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AIM: To investigate the contribution of angiotensin-converting enzyme inhibitor (ACEI) to the regulation of calpain system in infarcted myocardium. METHODS: Rat myocardial infarction (MI) model was established by permanent ligation of the left coronary artery. The treatment with the ACEI inhibitor rampril (1 mg·kg-1·d-1) was started 7 days prior to surgery. On day 1, 3, 7 and 14 after MI, protein levels of calpainⅠ, Ⅱ and calpastatin were determined in left ventricular free wall (LVFW), interventricular septum (IS) and right ventricule. RESULTS: CalpainⅠprotein level was increased in IS 14 d post MI, whereas the protein level of calpainⅡ was maximally increased in LVFW 3 d post MI. Rampril decreased protein up-regulation of calpainⅠ and Ⅱ, and reduced infarct size and interstitial fibrosis. Calpastatin protein expression was not affected by ACEI. CONCLUSIONS: CalpainⅠ is involved in cardiac remodelling in the late and calpainⅡ contributes to cardiac tissue damage in the early phase of MI. The heart protective effect of ACEI may be related to the inhibition of calpain system in the pathogenesis of myocardial infarction. 相似文献
3.
ZHANG En-guang ZHANG Huai-qin LIN Jie HUANG Wei-jian LI Shang-gong XU Li-xin 《园艺学报》2003,19(5):653-656
AIM:To examine the relationship between the activity of matrix metallproteinases(MMPs) and ventricular remodeling following myocardial ischemia in the rat.METHODS:The model of myocardial ischemia(MI) in the rat was established by isoprenaline(ISP). The activity of MMPs was measured by zymography and collagen concentration was assessed by the method of chloramine T, so did I/III collagen ratio by immunohistochemical staining. The microstructure of myocardium was also observed by electron microscope.RESULTS:The activity of MMP-2 in myocardial ischemia group (group M) increased by 5.8 folds at 1 st week(P<0.01), 2.3 folds at 2 nd week(P<0.01) and 1.7 flods at 4 th week(P<0.05) compared with control group (group C) and MMP-9's activity in group M increased by 4.9 folds (P<0.01), 1.9 flods(P<0.01) and 1.4 folds(P<0.05), respectively. Collagen amount and I/III collagen ratio in group M increased compared with that in group C at 2 nd week and 4 th week. It showed that cardiac myocytes in group M were necrosed and collagen grew abundantly in interstitium under electron microscope.CONCLUSION:The activity of MMPs in the myocardial interstitium increased following myocardial ischemia, then collagen amount and I/III collagen ratio increased, which may be the major causes of ventricular remodeling. 相似文献
4.
AIM:To study the relationship between myocardial HSP70 and PKC during myocardial ischemic preconditioning(IPC). METHODS: PKC inhibitor, polymyxin B(PMB) and PKC activator, phorbol 12-myristate 13-acetate(PMA) were applied to the models of myocardial ischemia/reperfusion in vivo and in vitro in rabbits, respectively, and the ventricular functions, PLA2 in the serum, and the expression of mycardial HSP70 mRNA were examined. RESULTS:IPC decreased PLA2 activity, improved the left ventricular function and increased the expression of myocardial HSP70 mRNA. Howerer, all these effects of IPC could be blocked by PMB. Interestingly, PMA mimicked IPC with attenuating the injuries of cardial myocytes and increasing myocardial HSP70 mRNA expression. CONCLUSION:PKC is involved in the myocardial HSP70 expression in case of ischemic preconditioning. 相似文献
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AIM:To examine the effect of external counterpulsation(ECP) on renin-angiotensin system(RAS) and hemodynamics in dogs with myocardial ischemia and their relationship. METHODS:Acute myocardial ischemia was induced by occluding the left anterior descending of the dogs. The local renin activity, angiotensin Ⅱ(AngⅡ) level, angiotension-converting enzyme(ACE) activity were tested by biochemical methods and hemodynamics was recorded by a 8-channel physiological recorder.RESULTS:Ischemia could actiivate renin,ACE and AngⅡ in cardiovasculature and ECP reduced them except for renin in ischemic myocardium. Ischemia also could activate RAS in lung and kidney, which play an important role on circulating RAS, and ECP reduced them. Furthermore, ECP could improve hemodynamics and there existed a close relationship between local AngⅡlevel and hemodynamics. CONCLUSION:ECP can reduce local RAS and improve hemodynamics in dogs with myocardial ischemia, which might be one of mechanisms underlying the protective effect of ECP on ischemic myocardium. 相似文献
6.
