The method of measuring cardiac-pump function with electromagneticflowmeter was studied in rats. CI, SVI, AFV and dF/dt measured in 20 nor-mal rats were 227 + 7 ml/kg/min, 0. 50 ? 0. 0.2ml/kg, 3. 35 ? 0. 17ml/secand 167 ? 9 ml/sec~2, respectively. The physiological status of the modelwithin 60 minutes was stable, When volume loading was given, CI and SVI of normal rats were incr-eased by 183 ? 8% and 190 ? 9%, AFV and dF/dt also increased significantlywith less degree (83 ? 8% and 64 ? 5%). The comparision of the pump function indices of the normal and themyocardial infarcted rats showed that during volume loading, the changesof pump function and its response curve were helpful to assess the damageof cardiac function.

The present study was performed to determine whether or not that cardiacrenin-angiotensin system (RAS) plays an important role in volume-overload myocardialhypertrophy. In order to control the increase of circulating RAS, aortacava fistula withnephrectomy (ACF+NT) rats were used in the experiment. The ventricular angiotensin Ⅰ,Ⅱ (Ang Ⅰ,Ⅱ) contents and angiotensin-converting enzyme (ACE) activities were measuredby means of radioimmunoassay and biochemical method. It was shown that in ACF+NTrats, the Ang Ⅱ contents and ACE activities in both left and right ventricles increasedsignificantly despite the plasma Ang Ⅰ, Ⅱ and renin activity remained at a lower level.These results indicate that: (1) Cardiac RAS as a relatively independent system, plays aregulatory role in the development of volume-overload cardiac hypertrophy; (2) The in-crease of Ang Ⅱ content was partly caused by the enhancement of ACE activities; (3) Atleast at the early stage of volume-overload cardiac hypertrophy, the circulating RAS maynot be a necessary promoter.

Objective To investigate the protective effect of 17?-estradiol (?E2) on cultured retinal neurons. Methods By using methods of the cultured retinal neurons, the effects of H 2O 2, ? E2, and tamoxifen, the estrogen receptor antagonist, on the cultured retinal neurons were observed. Results H 2O 2 significantly decreased cell viability in cultured retinal neurons in a dose- and time-dependent manner. When the retinal neurons were pretreated with ? E2 30 min prior to H 2O 2 treatment, cell viability was significantly increased (P

We studied the alteration of local and circulat-ing RAS during cardiac hypertrophy caused by ab-dominal aorta constriction (AC, with nephrectomyof left side) and aorta-vena fistula (AVF). Bothventricular and plasma angiotensin Ⅰ and Ⅱ (AngⅠ. Ⅱ), and plasma, renin actvity (RA) weremeasured by means of radioimmunoassay after twoand seven weeks of surgery. Despite the level ofplasma Ang Ⅰ, Ⅱ and RA were not enhanced, theventricular Ang Ⅰ and Ⅱ were increased signifi-cantly in AC rats (v. s. SO group P

Objetive To study the effects of captopri on AT1 and AT2 receptors of load-pressured hypertrophied cardiac muscles of adult rats.Methods Using the methods of narrowing and contraction of the aorta of adult healthy rats to establish the model of animals with hypertrophied cardiac and to observe the changes of receptors AT1 and AT2 of hypertrophied cardiac muscles of AC rats by comprehensive applications of cardiac-tube,immunity tissue chemistry and the technique of image disjunction.Results Left ventricular and cardiac muscles of rats were increased remarkably as the pressure-loading time lasted.After using captopri,left ventricular hypertrophied one was decreased more significantly than that in control group.The expression of receptor AT 1 was increased remarkably as the pressure-loading time lasted.The expression of receptor AT2 was increased transiently,after that reached about as high as control group.AT1/AT2 was increased one week after operation,and then was progressively decreased.After AC,captopri prevented hypertrophied cardiac muscles and receptor AT1 in cardiac muscles.AT1/AT2 was remarkably decreased.Conclusion Load-pressured cardiac hypertrophy may increase the expression of AT1.The expression of receptor AT 2 was increased transiently.The main working mechanism of captopri's preventing and treating the load-pressured cardiac hypertrophy in adult rats may be lowering the expression of AT1 and may effectively block the cardiac hypertrophy regulation precess of Ang ll via AT1 preventing load-pressured cardiac hypertrophy in adult rats.

AIM: To examine the effects of monocyte-endothelium interaction on the expression of CD36 in monocytes and observe the functions of cytokines in this process. METHODS: The monocytes and endothelial cells were cultured alone or cocultured together to form different cell culture conditions. The level of M-CSF in culture medium was determined by enzyme linked immune sandwich assay(ELISA) technique, and the expression of CD36 in monocytes was determined by flow cytometry. RESULTS: The expression of CD36 in monocytes was low in monocytes cultured alone but increased significantly when monocytes and endothelial cells were cocultured(P

AIM: To investigate the effects of AngⅡon the production of ET-1, NO from myocardial fibroblasts (MFs) of adult rat. METHODS: MFs were extracted by enzymatic digestion and anchorage velocity-dependent separation method. In this study, the changes of ET-1 and NO production from MFs in the second passage were examined by radioimmunoassay and by nitrate reductase-dependent assay, separatively. RESULTS: In a specific concentration range, AngⅡ increased ET-1 synthesis in MFs in a concentration-dependent manner. Losartan, the antagonist of angiotensin Ⅱ 1 type recepters (AT 1R), blocked the above effects. AngⅡ may inhibit NO synthesis in MFs. When MFs were treated with losartan+AngⅡ, the production of NO increased significantly, and was higher than that treated with the others( P

AIM: To observe the change of TNF-? mRNA in hypertrophic cardiac myocytes induced by pressure overload in rats and the effect of captopril. METHODS: Serum and heart were collected 42 days after the cardiac hypertrophy model made by pressure overload by abdomen aorta-constriction (AC). Hypertrophic parameter and the concentration of TNF-? in serum and left ventricle were determined by ELISA. TNF-? mRNA in cardiac myocytes was determined by in situ hybridization and analyze by ELIA image analysis system. The orientation of (TNF-?) mRNA in cardiac myocytes was also observed. RESULTS: Left ventricle hypertrophy was observed 42 days after operation. TNF-? mRNA in AC group elevated 98% compared to sham-operated group and descended 64.14% by captopril ((P

AIM: To identify the down-regulated genes in adult rat cardiac fibroblasts (CF) stimulated with angiotensin Ⅱ (AngⅡ). METHODS: Suppression subtractive hybridization (SSH) was performed between the CF stimulated by AngⅡ (driver) and unstimulated CF (tester) to generate subtractive cDNA library. The library was screened with dot blots hybridization to further verify the differentially expressed cDNA clones. Partial positive clones were sequenced and BLAST analyzed. RESULTS: Seventeen down-regulated genes related to intracellular signal transduction, transcriptional repression, deposition of fibrous matrix and cellular cytoskeletal rearrangement, and 4 new expression sequence tags (EST) were acquired. CONCLUSION: SSH is a powerful technique with high sensitivity for the detection and clone of down-regulated genes expressed in CF induced by AngⅡ, which is helpful to clarify the mechanism of cardiac remodeling.