Left ventricular long-axis ultrasound strain (GLS) is an ideal indicator for patients with anti-hypertension treatment.

BACKGROUND: Primary hypertension is one of the most well-known risk factors for cardiovascular disease. Currently, there is still no ideal indicator for left ventricular end-diastolic pressure. METHODS: 73 hypertension patients and 37 healthy people were enrolled in this study. Each member was examined with conventional echocardiography including multiple indicators such as Peak mitral valve flow velocity (E, A), E/A, left atrial volume index (LAVl), tissue Doppler (PW-TDI) peak velocities during early and late diastolic mitral valve flow (e '), E/e ', and GLS. We have collected clinical data from all enrolled members. The above cardiac ultrasound indicators were obtained before the antihypertensive treatment, one month and three months after treatment. RESULTS: Left ventricular end-diastolic pressure (LVEDP) was positively correlated and negatively correlated with GLS (r = 0.638, P < .01) and E/e' (r = -0.578, P < .05), respectively. The hypertensives had lower e' value and higher values of GLS, E/e', and LAVI than the control group (P < .05). GLS and E/e' were significantly lower in hypertension group than those in the Control group after one month and three months of treatment (P < .05). The improvement rate of GLS was significantly higher than those in the improvement rate of e', E/e', LAVI after treatment (p < .05). CONCLUSION: The GLS improvement rate was significantly higher than those of e', E/e' after one and three-month treatment. Therefore, GLS might be a potential ideal index for patients with anti-hypertension treatment. The results obtained in this study provide useful information for further study.

The Influence of Sex on Cardiac Physiology and Cardiovascular Diseases.

Cardiovascular disease (CVD) is the leading cause of death world-wide. Most of treatment strategies were based on studies conducted on male patients. Studies have shown that significant differences exist between the two sexes in the development of CVD. There are certain differences between men and women in the structure and physiological functions of the heart such as left ventricular mass index, resting heart rate, and contractile function. Accordingly, the pathological features of the heart such as the extend of hypertrophy, fibrosis, and remodeling are also different. In addition, different genders also affect clinical symptoms, responses to treatment and prognosis in the development of CVD. Therefore, it is important to take these differences into consideration when design treatment options for men and women.

Niacin regulates apolipoprotein M expression via liver X receptor­α.

Niacin is currently the most effective drug that increases HDL­C levels. Apolipoprotein M (ApoM) in humans is mainly found in plasma high­density lipoprotein (HDL). Little is known about the role played by niacin in ApoM expression. In this study, the effects of niacin on ApoM expression were assessed as well as the associated mechanism. Human liver cancer cell line HepG2 was treated with niacin alone or with liver X receptor­α (LXRα) inhibitor at multiple concentrations. The mRNA and protein expression of ApoM were assessed by qRT­PCR and western blotting. Specific LXRα shRNA was transfected into HepG2 cells to further evaluate the regulatory effects of LXRα on ApoM. An in vivo model was also established to investigate the LXRα inhibitor on the mouse ApoM levels. The comparisons among groups were evaluated using one­way ANOVA and Student­Newman­Keuls test. It was revealed that in HepG2 cells, niacin dose­dependently increased ApoM gene and protein expression levels. Niacin­induced upregulation of ApoM was attenuated by an LXRα inhibitor or LXRα shRNA, indicating that LXRα mediated this effect. Moreover, niacin treatment resulted in increased LXRα mRNA levels, in vivo and in vitro; niacin treatment resulted in increased ApoM gene and protein expression levels in mice. In conclusion, niacin upregulates ApoM expression by increasing LXRα expression in vivo and in vitro.

Expression of apolipoprotein M and its association with adiponectin in an obese mouse model.

