluding human. Ischemic preconditioning occurs in two phases:an early phase,which lasts 2-3h,and a late phase,which begins 12-24h later and lasts 3-4 days.The late phase of ischemic preconditioning can be induced by brief ischemic\heat shock protein and oxidize the nitrogen,among them, oxidize the nitrogen is much more noted.It is thought that oxidize the nitrogen play an important role in the cardioprotective effect of ischemic preconditioning. Recent studies incident:the heart is not only a dynamical organ that drives blood circulation,but also a latenet endocring organ.It can produce and secrete kinds of biological live material,especially RAS,which promote the application of angiotensin converting enzyme inhibitors in clinic.Presently, angiotensin converting enzyme inhibitors are used extensively for treatment of hypertension and chronic heart failure,and its cardioprotective effect against ischaemia-reperfusion injury has been shown in various animal models.Not only captril but also ramipril was used in second window of cardialprotection .Fosinopril as a new ACEI,its medicine function can keep on time long.It was excreted by kidney and liver. So studying its cardioprotective effect against ischaemia-reperfusion injury t is significant sense and practicable.To study the machanism of preconditioning and the late protective effect of the fosinopril,develop the resource of medicine.We observed the changes in infraction size and the quantiation of iNOS in the late preconditioning after pretreatment with fosinopril,elaborated the machanism and the cardioprotective effect of fosinopril in the late preconditioning is induced by NO.This study will provide the foundmental theorial evidence for clinical use.In this study,24 Wistar male rats were divided into 4 groups at random,4-6 rats in each group.Three of the experimental group,were pretreated with medicines salinesolution, fosinopril ,L-NAME respectively.24 hour before we made ischemiae-reperfusion model,wherea the control group was only pretreated with nomal salinesolution.Rats was injection medicine by vein of tongue bottom ,after 24 hour rats was made ischemiae-reperfusion models.After rats were anesthetize with 10% chloral hydrate,trachealintubaoon and 2 lead electrocardiogrphic monitoring mechine were connected .The next step was opening the chest to connect apirophprus (frequency 55 time/min the dampness measures 1.5mls/100gs),monitoring the electrocardiogram and recording it.Rear the heart after opening the chesy,expose the heart, ischemiae-reperfusion models were copied by closing the left coronary artery dicline before.Conscious rats underwent 30min coronary occlusion/2 hours reperfusion.We recorded the arrhythmia after ischemiae-reperfusion and gave grade point.At the end of experiment,taking off the heart quickly,cutting off artrium and right ventricleses.Left ventricleses was horizontal to cut into slice to slice.Myocardio infarction size of rats were examed:a piece of one tiussue was dyed with HE as control,the rest myocardial slice were dyed with TTC.Becauses the infarction could not be dyed,the left ventricleses was divided into two districts:purple and blue area,no colour area.We would distinct infarction from normal myocardial.Infarction size was exame by measuring the weight.Change of electrocardiogram of ischemiae-reperfusin was recorded by electrocardiogrphic monitoring mechinearrthymia was dave grade point according to the LOWN arrhythmia system.The quantitative aspects of the iNOS after ischemiae-reperfusion was examed by immunohistchemical method .Results showed:comparision of myocardial infarction size :Ischemiae reperfusion injury made all groups appear infarction arear,among them,compared with I/R group,infarction size of FOS group contract obviously.Compared with I/R group and FOS group respectively,there were difference too.Grade point of FOS grous was lower than that of I/R grous a...
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