| Acute myocardial infarction(AMI) is a type of coronary heart disease(CHD) which severly threatens the human health. And ventricular remoldling(VR) after AMI is a major cause for increased mortality. It is the broad sense of VR that because of the effects of hemodynamics and non-hemodynamics, the size and form of the heart have changed, the microstructure and the function of the heart have damaged. The narrow sense of VR is the geometrical changes of the infracted and/or non-infarcted area of the ventricle,and whose major display are the expansion of infracted area and non-infarcted myocardium.Though VR not increasing the infracted area,it can increase the area of functional MI and progressive expansion of heart which are the prelude of heart failure.The mechanisms of VR after AMI are not fully understood at present. Recently, nitric oxide (NO) is a hot topic of the research of cardiovascular disease. NO is produced in vivo from L-arginine by NO synthase (NOS). Three distinct isoforms of NOS are neural NOS(nNOS), endothelial NOS(eNOS) and inducible NOS (iNOS). Few iNOS is express in normal tissue and induced after the cells are stimulated. The high level of NO induced by iNOS may be toxic to healthy cells as a cytotoxic reactor. Recent studies have shown that iNOS expression is increased in the myocardium of falling hearts. Another study has shown that increased iNOS expression and high level of NO contribute to myocardial dysfunction and higher mortality after MI. But these studies are short-term research and the long-term effects of iNOS to AMI are not reported. We hypothesized that increased NO production from iNOSexpression causes VR after AMI. The aim of this study is to investigate the effects of iNOS and NO in VR after AMI, so we may find a new way to protect myocardial dysfunction and VR after AMI.In phase I ,sixty rats were included and divided into three groups. The model of AMI was made in group I and group II by isoproternol (Isop, 80mg/kg ) injected intraperitoneally(i.p). NS (lml/100g,i.p) substituted Isop in group III . After that, aminoguanidine(AG) was injected [600mg/( kg.d),I.p] in group I .NS(lml/100g) substitude AG in group II and group III. In phrase II , after four weeks after AMI, every rat was anesthetized by sodium amylobarbitone (30mg/kg) and heparinized. PESO tube was insert via right common carotid artery into left ventricle to record inner left ventricular end-diastolic pressure(LVEDP) and its differentiation. Heart rate,mean arterial pressure(MAP) and left ventricular systolic pressure (LVSP) are also recorded.Before hemodynamic measurements, serum was obtained via coccygeal vein and stored at -20 癈 for determining the content of NO and iNOS. The rats were killed by opening chest. The heart was removed quickly and washed in iced NS and dried by filter paper. After great vessels, atria, pericardium and right ventricle removed, left ventricle was weighed, fixed with 4% formaldelyde solution, dehydrated routinely, embedded with paraffin and cut along the short axis into 2- u m- thick slices from lower 1/3 part of left anterior ventricles .After staining with hematoxylin-eosin, the slices were observed for histological changes, such as the size of the cells. The diameters of cells were measured by optical soft of colour pathological analysis.The results showed:(1) The expression of NO and iNOS was significantly greater in group II compared with group I and III [(77.20 + 6.46 and 18.52 1.03)Vs (36.88 6.78 and 9.46 0.80),(38.75 6.92 and 9.37 0.90) P<0.01].But there are no significant differences between group I and groupIII (P>0.05). Furthermore, the contents of cNOS in three groups have no statistical significance (18.40 1.08 Vs 18.24 1.3 1,1 8.90 1.16,P>0.05), indicating that AG is a selective iNOS inhibitor and reduces the expression of iNOS and NO-, (2) Hemodynamic parameters:There no significant differences in groups about heart rate(HR) (323.75 15.21 Vs 322.75 13.52,321.75 13.21,P>0.05), MAP(1 10.5 7.24 VS 108.75 + 7.41, 1 10.25 7.34,P>0.05) and LV...
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