The aim of the present study was to explore the association between apolipoprotein M (ApoM) and adiponectin, and the underlying mechanism, via observation of ApoM expression in an obese mouse model. For in vivo experiments, mice were randomly distributed into four groups: Control group, obese group, obese group treated with adiponectin, and normal group treated with adiponectin. Body weight, plasma adiponectin, blood glucose and fasting insulin were measured and visceral adipose tissue was weighed at the end of the experiment. ApoM and transcription factor forkhead box A2 (Foxa2) mRNA expression in the mouse liver was evaluated and the protein level of ApoM detected. For in vitro experiments, an insulin-resistant (IR) hepatic cell model was established by inducing the HepG2 cell line with a high concentration of insulin. Following treatment with adiponectin, changes in ApoM and Foxa2 mRNA expression and ApoM protein expression were evaluated in the control and IR HepG2 cells. Results demonstrated that compared with the control group, body weight, visceral adipose tissue weight, blood glucose, fasting insulin and insulin-resistance index (HOMA-IR) were significantly increased in the obese group, whilst plasma adiponectin, ApoM mRNA expression, Foxa2 mRNA expression and ApoM protein in the mouse liver were all significantly decreased. Following intervention with adiponectin in obese mice, blood glucose, insulin and HOMA-IR were significantly decreased, whilst plasma adiponectin, ApoM mRNA expression, Foxa2 mRNA expression and ApoM protein were all significantly increased. However, no significant difference was observed in visceral adipose tissue weight following the intervention of adiponectin in obese mice. In vitro, in the absence of intervention, ApoM and Foxa2 mRNA expression and ApoM protein expression were significantly lower in IR HepG2 cells compared with HepG2 cells. Following intervention with adiponectin on IR HepG2 cells, ApoM and Foxa2 mRNA expression and ApoM protein expression were significantly increased. However, the intervention did not have any effect on HepG2 cells. In conclusion, intervention with adiponectin elevated ApoM mRNA expression, potentially via relieving IR and upregulating Foxa2 mRNA expression.

Correlation Between Apolipoprotein M and Inflammatory Factors in Obese Patients.

BACKGROUND The aim of this study was to observe apolipoprotein M (ApoM) level in obese patients and to explore its correlation with inflammatory factors. MATERIAL AND METHODS A total number of 96 participants were recruited and divided into 2 groups: the control group (or healthy group) whose participants had normal body weight (n=58), and the obese group with all its participants diagnosed with obesity (n=38). Data on blood pressure, body weight, height, body mass index, diastolic function of brachial artery endothelium, fasting venous blood glucose, blood lipids, plasmatic ApoM, interleukin-6 (IL-6), C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), fasting insulin, and adiponectin levels were collected for both groups. RESULTS In the obese group, the levels of plasmatic ApoM, high-density lipoprotein cholesterol (HDL-C), and plasmatic adiponectin were significantly (p<0.05) decreased compared to the control group, and the levels of IL-6, TNF-α, CRP, and fasting insulin were significantly increased (p<0.05) compared to the control group. For the obese group, plasmatic ApoM level was positively correlated with HDL-C level and negatively correlated with levels of IL-6, TNF-α, CRP, insulin, and insulin resistance index. However, no significant correlations were revealed between plasmatic ApoM and the diastolic function of brachial artery endothelium, adiponectin level, blood pressure, and blood glucose level. CONCLUSIONS Obese patients showed significantly lower plasmatic ApoM levels than people with normal body weight, and ApoM level showed a strong correlation with CRP, TNF-α, and IL-6 levels, which indicated that ApoM might be regulated by these inflammatory factors.

Protective Effects of Pterostilbene Against Myocardial Ischemia/Reperfusion Injury in Rats.

