Objective: To assess the autonomic nervous impairment in chronic renal failure and its related factors. Methods: Forty adults were randomly selected including in patients in the nephrology ward and healthy subjects for routine medical examination. The subjects were classified into 4 groups: normal subjects(NS),normal renal function,nitremia, uremic patients. The time domain measurements of heart rate variability(HRV) and ambulatory blood pressure were analyzed simultaneously . Results: (1) There were significant differences as compared with normal subjects in the time domain measurements of HRV in uremic group. It decreased significantly when the patient was defined as end stage chronic renal failure. There were no significant differences between NS,normal renal function group and nitremic group. (2) Time domain measurements of HRV was significantly lower( P

Objective: To assess the autonomic nervous impairm ent in chronic renal failure and its related factors. Methods: F orty adults were randomly selected including in-patients in the nephrology ward and healthy subjects for routine medical examination. The subjects were classifi ed into 4 groups: normal subjects(NS)，normal renal function，nitremia， uremic patients. The time domain measurements of heart rate variability(HRV) and ambula tory blood pressure were analyzed simultaneously . Results: (1) There were significant differences as compared with normal subjects in the time domain measurements of HRV in uremic group. It decreased significantly when the patient was defined as end stage chronic renal failure. There were no significan t differences between NS，normal renal function group and nitremic group. (2) Ti me domain measurements of HRV was significantly lower(P<0.05) in uremia with renal hypertension than in uremia with normal blood pressure. Conclusio n: (1) Patients with chronic renal failure(HRV) have their cardiac auton omic nervous system impaired conspicuously in the course of uremia. (2) There is a positive correlation between cardiac autonomic nervous system impairment in p atients with CRF and renal function levels. Uremia itself is an independent fact or for the impairment of cardiac autonomic nervous system. (3) Renal hypertensio n with uremia may intensify the impairment of cardiac autonomic nervous system of the patients.

Objective:To investigate the effects of OX-LDL on the formation and progression of atherosclerosis. Methods: (1) The thoracic aorta smooth muscle cells(VSMC) of male Sprague-Dawley rat were primarily cultured in vitro. Different concentrations of OX-LDL(50,100,150,200 ?g/ml) were co-incubated with the cells respectively. MTT method was used to detect the cell proliferation after 24, 48 and 72 h. (2) pCOLH22. 4 and pCOLH2l. 6, recombinants of human a2( I ) procol-lagen gene 5' flank sequence ( - 2. 4 kb and -1. 6 kb in size) and CAT reporter gene, were used to transiently transfect smooth muscle cells with FuGENE Transfectant Reagent. The effect of OX-LDL (150 ?g/ml) on the plasmid were determined by CAT-EL1SA. Results: (1)OX-LDL accelerated the proliferation of VSMC in dose-dependent manner. (2)OX-LDL enhanced the promoter activities of human a2( I ) procollagen gene significantly. Conclusion: OX-LDL can accelerate the proliferation of VSMC and the formation of type I collagen,which facilitates the formation and progression of atherosclerosis.

Objective: To observe the effects of angina pector is on severe ventricular arrhythmia and QTd in patients with first acute myocard ial infarction(AMI). Methods: One hundred and eight-four cases of first AMI were divided into 2 groups: PA group, angina pectoris occurred with in 24 h before AMI onset (n=58), NPA group, no preceeding angina pectori s occurred (n=126). Occurrence of complications and QTd were investigated du ring hospitalization. Results: The basic clinical characteristic s, coronary risk factors, medication before infarction, treatments after admissi on with antiarrhythmic agents, site of infarction, successful rate of thrombolys is and peak CK, CK-MB were not statistically different. Early QTd in PA group and NPA group were (56.22±18.40) ms vs (84.45±21.90) ms, respectively, P <0.05, late QTd in PA group and NPA group were (50.67± 16.34) ms vs (64.1 8(16.41) ms, respectively, P<0.05. Comparison with NPA group, incidence of severe ventricular arrhythmia, heart failure, cardiogenic shock and rate of car diac mortality in-hospital was lower in PA group. Conclusion: P reinfarction angina pectoris can significantly reduce the incidence of severe ve ntricular arrhythmia and QTd in the patients with first AMI, sugges ting that these favorable effects might be associated with protective effects of ischemic preconditioning on myocardium and ventricular pump function and improv ement of repolarizative asynchronism in ventricular myocardium.

