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<正>苹果优良新品种原色图谱11.50元中国农业百科全书·果树卷60.50元生物学卷66.00元昆虫卷55.00元农药卷71.00元     

Effects of angiotensionⅡon metalloproteinases and matrix in hypertrophied myocardium from infarcted rats

AIM: To investigate the roles of angiotensionⅡ (AngⅡ) receptors (AT₁, AT₂) antagonists on matrix metalloproteinases (MMPs) and extracellular matrix (ECM) system in septal myocardium from infarcted rats.METHODS: The model of rat myocardium infarction (MI) was established by permanent ligation of the left coronary artery. The treatments of the AT₁ receptor antagonist valsartan (10 mg·kg^-1·d^-1) or AT₂ receptor antagonist PD123319 (30 mg·kg^-1·d^-1) were started 7 days prior to surgery. On day 14 after MI, protein levels of MMP-2, 3, 9, fibronectin (FN), tenascin-C (TN-C) in interventricular septum (IS) were determined. The distributions of FN and TN-C were also determined by immunofluorescence.RESULTS: Pathological changes of IS on day 14 after MI showed typical myocardial hypertrophy. Protein expressions of MMP-2, 3, 9 and TN-C of IS in banding group were higher than those in sham-operation group (P<0.01). The expressions of TIMP-1 and FN were lower than those in sham-operation group (P<0.01). Protein expressions of MMP-2, 3, 9 and TN-C in valsartan group were obviously lower than those in banding and PD123319 groups (P<0.01). TIMP-1 and FN protein expressions in valsartan group were higher than those in banding and PD123319 groups (P<0.01). No difference between banding and PD123319 groups was observed (P>0.05).CONCLUSION: AngⅡis involved in myocardium remodeling in infarcted rats, which is mediated via AT₁ receptor to degrade matrix by MMPs. The heart protection of AT₁ receptor antagonists may relate to inhibition of MMPs.     

Effect of adenosine on vWF in the infarcted reflow and no-reflow myocardium of mini-swines

AIM:Adenosine is experimentally and clinically effective in preventing even reversing myocardial infarction no-reflow,though the mechanisms are still not to be verified.This study was sought to evaluate the effect of adenosine on von willbrand factor (vWF) in the infarcted reflow and no-reflow myocardium of mini-swines.METHODS: Twenty-four animals were randomized into 3 study groups: 8 in controls,8 in adenosine-treated and 8 in sham-operated.The mini-swines were subjected to 3 hours of coronary occlusion followed by 60 minutes of reperfusion except those in the sham-operated group.The normal,infracted reflow and no-reflow myocardium was divided after experiment.vWF in both blood sample and myocardium was determined.The gene expression of vWF was also quantified.RESULTS: (1) In control group,vWF in blood sample significantly increased (P<0.01).In adenosine treated group,the level of vWF was significantly lower than that in control group (P<0.05).(2) vWF in both infarcted reflow and no-reflow myocardium significantly increased (both P<0.01),while the level of vWF in no-reflow myocardium was significantly higher than that in infarcted reflow myocardium (P<0.01).In adenosine-treated group,the level of vWF in infarcted reflow myocardium was significantly lower than that in control group (P<0.01).(3) The gene expression of vWF in infarcted reflow myocardium significantly up-regulated (P<0.01),while that of vWF in no-reflow myocardium significantly down-regulated (P<0.01).In adenosine-treated group,the level of vWF mRNA in infarcted reflow myocardium was significantly lower than that in control group (P<0.01).CONCLUSION: The endothelium injury is one of the important mechanisms for no-reflow phenomenon.Adenosine prevents endothelium from injury to reduce no-reflow.     

Effects of external counterpulsation on renin-angiotensin system and hemodynamics in dogs with myocardial ischemia

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.     

