| Recently years, coronary heart disease has become a hazard to our countryand even the world human health. Despite the timely and effective treatmentcan reduce the degree of myocardial ischemia, raise survival rate of thepatients, but any reperfusion injury inevitable. For example: reperfusionarrhythmia, myocardial systolic dysfunction, endothelial function obstacle,myocardial cell apoptosis etc, which directly affects the treatment effect andprognosis. Therefore, searching for the effective and reasonable treatment toreduce myocardial ischemia-reperfusion injury has important clinicalsignificance.In1986, Murry firstly proposed the concept of ischemic preconditioning,namely, myocardium has a strong tolerance in a long-time ischemia-reperfusion if it has suffered repeated short-term myocardial ischemia andreperfusion. This method increases the tolerance of myocardium to reperfusion.However, in clinical, the time of myocardial ischemia is unpredictable, so that,the clinical application of Preconditioning is greatly limited. In2003, Zhaoproposed the concept of ischemic postconditioning in the test of dogs. In earlyreperfusion, repeated coronary occlusion and reperfusion can significantlyreduce myocardial infarction area and reperfusion injury.Many study of variety animal models confirmed that ischemicpostconditioning have protective effect on the heart, similarly as ischemicpreconditioning. Subsequently, different organs such as brain, liver, kidney inthe different species of animal have also been shown to have different degreesof protection. With the deepening of the study, the research of remote ischemicpostconditioning has been addressed from brain, liver, kidney and other vitalorgans to skeletal muscle. Remote ischemic postconditioning of skeletalmuscle is simple, safe, and convenient. Studies have confirmed that the ischemia-reperfusion of the skeletal muscle can reduce myocardial cellapoptosis and reperfusion injury. But the mechanism of this protection and theInfluence of Bcl-2on Remote Ischemic Postconditioning is not clear.Objective: To observe whether there is a protection of remotepostconditioning to myocardial ischemia and reperfusion, whether Bcl-2is theprotection factor of remote postconditioning.Methods:18healthy New Zealand rabbits were randomly divided into3groups:1) Con: By the thoracotomy exposed the heart,45minutes of leftcircumflex artery (LCX) occlusion followed by120minutes of coronaryartery reperfusion.2) RPostC (Remote postconditioning):the bilateral external iliac artery（EIA）were occluded for5minutes and followed by1minutes of reperfusion,1circle at39minutes of coronary artery ischemia，then reperfusion120minutes with LCX.3) HA14-1+RPostC: the selective Bcl-2inhibitor HA14-1(2mg/kg) wasadministered by intraperitoneal injection30minutes before coronaryocclusion; the EIAs were occluded for5minutes and followed by1minutes ofreperfusion,1circle at39minutes of coronary artery ischemia， thenreperfusion120minutes with LCX.The model of ischemia reperfusion was produced by45minutes occlusionand120minutes reperfusion of left ventricular branch of the left coronaryartery. The skeletal muscle ischemia reperfusion model was produced byregular occlusion and reperfusion of the external iliac arteries. Myocardialischemia and myocardial infracted area was measured using area calculationand weight measurement methods by Evans blue (Evans) and TTC doublestaining. Plasma creatine kinase (CK) activity and lactate dehydrogenase(LDH) activity were measured at baseline，the end of ischemia, after60minand120min of reperfusion respectively.Results:1Hemodynamic parameters in three groups: 1.1HemodynamicsThe hemodynamic paramenters included heart rate (HR) and mean arterialblood pressure (MAP). The heart rates (HR, bpm) and mean arterial pressure(MAP, mmHg) were not different statistically between every group at baseline,the end of ischemia,60min and120min reperfusion.1.2Baseline dataIn the experiment, the body weight (G), left ventricular mass (LV) andischemic area of left ventricle caused by ligation between every group had nosignificant difference (P>0.05).2Myocardial ischemia and infarction2.1The comparison of the ischemic areas among the three groups.Myocardial ischemia size was expressed by area ratio (area at risk/leftventricle, IZ/LVs) and weight ratio (weight of area at risk/left ventricle,IZ/LVg). Myocardial ischemia extent had no statistically difference betweenevery group (P>0.05).2.2The comparison of the infarction areas in the three groups.Myocardial infracted size was expressed by area ratio (NZ/IZs) and weightratio (NZ/IZg). Compared with the Con group (64.25(19.40)), NZ/IZs ofRPostC group (28.71(8.36)) was significantly reduced (P<0.05). The area ratioof myocardial infarction in HA14-1+RPostC group (67.28(11.69)) comparedwith the RPostC group was significantly increased (P<0.05), and there is nostatistical difference between Con group and HA14-1+RPostC group (P＞0.05). The NZ/IZg in three groups had no statistically difference (P＞0.05).3Creatine Kinase (CK) and Lactate Dehydrogenase (LDH) observation:CK had no statistically different between three groups (P>0.05).LDH baseline in every group had no significant difference (P>0.05). At60min and120min of reperfusion, compared with the Con group, LDH of theRPostC group had a trend to reduce, but these results did not reach statisticalsignificance (P>0.05).Conclusions:1The study found that early reperfusion in rabbits’ external iliac arteries given by a short ischemia and reperfusion could reduce myocardial reperfusioninjury.2The myocardial protection of skeletal muscle ischemic postconditioning ismediated by the protein of Bcl-2. |
PDF Full Text Request