To study the effects of high salt intake together with cold stress on rat cardiac renin angiotensin aldosterone system (RAAS) in rats. Male Wistar rats were randomly divided into four groups: control, high salt (8%NaCl), cold stress (5 2℃) and compound group (8%NaCl+cold stress). Blood pressure and body weight were measured once a week. The experiment ran for 8 weeks. Renin activity (RA), angiotensinⅡ (AngⅡ), and aldosterone (Aldo) in plasma and left ventricle were determined with radioimmunoassay. Angiotensin II receptor mRNA was determined with RT PCR. The results showed that ①Rats in compound group had higher blood pressure than rats in the other three groups ( P

Objective To investigate the effects of nuclear factor ?B (NF ?B) activation and tumor necrosis factor ?(TNF ?) expression on the progressive heart failure following myocardial infarction in rats. Methods Male rats were randomized for the proximal left anterior descending branch coronary artery ligation and then killed at 4, 8 and 12 weeks after ligation for the examination of hemodynamic parameters, ventricular mass index, protein expression of TNF ?, and NF ?B activity. Sham operated rats were used as the control group. Results Compared with the sham operated group, the myocardial infarction rats showed significant decreases in mean arterial pressure(MAP), maximal ascending and descending velocity of the left ventricular pressure(?dp/dt max ) and a significant increase in left ventricular end diastolic pressure(LVEDP) ( P

Objective To investigate the stroke caused by a combination of genetic and environmental factors Though epidemiological studies have provided evidence of genetic influence on the occurrence of human stroke,however,the role of environmental risk factors to the development of stroke is still not well known. Methods Using cold stimuli plus high salt intake as environmental risk factors, we established a hypertension model in rats, for producing a complicated stroke, then, applied a new technique, suppression subtractive hybridization(SSH),to identify the differential genes which were specifically expressed in total rat cerebrum tissues in between two populations, namely the control and the stroke groups. Results Using this SSH approach, totally 288 clones were generated in our study from a subtractive libraries, among them,226 clones were usable and analyzed The average length of this group is (286 6?120 3) bp Among those clones, 126 clones represented sequences with significant identity to the known genes, 78 were matched to existing ESTs in dbEST but not to any known gene sequences, and the remaining 22 were novel transcripts exhibiting no similarity to any known sequences Mitochondrial transcripts were observed at a high rate of 26 5% Mitochondrial genes may play important roles in causes and effects of stroke. Conclusions Our investigation suggests that environmental risk factors may induce an increased sensitivity to stroke through genetic influence Also we will identify the genes responsible for stroke in this rat model

Objective To determine the relationship and significance between the acute ischemia, hypoxia and the production of VEGF in rat myocardium and the influence of EDS on expression of VEGF protein in myocardium Methods To establish the model of AMI in rats, Wistar rats were randomly divided into control group, AMI group (1,3,7 day) and EDS group (0, 40 mg/day) Myocardial enzymes, VEGF protein, microvascular density and infarct size were detected Rat cardiac myocytes cultured primarily received EDS 100 ?g/ml in normal and hypoxia condition After 24 hours, VEGF was detected with immunohistochemical technique Results The production of VEGF was higher with ischemia and hypoxia time, the positive relationship was found between the time of AMI and the production of VEGF EDS reduced the concentration of serum myocardial enzymes (CK MB), enhanced the formation of collateral circulation,microvascular density and cardiac function; decreased infarct size In addition, EDS could enhance expression of VEGF protein in cardiac myocytes of rat in normal and hypoxia condition Conclusion Acute ischemia strongly stimulated the production of VEGF in myocardium, which played an important role for autoprotection of ischemic myocardium EDS could promote the establishment of cardiac collateral circulation and enhance microvascular density in infarct zone by upregulation of VEGF protein expression

Objective　To evaluate the role of transfected angiotensinⅡ(Ang Ⅱ) receptor AT1 anti-sense nucleotide (AT1A) in the expression of subtypes of AngⅡ receptor mRNA, synthesis of protein and nucleic acid in cardiomyocytes. Methods　AT1 cDNA sequence (476 bp) was cloned with RT-PCR and reversely inserted into PcDNA3.1 (5.4 kb) to construct an intact plasmid containing AT1A (PAT1A). The plasmid was then transfected into the cultured cardiomyocytes and identified with RT-PCR and Western blot. The synthesis of protein and nucleic acid identified by 3H-Leu and 3H-TdR incorporation, and expressions of AT1 and AT2 mRNA by RT-PCR, were compared between transfected and nontransfected cardiomyocytes after being stimulated with 10-7 mol/L AngⅡ for 24 h. Results　The plasmid PAT1A were successfully constructed. The AT1 mRNA and its protein were expressed significantly less in the transfected cardiomyocytes than in the control (P<0.01). In the transfected cardiomyocytes, AT1 mRNA expression was markedly decreased, but that of AT2 mRNA obviously increased (P<0.01) when compared with the nontransfected cardiomyocytes after stimulation for 24 h with AngⅡ 10-7 mol/L; no significant difference was found in 3H-Leu and 3H-TdR incorporation between them. Conclusion　After the cardiomyocytes was tranfected with AT1A, the expression of AT1 mRNA was markedly suppressed，while AT2 mRNA up-regulated at the same time. Our results indicate that AT1A blocking can not effectively interrupt the Ang Ⅱ-induced synthesis of the protein and nucleic acid in cardiomyocytes.