Effect of high-fructose diet on adipose tissue renin-angiotensin system in rats

AIM: To observe the effects of high-fructose diet on adipose tissue inflammation and renin-angiotensin system (RAS), and to reveal the role of Toll-like receptor 2 (TLR2) in this process.METHODS: Male SD rats (n=16) were randomly divided into control group, high fructose group, high fructose+siRNA negative control group, and high fructose+TLR2-siRNA group. The rats in control group were fed with a standard chow diet. The rats in high fructose group were fed with a diet with 60% fructose, and the rats in high fructose+TLR2-siRNA group and high fructose+siRNA negative control group were transfected with TLR2 siRNA and scrambled siRNA, respectively. Serum uric acid was measured and visceral adipose tissue was weighed at the 14th week. The levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), angiotensinogen (AGT), and angiotensin Ⅱ (Ang Ⅱ) were measured by ELISA. Infiltrating macrophages in the adipose tissues were measured with immunohistochemistry. The mRNA expression of IL-6, TNF-α, monocyte chemoattractant protein-1 (MCP-1), AGT, angiotensin-converting enzyme 1 (ACE1), angiotensin Ⅱ type 1 receptor (AT1R), and angiotensin Ⅱ type 2 receptor (AT2R) was detected by RT-qPCR. The protein level of TLR2 was determined by Western blot.RESULTS: High fructose-fed rats showed elevated serum uric acid, raising fat content, higher serum concentrations of IL-6, TNF-α, AGT and AngⅡ, and more infiltrating macrophages in the adipose tissues (P<0.05). Moreover, the mRNA levels of IL-6, TNF-α,MCP-1, AGT, ACE1, AT1R and AT2R in the adipose tissues were increased (P<0.05). When high fructose-fed rats were transfected with TLR2-siRNA, the dramatic decreases in TLR2 protein level and number of infiltrating macrophages in the adipose tissues were found. Both in serum and adipose tissues, the mRNA levels of inflammatory cytokines and RAS components were all significantly decreased (P<0.05).CONCLUSION: High-fructose diet up-regulates RAS in adipose tissues via activation of TLR2 inflammation signaling pathway.     

Effects of non-excitatory electric stimulation on cardiac function in normal and infarcted heart rabbits and it's regional effect on myocardium

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/dt_max) were observed. RESULTS: In the normal and MI groups, LVSP, +dp/dt_max significantly increased, and LVEDP, -dp/dt_max 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.     

Effects of the calpain system expression on atrial structural remodeling in canine with atrial fibrillation

AIM: To evaluate the influence of the calpain system mRNA and protein expression on the progress of atrial structural remodeling in fibrillating canine.METHODS: 17 dogs were randomly divided into 2 groups: normal control group (SR,n=6) and atrial fibrillation (AF,n=11) group.AF was induced by rapid pacing for 8 weeks and all dogs underwent transthoratic echocardiography before and after rapid pacing.The mRNA and protein expression of calpainⅠ,calpainⅡand calpastatin were assessed by real-time quantitative PCR and Western blotting,respectively.RESULTS: Compared with SR group,the left atrial diameters and the content of calcium in atrial myocardium increased significantly in AF group (P<0.05).There was no significant difference in mRNA expression of calpainⅠand calpainⅡ (P>0.05) between two groups.The expression of calpastatin mRNA was upregulated significantly in AF group (P<0.05).The levels of calpainⅠand calpainⅡprotein were significantly increased in AF group compared with SR group (P<0.05).The expression of calpastatin protein was significantly decreased in AF group (P<0.05).The calpainⅠand calpainⅡprotein levels were positively correlated with the left atrial diameter.The calpastatin protein level was negatively correlated with the left atrial diameter (P<0.05).CONCLUSION: The changes of the calpain system protein expression in AF result in the disturbance of calpain/calpastatin system and degradation of many proteins,which may play an important role in mechanism of atrial remodeling.     

Effect of hypoxia on persistent sodium current in ventricular myocytes from 3-week infarcted rat heart

AIM: To investigate the effect of hypoxia on persistent sodium current (INap) in single ventricular myocyte isolated from acute myocardial infarction (AMI) heart of rats and to study the mechanisms of cardiac arrhythmias that occur after AMI. METHODS: AMI model was induced by ligating the left anterior descending coronary artery in rats. The whole-cell patch clamp technique was used to record the current in epicardial myocytes in infarcted region from rats at 3 week after AMI. RESULTS: In normoxic conditions, the current density of INap in cardiomyocytes of fake operation (FO) and AMI hearts was 0.144±0.022 pA/pF (n=9), 0.121±0.013 pA/pF (n=9，P<0.01)， respectively, which was blocked by tetrodotoxin (TTX). The amplitude of INap was gradually increased with the prolongation of hypoxia time, but the increase in extent of INap in FO cells was significant bigger than that in AMI cells. The INap was blocked by 1 mmol/L glutathione. CONCLUSIONS: After AMI, the amplitude of INaP in infarcted and noninfarcted myocardium showed differences both in normoxic and hypoxic conditions, which increased dispersion of repolarization. This may be one of the reasons of reentrant ventricular arrhythmias that occur after AMI.     