TANG Yi-da YANG Yue-jin RUAN Ying-mao LI Yong-li ZHOU Yan-wen TIAN Yi GAO Run-lin CHEN Ji-lin CHEN Zai-jia 《园艺学报》2002,18(9):1115-1118
AIM:To compare the effects of carvedilol, cilazapril and their combination on left ventricular remodeling(LVRM) after acute myocardial infarction(AMI) in rats. METHODS: Twenty-four hours after AMI operation, 100 surviving rats were randomly assigned to: ①AMI control(n= 25), ②AMI+carvedilol(1 mg·kg-1 ·d-1, n= 25)(C1), ③AMI+cilazapril(1 mg·kg-1 ·d-1, n= 25)(Z1), and ④ AMI+combination(n= 25) groups. Sham-operated group(n= 17) were selected randomly. After 4 weeks of therapy with the drugs gastric gavage, hemodynamic and pathological studies were performed. RESULTS: There were no significant differences in MI size among the four AMI groups(all P> 0.05) Left ventricular(LV) end diastolic pressure(LVEDP), volume(LVV), weight(LVW) and septal thickness(STh) were all higher and left ventricular pressure maximal rate of rise and fall(±d p /d t) were lower(all P< 0.01) in AMI group than sham-operated group. The LVEDP, LVV, LVW and STh were all lower and ±dp /dt were higher in Z1, C1, and combination groups than those in AMI group(P< 0.05, P< 0.01), with LVEDP and STh were more lower in the combination group than in the two monotherapy group(P< 0.05, P< 0.01), but there were no significant differences in other variables among the three therapy groups. CONCLUSION: Carvedilol, cilazapril and their combination all can prevent from LVRM after AMI in rats, improve hemodynamics and LV function, with the combination superior. 相似文献
7.
LIU Nian NIU Hui-yan LI Yang ZHANG Cun-tai ZHOU Qiang RUAN Yan-fei PU Jun LU Zai-ying 《园艺学报》2004,20(12):2227-2231
AIM: To elucidate the mechanism of arrhythmia in healed myocardial infarction (HMI), and to investigate the changes of action potential duration (APD),transient outward potassium current (Ito), delayed rectifier potassium current (IK) and inward rectifier potassium current (IK1) of left ventricular myocytes in noninfarcted zone of HMI. METHODS: 12 rabbits were randomly assigned in two groups: HMI group (thoracotomy and ligation of the circumflex coronary); sham-operated group (thoracotomy but no conorary ligation). 3 months after operation, whole cell patch clamp technique was used to record APD, Ito, IK and IK1 of ventricular myocytes in non-infarcted zone. RESULTS: Membrane capacitance was larger in HMI group than that in sham-operated group. Action potential duration was lengthened significantly in HMI group and early after depolarization (EAD) appeared in HMI group. The densities of Ito, IK,tail and IK1 were reduced significantly in HMI group (P<0.01), from (6.72±0.42) pA/pF, (1.54±0.13) pA/pF and (25.6±2.6) pA/pF in Sham-operated group to (4.03±0.33) pA/pF, (1.14±0.11) pA/pF and (17.6±2.3) pA/pF, respectively. CONCLUSION: The reduced densities of Ito, IK,tail and IK1 in ventricular myocytes of non-infarcted zone in HMI are responsible for the prolongation of APD and the presentation of EAD, which play important roles in the malignant arrhythmia of HMI. 相似文献
8.
AIM: To investigate the effects of long-term TCV116 on left ventricular remodeling and heart function after myocardial infarction. METHODS: Myocardial infarction (MI) was caused by ligation of the left anterior descending coronary artery in rats. One week after the surgical performance, the surviving rats were randomly assigned to the following treatment protocols: (1) MI rats with no therapy; (2) MI rats treated with TCV116 2 mg/kg per day; (3) Sham-operated control; (4) Sham-operated rats, treated with TCV116 2 mg/kg per day. At 22 weeks, cardiac hemodynamic parameters such as MAP, LVSP, dp/dtmax and LVEDP, and histomorphometric parameters such as LVW/BW and LVCA/BW were measured, mRNA of cardiac genes such as βMHC, BNP, TGF-β1, collagen I and III were quantified, and survival rates were calculated. RESULTS: Compared with sham-operated rats, MI rats without therapy showed significant increases in histomorphometric parameters as well as in mRAN expressions of cardiac genes (P<0.01); While their hemodynamic parameters were significantly impaired (P<0.01), and survival duration shortened (P<0.05). Compared with MI rats without therapy, MI rats treated with TCV116 showed significant attenuation of mRAN expression of cardiac genes (P<0.01); While their hemodynamic parameters were significantly improved (P<0.05 or P<0.01), and survival duration extended (P<0.05). CONCLUSION: Treatment with long-term angiotensin II type 1 receptor antagonist may improve left ventricular remodeling and cardiac function after MI in rats. 相似文献
9.
AIM: To investigate the influences of electric stimulation applied during the absolute refractory period (ARP) on the cardiac function of normal rabbits and rabbits after myocardial infarction (MI) and to observe the regional effects of this electric stimulation. METHODS: 64 rabbits were randomly assigned to normal and MI groups and each group was then divided into the anterior and posterior groups. A thoracotomy was performed 4 weeks after MI in rabbits. One set of electrodes was inserted into the anterior and posterior wall of left ventricle of the anterior and posterior groups, respectively. Current pulses were delivered during the ARP (called CCM) during sinus rhythm in rabbits. The left ventricular systolic pressure (LVSP) and the left ventricular end diastolic pressure(LVEDP) as well as maximum positive and negative left ventricular pressure change (±dp/dtmax) were observed. RESULTS: In the normal and MI groups, LVSP, +dp/dtmax significantly increased, and LVEDP, -dp/dtmax were reduced during CCM stimulation compared with the baseline (P<0.05). In the normal rabbits, electric stimulation in the anterior group improved the cardiac function more significantly than that in the posterior group (P<0.05). In the MI rabbits, there was no difference between the anterior and the posterior groups (P>0.05). CONCLUSION: Electric stimulation delivered during the ARP significantly enhances the contractility and the relaxation of myocardium in normal rabbits and rabbits after MI, and the effects of CCM stimulation on heart are regional. 相似文献
10.