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Experimental Study Of Promoting Effect And Its Mechanism Of Delayed Ischemic Preconditioning On Myocardial Neovascularization In Infarct Border Zone For Rats With Non-Reperfusion Myocardial Infarction

Posted on:2011-12-01Degree:DoctorType:Dissertation
Country:ChinaCandidate:J S ChengFull Text:PDF
GTID:1114360305967939Subject:Internal Medicine
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Objective To study if delayed ischemic preconditioning (DIPC) can promote myocardial neovascularization and its effects in infarct border zone of rats with myocardial infarction induced by permanent coronary artery ligation and to explore the possible mechanism.Methods Adult rats were randomly divided into 5 groups. IPC group:blood supply for anterior descending coronary arteries was restricted for 6 minutes and then restored for 6 minutes, which were repeated 4 times; IPC+AMI group:coronary arteries of rats in IPC group were ligated 24h later; Sham group:Thoracotomy was done as that to IPC group without blocking blood flow to coronary arteries; AMI group:coronary arteries of rats in Sham group were ligated 24h later; control group:nothing was done with rats.With regard to IPC+AMI group,AMI group and control group, first, left ventricular short axis fractional shortening (FS) was checked 14d after infarction with ultrasound firstly and infarction area was measured with Masson staining after the rats were putting to death. Myocardial neovascularization in infarct border zone was checked 3d,7d and 14 after infarction with immunohistochemical staining. As to IPC group and Sham group, myocardial neovascularization in ischemic zone was detected 24h after IPC with immunohistochemical staining, so was myocardial VEGF and PDGF-B expression in ischemic zone Oh,6h,12h and 24h after IPC.Results Compared with those of rats in AMI group, FS value of rats in IPC+AMI group raised evidently, infarction area decreased 14d after infarction,capillary density of myocardium in infarct border zone increased 3d and 7d after infarction and arteriole density increased too 14d after infarction. Compared with those of rats in Sham group, capillary density of myocardium in ischemic zone of rats in IPC group increased and myocardial VEGF and PDGF-B protein expression in ischemic zone raised 24h after ischemia.Conclusion For rats with non-reperfusion myocardial infarction, DIPC reduces infarct size and improves heart function, promotes myocardial angiogenesis and arteriogenesis in infarct border zone, whereas increased expression of VEGF and PDGF-B in ischemic myocardium in rats may contribute to proliferative capillary and arteriole. Objective To study if delayed ischemic preconditioning can exert cardioprotective effect on ageing rats with myocardial infarction,and explore angiogenesis in ischemic myocardium in ageing rats subject to ischemic preconditioning.Methods Ageing rats were randomly divided into 5 groups. IPC group:blood supply for anterior descending coronary arteries was restricted for 6 minutes and then restored for 6 minutes, which were repeated 4 times; IPC+AMI group:coronary arteries of rats in IPC group were ligated 24h later; Sham group:Thoracotomy was done as that to IPC group without blocking blood flow to coronary arteries; AMI group:coronary arteries of rats in Sham group were ligated 24h later; control group:nothing was done with rats.With regard to IPC+AMI group,AMI group and control group, first, left ventricular short axis fractional shortening (FS) was checked 14d after infarction with ultrasound firstly and infarction area was measured with Masson staining after the rats were putting to death. Myocardial neovascularization in infarct border zone was checked 3d,7d and 14 after infarction with immunohistochemical staining. As to IPC group and Sham group, myocardial neovascularization in ischemic zone was detected 24h after IPC with immunohistochemical staining, so was myocardial VEGF and PDGF-B expression in ischemic zone Oh,6h,12h and 24h after IPC.Results The survive rate of rats in IPC+AMI group and AMI group was low(IPC+AMI group vs. AMI group:5.9%(1/17) vs.15.8%(3/19),P>0.05), whereas the death rate is so high that we can't evaluate heart function,detect infarct size and measure neovascular density in infarct border zone myocardium.Compared with sham group, angiogenesis was seen increased in ischemic myocardium for rats in IPC group,but difference was no significance(IPC group vs. sham group:2367±216counts/mm2 vs.2 267±121 counts/mm2,P>0.05).Immunohistochemistry staining shows that VEGF protein expression in ischemic myocardium in ageing rats after IPC increased markedly(IPC group vs. sham group:0.17±0.02 (mean density) vs.0.10±0.01 (mean density),P<0.05), PDGF-B protein expression in ischemic myocardium in ageing rats after IPC increased markedly too(IPC group vs. sham group:0.14±0.00 (mean density) vs.0.02±0.01 (mean density),P<0.05).Conclusion Delayed ischemic preconditioning enhance death rates in ageing rats with myocardial infarction,angiogenesis was not increased markedly in ischemic myocardium for ageing rats subject to ischemic preconditioning.
Keywords/Search Tags:delayed ischemic preconditioning, acute myocardial infarction, angiogenesis, arteriogenesis, rat, ageing
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