Salvia extract promotes angiogenesis of myocardium in rats with myocardial infarction

AIM: To determine the effect of salvia extract on angiogenesis of the myocardium in the rats with myocardial infarction (MI) and to analyze its possible mechanism. METHODS: Left coronary artery of Sprague-Dawley rats was ligated to establish a MI model. The rats were randomly divided into MI model group, 3 different dose groups of salvia (10, 20 and 40 mg·kg^-1·d^-1), and sham operation group. Each group consisted of 8 rats. The rats in all treatment groups were orally administered with the salvia extract, and the rats in MI group and sham operation group were fed with the same volume of saline. The rats were sacrificed 4 weeks later. The hemodynamic changes of the rats were determined, and the segmental heart samples were used for morphological observation by hematoxylin and eosin staining, Masson staining, or electron microscopic analysis. The expression of vascular endothelial growth factor (VEGF) and cluster of differentiation 34 (CD34) was analyzed according to immunohistochemistry. RESULTS: Compared with sham operation group, the morphological changes of the myocardium in MI group were disordered, part of myocardial cell outline disappeared, and obvious fibrosis in the necrosis myocardial tissue and fuzzy or disappearing microvascular ultrastructure were also observed. Compared with MI group, the number of new microvessels in all the treatment groups increased obviously, and the morphological changes of the endothelial cells were relatively complete according to electron microscopy. Compared with sham operation group, the protein expression of VEGF and CD34 in the cytoplasm of the myocardial tissues in MI group increased only a little. Compared with MI group, the protein expression of VEGF and CD34 in the cytoplasm of the myocardial tissues in all treatment groups increased significantly (P<0.01). CONCLUSION: Salvia extract obviously promotes angiogenesis of the myocardial tissues in the rats after myocardial infarction.     

Alteration of local renin-angiotensin system of dogs with myocardial ischemia and external counterpulsation treatment

AIM:To examine the alteration of local renin-angiotensin system of dogs with myocardial ischemia and external counterpulsation treatment and its mechanism. METHODS:Acute myocardial ischemia was induced by occluding the LAD of ischemic and ECP groups. The tissue renin activity and angiotensin(AngⅡ) level in ischemic myocardium and aorta were measured. The expression of angiotensinogen and renin mRNA were detected by RT-PCR. RESULTS:Renin activity, AngⅡ level in ischemic myocardium and AngⅡ level in aorta of ECP group were lower than those of MI group. Except for renin in ischemic myocardium, angiotensinogen mRNA and renin in ischemic myocardium and angiotensinogen mRNA in aorta of ECP group were reduced to normal level. CONCLUSION:The inhibitory effect of ECP on cardiovascular renin activity and angiotensinogen gene expression could be one of the mechanisms by which ECP protects ischemic myocardium.     

Effects of dietary sodium on the expression of angiotensinogen mRNA in myocardium of rats with congestive heart failure

AIM:This study was designed to investigate the effects of sodium restriction and sodium supplementation on the expression of angiotensinogen mRNA in myocardium of rats with congestive heart failure(CHF).METHODS:Radioimmunassay and in situ hybridization techniques were used to determine the angiotensin Ⅱ(AngⅡ)contents and the expression of angiotensinogen(ANG)mRNA in myocardium, respectively.RESULTS: In sodium restricted group, the plasma sodium was obviously lower than that in CHF group(P＜0.05), while the contents of AngⅡ,the expression of ANG mRNA in myocardium and the ratio of heart weight/body weight(HW/BW)were significantly higher than those in CHF group (P＜0.05 or P＜0.01). It was also found that the AngⅡ, the mRNA contents in rat myocardium and the ratio of HW/BW were not significantly changed in case of sodium supplementation. CONCLUSION:Restriction of sodium intake can further activate the local renin-angiotensin system in CHF heart.