Objective To observe the effects of antihypertensive agents on renin angiotensin aldosterone system, blood pressure and myocardial hypertrophy induced by high salt diet plus cold stress. Methods Fifty male Wistar rats weighting 200～250 g were divided into 5 groups: control, saline, captopril, betaloc and nitrendipine. The rats treated with dugs or saline were fed with high salt diet(8% NaCl) and subjected to cold stress 4 hours a day. Blood pressure and body weight were measured once a week. Rats were sacrificed and then the gross weight of hearts was measured 8 weeks later. Renin activity(RA), angiotensinⅡ(AngⅡ) and aldosterone(Aldo) in the left ventricular wall were determined by radioimmunoassay. Results ① Levels of RA, AngⅡ and Aldo of rat left ventricular wall in betaloc group were significantly lower than those in saline, captopril and nitrendipine groups( P

Forty-eight cases of atrial septum secundum defect were repaired and followed up with M-mode echocardiography postoperatively for three months to three yaers respectively.All the cases showed a significant reduction of the inner diameter of the right ventricle after operation,and in 23% of the cases, the inner diameter even returned to the normal range. In 92% of the acses, the intervetricular septal paradoxical motion resumed the normal pattern. In most cases, the inner diameter of the left ventricle increased markedly.In 11 cases with repeated follow-up studies, it was found that three months after operation, the interventricular septal paradoxical motion became normal in 7 cases and the motion flattened in three cases. In 18 cases with a 3-year follow-up history, it was found that the recovery of the heart condition showed no relation to the age of the patient. This is likely to suggest that the age factor exerts no influence on the postoperative recovery of the cases having the atrial septal defect repaired.

Objective　To explore the effect of hypoxia on the apoptosis of cultured human umbilical vein endothelial cells（HUVECs） and the role of vascular endothelial growth factor（VEGF） in inhibition of apoptosis． Methods　①Culture and identification of HUVECs．②Establishment of hypoxic model（0，12，24，48 h）in HUVECs．③Incubation of HUVECs with VEGF(0 ng, 100 ng) under hypoxic condition for 24 h. ④Detection of apoptosis of HUVECs with TUNEL method． Results　The percentages of apoptosis were different under different hypoxic conditions． The longer hypoxic time was，the higher apoptosis percentage was．VEGF reduced the apoptosis of HUVECs induced by hepoxia． Conclusion　Over-apoptosis EVCs in one of the important factors for the impairment of endothelial function. HEGF inhibits the apoptosis of HVCs and having a pretive function on them.

Fifty cases with chronic rheumatic valvular disease were examined with two dimensional echocardiography to evaluate the valvular pathology preoperatively. The echocardiographic findings were correlated and compared with the operative findings.It was found that 89% of the thickening pattern cases and 75% of the funnel-shaped cases showed thickening of the leaf-lets- All the 28 membranous cases showed diastolic doming and restricted tip motion of the anterior leaflet in different degrees. In the 4 funnel-shaped cases, 3 showed restricted tip and body motion of the leaflets and the 4th case showed stiffness of the leaflet base. 63% of the mitral regurgitation cases were confirmed at operation.It is concluded that preoperative evaluation of the valvular pathology with two dimensional echocardiography is helpful in selection of suitable operative candidates.

Objective: To understand the effect of Carvedilol on mitochondrial oxidative phosphorylation function during the development of pressure overload induced left ventricular hypertrophy in rats and its mechanism.Methods: Male SD rats were randomized into 6 groups: 5-and 15-week coarctation of the abdominal aorta(H5,H15),5-and 15-week Carvedilol intervention(HR5,HR15) and 5-and 15-week sham operation(S5,S15).Hemodynamics and ventricular remodeling parameters were measured,and the mitochondrial respiratory function was detected by Clark oxygen electrode.Results: Compared with S5,mitochondrial state 3 and 4 respiration and the oxidative phosphorylation rate(OPR) were increased and the respiratory control rate(RCR) decreased significantly in the H5 group.In comparison with S15,state 3 respiration,OPR and RCR were reduced significantly in the H15group.Carvedilol increased the three parameters and restored them to the level of the S15.Conclusion: Mitochondrial respiratory function decreased during the development of pressure overload induced left ventricular hypertrophy in rats.Carvedilol could protect mitochondrial respiratory function and improve myocardial energy metabolism,which might be a mechanism underlying its protective effect on myocardium.