Pterostilbene (PTB) has been suggested to protect against myocardial ischemia/reperfusion (MI/R) injury. Gas6/Axl signaling has been suggested to play an important role in cell survival. However, the interaction between PTB and Gas6/Axl signaling in MI/R remains unclear. This study aims to evaluate the role of Gas6/Axl signaling in the protective effects of PTB against MI/R injury. In experiment 1, the rats were subjected to 30 min of ischemia, followed by 3, 6, and 12 h of reperfusion, respectively. In experiment 2, the rats were administered intraperitoneally with PTB or vehicle and subjected to MI/R injury. The results suggested that the expression of Gas6 and Axl decreased significantly after MI/R injury. PTB treatment conferred a cardioprotective effect with an improved post-ischemic cardiac function, a reduced myocardial infarct size, and decreased lactate dehydrogenase and creatine kinase-MB in the serum, a decreased oxidative stress and inflammation, and a reduced number of apoptotic cardiomyocytes. Moreover, PTB treatment up-regulated the expression of Gas6, Axl, and Bcl-2 and down-regulated Bax expression. Our findings suggest that PTB treatment exerts cardioprotection against MI/R injury via attenuating inflammatory response, oxidative stress, and apoptosis and up-regulating the expression of Gas6 and Axl. The application of PTB may be a new strategy for the treatment of MI/R injury.

Losartan Attenuates Myocardial Endothelial-To-Mesenchymal Transition in Spontaneous Hypertensive Rats via Inhibiting TGF-ß/Smad Signaling.

BACKGROUND: Losartan plays an important role in the inhibition of myocardial fibrosis. But the underlying mechanism is not entirely clear. Emerging evidences have indicated that endothelial-to-mesenchymal transition (EndMT) plays a crucial role in cardiac fibrosis. Here the present study aims to first investigated the effect of Losartan on EndMT in cardiac fibrosis of spontaneous hypertensive rats (SHRs). METHODS: Male SHRs were randomly divided into three groups and fed for 12 weeks, namely the SHR group (Group S), the Losartan-treated group (Group L) and the Prazosin-treated group (Group P). Wistar-Kyoto rats served as controls (Group W). The histological changes were evaluated by Masson's trichrome. Co-expression of CD31 and fibroblast-specific protein 1 (FSP1) were used as the markers of EndMT through immunofluorescence. The expressions of FSP1, CD31, TGF-ß, Smad were detected by Western blot analysis. RESULTS: It was identified that elevated blood pressure induced a significant increase in myocardial fibrosis and EndMT in SHRs, which was reversed by Losartan and Prazosin treatment. Furthermore, the activity of TGF-ß/Smad signaling was detected in the four groups. TGF-ß/Smad signaling was activated in SHRs and suppressed by Losartan or Prazosin treatment. Losartan exhibited more efficiently than Prazosin in inhibiting TGF-ß/Smad signaling activation, EndMT and myocardial fibrosis. CONCLUSION: These results showed that EndMT played an important role in promoting hypertensive cardiac fibrosis, and that losartan could suppress cardiac fibrosis through the inhibition of EndMT via classical TGF-ß/Smad pathway.

Neferine inhibits angiotensin II-induced rat aortic smooth muscle cell proliferation predominantly by downregulating fractalkine gene expression.

Neferine inhibits the angiotensin II (AngII)-induced proliferation of vascular smooth muscle cells (SMCs), but the underlying mechanism is unclear. The aim of this study was to explore the mechanism underlying the effect of neferine on the proliferation of vascular SMCs. Rat aortic SMCs (RASMCs) were used and fractalkine (Fkn) gene expression was measured by quantitative polymerase chain reaction and western blot analysis. The proliferation of RASMCs was analyzed by MTT assay and flow cytometry. It was revealed that AngII induced Fkn expression in a dose- and time-dependent manner. Fkn-knockdown with small interfering RNA attenuated the AngII-induced RASMC proliferation. Furthermore, neferine inhibited Fkn expression and attenuated the AngII-induced RASMC proliferation. These findings suggest that the Fkn gene may play an important role in AngII-induced RASMC proliferation and that neferine acts to attenuate AngII-induced RASMC proliferation by inhibiting Fkn expression.

Total flavonoids from Plumula Nelumbinis suppress angiotensin II-induced fractalkine production by inhibiting the ROS/NF-κB pathway in human umbilical vein endothelial cells.

