| Objective: Ischemic preconditioning (IP) refers to a mechanism whereby brief periods of ischemia reperfusion render a tissue relatively resistant to the harmful effects of a subsequent prolonged period of ischemia. Some studies have demonstrated that a remote myocardial protection can be conferred by an early brief ischemia of a remote myocardial region or even by brief ischemia of a remote organ. This phenomenon was called remote ischemic preconditioning or preconditioning at a distance (RPC). The mechanisms by which remote preconditioning protects the heart are less well understood. Studies showed the adenosine, bradykinin, opioid receptors, protein kinase that released by area after ischemic and reperfusion can stimulate afferent nerve, by nervous reflex, then triggers and signaling pathways such as adenosine, bradykinin, opioid receptors, protein kinase C, tyrosine kinase, mitogen activated protein kinase (MAPK), and ATP-dependent potassium channels in myocardium are activated to protect the heart form ischemic. As a heterodimers, hepatocyte growth factor (HGF) has a chainαwhose molecular is 69KD and a chainβwhose molecular is 34KD. The gene of HGF is in chromatin 7. HGF is a mesenchyme-derived pleiotropic factor which regulates cell growth, cell motility, and morphogenesis of various types of cells. As a protection to heart, HGF has already experimental used to myocardium after ischemic injured. But it was unclear that the effect of HGF on ischemia myocardium after RPC. The purpose of this study was to explore the cardioprotective effect of HGF on ischemia myocardium after RPC by observing the change of HGF gene in the ischemic myocardium after acute myocardial infarction and acute myocardial infarction after RPC, which the theory can be supplied to treatment the ischemic heart disease in clinic.Methods: 1 The rats were divided into four groups:①acute myocardial infarction group (AMI): The method of ligating the left anterior descending coronary artery were used to cause AMI.②limb ischemic preconditioning group (LIP): Rats both femoral artery were underwent four cycles of 5-minute occlusion and reperfusion by a bulldog clamp before the experiment was continued as in Group①.③renal ischemic preconditioning group (RIP): Rats both renal artery were underwent three cycles of 5-minute occlusion and reperfusion by a bulldog clamp before the experiment was continued as in Group①.④control group :using the normal rats as control. Rats were sacrificed and took myocardium tissue in 1hour, 2 hour, 4 hour, 6 hour and 12 hours after ligating the LAD except group④. 2 objective: The changes of electrocardiographic were recorded after surgery, The infarct size of the myocardium were measured at the end of 12h after the ligating left anterior descending coronary artery , the area at risk (AAR) and infarct size (IS) was determined by negative staining. 1. 0% Evans blue and triphenyitetrazoiium chioride (TTC). Infarct size (IS) and the area at risk (AAR) were determined by gravimetric analysis. The AAR was expressed as percentage of the weight of left ventricle (AAR/ LV%),and IS was expressed as percentage of the weight of AAR (IS/ AAR%). HGF gene expression in ischemic myocardium: The levels of HGF gene expression in myocardium tissue were measured by reverse transcriptase-polymerase chain reaction (RT-PCR). The relative expression quantity of specific land was represented with the ratio of land densitomery unit of HGF to that ofβ-actin. We drew assistance from the SPSS13.0 software to analyze the data.Results: 1 The AMI model was established succeefully: The electrocardiographic ST segment was elevated significantly after the ligating. It showed that the AMI model had established. The color of kidney, limb became to dark after occlusion. It showed that the RIP, LIP model had established.2 The infarct size of the myocardium: After stained by evans and TTC, the myocardium was allowed differentiation among the viable (brick red), necrotic (dark) and normal areas (blue). Infarct size (IS) and the area at risk (AAR) were determined. The myocardial IS was decreased significantly in both RIP and LIP group compared with AMI group, and those were 46.18%±6.15%, 46.92%±6.69% and 66.44%±13.68% respectively( P < 0. 05).3 The gene expression of HGF: The gene expression of HGF was increased significantly in AMI group (0.61±0.16 at 4h, 0.68±0.11 at 6h, 0.71±0.18 at 12h compared with control 0.47±0.11, P<0.05). The gene expression of HGF was depressed significantly in RIP group (0.31±0.06 at 4h; 0.35±0.08 at 6h; 0.31±0.06 at 12h) and in LIP group (0.40±0.08 at 4h; 0.47±0.17 at 6h; 0.41±0.11 at 12h) compare to those in AMI group at the same time point ( P < 0. 01).Conclusion: 1 The infarct size of AMI was reduced after RPC in our study, which demonstrated that RPC is quite effective in protecting the myocardium from ischemia injury. Exploring the mechanisms of RPC is very useful to prevent and to treat AMI in clinic.2 The gene expression of HGF were decreased in myocardium of rats after RPC, it means that HGF palys a important role in RPC and may be one of the molecular mechanisms of cardioprotection after RPC.
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