Experimental Study Of The Effect Of Netrin-1on In Vivo Myocardial Ischemia Reperfusion Injury In Rats

Objective:To observe the effect and mechanism of Netrin-1on in vivo myocardialischemia reperfusion injury in rats. For the clinic with myocardial protection aboutcardiopulmonary bypass with a new strategy.Metholds:Twenty male Sprague-Dawley rats,weight (400-450)g,were randomly dividedinto two groups(each=10): I/R+Netrin-1and I/R groups. To establish of myocardialischemia reperfusion model of no blood priming of rats with deep hypothermiccirculatory arrest (DHCA). Two groups of rats were given tracheal intubation ingeneral anesthesia, mechanical ventilation, and cardiopulmonary bypass intubation,while rates were cooled to a rectal temperature of16℃to18℃within30minutes,cardiac arresting, and given by DHCA30min, then rewarming within40minutes,animals were weaned from cardiopulmonary bypass at36.6℃. Bloodsamples were collected at the before of CPB,15min after rewarming and2h afterCPB for determination of myocardial injury markers of cardiac troponin I (cTn I)and heart fatty acid binding protein (HFABP). These was measured byEnzyme-linked immunosorbent assay (ELISA). Heart samples were collected fordetection of myocardial cell apoptosis with TUNEL method and detection of localmyocardial DCC protein index with Western-blot method. hematoxylin and eosin(HE) staining of cardiac tissue specimens were observed in the MyocardiumPathological Changes.Blood samples were collected at the before of CPB,15minafter CPB and DHCA,at the termination of CPB and2h after CPB for blood gasanalysis.Results:The I/R+Netrin-1group than in I/R group: serum cardiac troponin I (cTn I)and heart fatty acid binding protein (HFABP) expression was significantly reduced;myocardial apoptosis after myocardial ischemia-reperfusion injury decreased27.5% (P <0.05); the expression of DCC increased (P <0.05). HE staining microscopicobservations showed that I/R+Netrin-1group significantly reduced myocardialcell injury. At the same time, We found that I/R+Netrin-1group of myocardialcell injury is reduced significantly through HE staining in light microscopyobservation.Conclusions:(1)myocardial ischemia reperfusion model of no blood priming of rats withdeep hypothermic circulatory arrest (DHCA) is the ideal model of study ofmyocardial and other organs protection during cardiopulmonary.(2)Netrin-1onmyocardial ischemia reperfusion injury has a protective effect, its mechanism maybe related with DCC.