Objective: To investigate the efficacy and safety of naftopidil on patients with mild-to-moderate essential hypertension. Methods: A prospective, open study was performed in patients with hyp ertension. Forty patients were administered naftopidil for 8 weeks. Results:BP decreased significantly 2 weeks after administration an d reached to its trough at week 4. The magnitudes were 2.28 kPa (17.1 mmHg) and 1.43 kPa (10.7 mmHg) for SBP and DBP, respectively. The effect lasted to the end of experiment. HR had no change.The total effective rate was 82.05%.There was n o significant change in liver and renal function and electrocardiograph. Conclusion: Naftopidil has a stable hypotensive effect and the complia nce is good.

It is now clear that continued stimulation o f the neurohormonal system in heart failure (HF) has serious deleterious effects on the heart. The increase of circulating catecholamines exerts direct toxic ef fect on cardiac myocytes, increases membrane permeability and myocardial fibrosi s; lead to aggravation of HF. β-blockers are commonly used in the treatment of HF including propranolol, metoprolol, bisoprolol, bucindolol and carvedilol. These drugs are used in combination with ACEIs, digitalis and diuretics. Genera lly, the benefits of β-blockade therapy in HF include improving symptoms, decr easing morbidity, mortality, elevating need for hospitalization and quality of l ife. β- blockade therapy arrests and reverts LV remodeling and improves the ri sk of life threatening arrhythmias and sudden cardiac death. A few serious adver se effects include hypotension, heart blocks, bradycardia and fluid retention.

Objective: To investigate the relationship between serum HGF levels and clinical severity of essential hypertension (EH). Methods: The serum HGF concentrations of 44 patients with EH were measur ed by ELISA. Results: The serum HGF levels in patients with EH w ere higher than that in control. Furthermore, the serum HGF levels of EH patient s with coronary atherosclerosis (CAS) were significantly higher than those of EH patients without CAS ［(920.8±250.0） pg/ml vs （747.9±132.1） pg/ml, P <0.01］ or control ［（643.8±98.2） pg/ml, P<0.01)］.The changes of HGF l evel were correlated with the clinical courses (r=0.63, P<0.01) and stag es (r=0.69, P<0.01) of hypertension. Conclusion: HGF may be considered as a new index for the severity of hypertension and an useful bio chemical parameter for estimating the development of atherosclerosis.

AIM: To investigate the mechanism underlying insulin-stimulated increase in glucose uptake during low-flow myocardial ischemia. METHODS: The expression of myocardial GLUT1 polypeptide was determined by semiquantitative immunoblotting. The expression of GLUT1 mRNA was determined by semiquantitative Northern blotting. RESULTS: After infusing insulin during low- flow myocardial ischemia for 8 h,the expression of both GLUT1 mRNA and GLUT1 polypeptide was significantly higher in experimental myocardium than that in normal myocardium. The glucose uptake was upregulated at the same time in the exprimental myocardium. CONCLUSION: Insulin enhances the expression of GLUT1 mRNA and GLUT1 polypeptide in ischemic myocardial regions. GLUT1 expression may be an important mechanism by which myocardial cells enhance glucose uptake and metabolism during low-flow myocardial ischemia. [

Objective: To investigate whether insulin stimulates the translocation of glucose transporter-4 (GLUT4) and glucose uptak e in ischemic myocardium. Methods: Plasma concentration of gluc ose, lactate, free fatty acid and insulin were determined by autoanalyser, and G LUT4 was studied by Western blotting analysis. Results: Insulin increased GLUT4 significantly in sarcolemma of ischemic myocardium ［(25±4)% vs (40±6)%］, and GLUT4 content in intracellular membrane decreased proporti onally. The glucose uptake increased significantly in insulin-ischemic myocardi um. The uptake of insulin-ischemic myocardium was almost 2 times that of ischem ic myocardium. Conclusion: Insulin stimulation results in GLUT4 translocation and increases glucose uptake in ischemic myocardium. When myocardi al ischemia occurs, insulin is helpful in increasing myocardial glucose uptake a nd utilization.