| Research background:As we known, coronary heart disease(CHD) has become one of most lifethreatening diseases. Currently, the main way to treat CHD is to reopen the oc clusive coronary and restore its blood-supply as soon as possible. In most case s, patients' conditions could improve after this treatment, however, sometimes,with the revascularization, arrhythmia and organic injury was found, it may ca use reperfusion injury. Ca2+ play an important role in curing reperfusion injury,so the main research direction for related fields is to find an effective metho d to reduce the ischemia-reperfusion injury. Remote ischemic postconditioning(RIP) has good operability and damages slightly to target organ, which draw re searchers' attention soon. However, currently, the exact mechanism of RIP is c omplicated and unclear. At present, the results of some studies shows that its mechanism is to invoke the PI3k-AKt-e NOS access of cells and then to arouse the downstream target molecules further. Other study results also reveal that NCX can act as the role to transit the calcium ion into cells in the process of reperfusion. However, there are no related reports on the issue that whether t here is a relation between PI3k-AKt-ENOs access and NCX during the postcon ditioning.Object:To explore the relationship between PI3k-AKt-ENOs and NCX in the process of remote postconditioning.method:Forty adult rabbits were divided into five groups randomly(each=8).(1)Control group: rabbits were underwent surgical procedures and passed the suture under the left anterior descending branch(LAD) but not tightened it;(2)Ischemia/reperfusion group( group I/R) : ischemia 45 min followed by reperfusion 3h;(3)remote ischemic postconditioning group(group RIP):the rabbits' left arterial cruralis was occlusion 25 min and followed by 5 min reperfusion while LAD was ischemic 30 min and then reperfused 180 min;(4)NCXi group: rabbits were injected with 3mg/kg KB-R7943 before blood supply,then they were gave the same treatment as group RIP.(5) remote ischemic postconditioning and NCXi group:rabbits were injected with 3mg/kg KB-R7943 before blood supply. then they were gave the same treatment as group RIP.Results:There are not significant differences in CK concentration of five groups before ischemia(P>0.05). At the end of repufusion 180 min, in addition to the group control,the concentrations of CK in the remaining four groups are higher than before ischemia. The CK concentration of group I/R was higher than that of group Control(P<0.01). The concentration of CK in group RIP was lower than that of group I/R(P<0.01). The CK concentration of group RIP+NCXi was lower than that of group RIP(P<0.01).The cell apoptosis:rate of myocardial cell of control group is significantly smaller than the rest four groups(p<0.01). The group I/R has the biggest death rate of myocardial cell(p<0.01). The death rate of myocardial cell of group RIP is smaller than group NCXi(p<0.05).The expression of p-AKt protein in I/R group was higher than control group(p<0.05). The other three groups are bigger than control group significantly. The expression of P-AKt protein in group NCXI was smaller than group RIP and NCXi+RIP group( p<0.01). The expression of P-AKt protein in group RIP was smaller than NCXi+RIP group(p<0.01).The expression of e NOS in Control group was smallest(p<0.01).The other four gruop was significantly higher than Control group.The expression of e NOs protein in group NCXi was higher than that of group I/R(p<0.01). The expression of e NOs protein in group RIP was higher than that of group NCXi(p<0.01).The expression of e NOs protein in group NCXi+RIP was higher than that of group RIP(p<0.01).The expression of NCX protein in control group was smallest. The expression of NCX protein in I/R group was biggest. The expression of NCX protein in NCX was a litter smaller than group NCXi(p<0.01). The expression of RIP is a bit bigger than group NCXi(p<0.01).The expression of e NOS m RNA in I/R group was higher than control group( p<0.01). The other four groups are higher than control group significantly. The expression of e NOS protein in group NCXi was smaller than group RIP and NCXi+RIP group( p<0.01). The expression of e NOS protein in group RIP was smaller than NCXi+RIP group(p<0.01).The expression of NCX m RNA in control group was smaller than the other four group significantly..I/R group has most NCX m RNA(p<0.01). NCX m RNA in RIP+NCXi group is smaller than NCXi group(p<0.01). NCX m RNA in NCXi group is smaller than RIP group(p<0.01).Conclusion1.Remote postconditioning may protect myocardium with the help of PI3kAKt-e NOS access.2.Inhibition NCX reverse transportation may reduce the death rate of myocardial cell to protect myocardium.3.Inhibition NCX reverse transportation may protect myocardium with the PI3k-AKt-e NOS access. |
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