Angiotensin II (Ang II) is a neuroendocrine factor that promotes hypertension and has been implicated in vascular inflammation through the induction of reactive oxygen species (ROS) and proinflammatory genes in endothelial cells. However, relatively little attention has been paid to the effect of Ang II on fractalkine (FKN), an important chemokine involved in endothelial dysfunction. In the study, we aimed to investigate the protective role of total flavonoids from Plumula Nelumbinis (TFPN), the main component extracted from Semen Nelumbinis, in Ang II-induced oxidative stress injury in human umbilical vein endothelial cells (HUVECs). Furthermore, we studied whether TFPN could attenuate the Ang II-induced generation of ROS and the activation of nuclear factor-κB (NF-κB); whether these Ang II-induced effects were inhibited by apocynin (a nicotinamide adenine dinucleotide phosphate oxidase inhibitor) and pyrrolidine dithiocarbamate (an NF-κB inhibitor). In the present study, it was observed that total flavonoids from Plumula Nelumbinis (TFPN), the main component extracted from Semen Nelumbinis, concentration-dependently inhibited the FKN production induced by Ang II in human umbilical vein endothelial cells (HUVECs). Furthermore, TFPN attenuated the Ang II-induced generation of ROS and the activation of nuclear factor-κB (NF-κB); these Ang II-induced effects were also inhibited by apocynin (a nicotinamide adenine dinucleotide phosphate oxidase inhibitor) and pyrrolidine dithiocarbamate (an NF-κB inhibitor). In conclusion, the findings of the present study indicate that TFPN attenuate Ang II-induced upregulation of FKN by inhibiting the ROS/NF-κB pathway in HUVECs and thus have a suppressive effect on vascular inflammation.

[QT dispersion in acute pulmonary embolism].

OBJECTIVE: To explore the alteration and the clinical significance of QT dispersion in acute pulmonary embolism (PE). METHODS: From May 2011 to April 2012, 42 hospitalized PE patients in Xiangya Hospital of Central South University were enrolled, and divided into a high-risk group and a non-high-risk group according to the clinic state on admission. Another 30 healthy subjects with matched age and genders were enrolled as a normal control group. QT interval was measured manually in 12- lead conventional electrocardiogram within 24 hours on admission and after the treatment. QT dispersion (QTd) and heart rate-corrected QT dispersion (QTcd) were also calculated. All patients were followed up during hospitalization, and were divided to a death group and a survival group. RESULTS: QTd and QTcd in the high-risk group [(70.2±34.0), (88.1±43.3) ms] and the non-high-risk group [(49.3±21.8), (59.1±26.2) ms] were significantly higher than those in the normal control group[(33.2±12.4), (36.7±14.2) ms] (P<0.05), while QTd and QTcd in the high-risk group were significantly higher than those in the non-high-risk group (P<0.05). The interval of electrocardiogram was (5.6±2.5) days between 24 hours on admission and after the treatment (ECG). QTd and QTcd were reduced significantly after the treatment in the survival group [(41.0±16.4), (47.4±18.0)ms] compared with those on admission [(54.0±33.0), (67.2±40.5)ms] (P<0.05), but the QTd and QTcd after the treatment were also significantly higher than those in the normal control group (P<0.05). There was no significant difference in the QTd and QTcd between 24 hours on admission and after the treatment in the death group (P>0.05). Logistic regression showed that high-risk of PE, right ventricular dysfunction and high QTcd after the treatment were the main risk factors of hospital death. CONCLUSION: QTd and QTcd are increased in PE. PE patients with right ventricular dysfunction, high-risk of PE, and high QTcd after the treatment suggest weak prognosis.

High levels of glucose induce "metabolic memory" in cardiomyocyte via epigenetic histone H3 lysine 9 methylation.

Diabetic patients continue to develop inflammation and cardiovascular complication even after achieving glycemic control, suggesting a "metabolic memory". Metabolic memory is a major challenge in the treatment of diabetic complication, and the mechanisms underlying metabolic memory are not clear. Recent studies suggest a link between chromatin histone methylation and metabolic memory. In this study, we tested whether histone 3 lysine-9 tri-methylation (H3K9me3), a key epigenetic chromatin marker, was involved in high glucose (HG)-induced inflammation and metabolic memory. Incubating cardiomyocyte cells in HG resulted in increased levels of inflammatory cytokine IL-6 mRNA when compared with myocytes incubated in normal culture media, whereas mannitol (osmotic control) has no effect. Chromatin immunoprecipitation (ChIP) assays showed that H3K9me3 levels were significantly decreased at the promoters of IL-6. Immunoblotting demonstrated that protein levels of the H3K9me3 methyltransferase, Suv39h1, were also reduced after HG treatment. HG-induced apoptosis, mitochondrial dysfunction and cytochrome-c release were reversible. However, the effects of HG on the expression of IL-6 and the levels of H3K9me3 were irreversible after the removal of HG from the culture. These results suggest that HG-induced sustained inflammatory phenotype and epigenetic histone modification, rather than HG-induced mitochondrial dysfunction and apoptosis, are main mechanisms responsible for metabolic memory. In conclusion, our data demonstrate that HG increases expression of inflammatory cytokine and decreases the levels of histone-3 methylation at the cytokine promoter, and suggest that modulating histone 3 methylation and inflammatory cytokine expression may be a useful strategy to prevent metabolic memory and cardiomyopathy in diabetic patients.

Phenylethanolamine N-methyltransferase gene promoter haplotypes and risk of essential hypertension.

BACKGROUND: Phenylethanolamine N-methyltransferase gene (PNMT) catalyzes the synthesis of epinephrine and plays an important role in regulating cardiovascular function. Genetic variation in the PNMT promoter is reportedly associated with the risk of essential hypertension in certain population. METHODS: In the present study, we explored the association of two common PNMT promoter single-nucleotide polymorphisms (SNPs) G-367A (rs3764351) and G-161A (rs876493) and their haplotypes with the risk of essential hypertension in a Han Chinese population, using 316 pairs of age-, sex-, and geographically matched essential hypertension patients and normotensive controls. RESULTS: No significant difference in allele and genotype frequencies at either G-367A (rs3764351) or G-161A (rs876493) was observed between essential hypertension patients and normotensive controls. However, the 2-SNP AA haplotype was found significantly more common in normotensive controls than in essential hypertensive patients (P = 0.01; adjusted odds ratios, 0.17; 95% confidence interval, 0.05-0.58). CONCLUSIONS: The 2-SNP AA haplotype in the PNMT promoter is associated with decreased risk of essential hypertension in Han Chinese. This is the first evidence of an association between a PNMT promoter haplotype and the risk of essential hypertension.

Protective effect of neferine on endothelial cell nitric oxide production induced by lysophosphatidylcholine: the role of the DDAH-ADMA pathway.

Neferine, extracted from the seed embryo of Nelumbo nucifera Gaertn., has multiple cardiovascular pharmacological effects. The dimethylarginine dimethylaminohydrolase (DDAH) - asymmetric dimethylarginine (ADMA) system is a novel pathway for modulating nitric oxide (NO) production. The aim of this study was to investigate whether the protective effect of neferine on endothelial NO production was related to the DDAH-ADMA pathway. Human umbilical vein endothelial cells (HUVECs) were first exposed to neferine (0.1, 1.0, or 10.0 µmol/L) for 1 h, and then incubated with lysophosphatidylcholine (LPC; 10 µg/mL) in the presence of neferine for 24 h. The medium was collected for measuring the levels of NO, maleic dialdehyde (MDA), as well as ADMA. The endothelial cells were collected for measuring DDAH activity and the level of reactive oxygen species (ROS). LPC significantly decreased NO concentration and DDAH activity and increased the levels of ADMA, ROS, and MDA. Neferine could partially counteract the changes induced by LPC. These findings suggested that neferine could modulate the DDAH-ADMA pathway via its antioxidant properties, which was involved in its beneficial effect on endothelial NO production.

Left ventricular systolic synchrony in dilated cardiomyopathy patients with normal QRS wave.

OBJECTIVE: To evaluate the distribution characteristics of left ventricular systolic dyssynchrony (LV-SD) in dilated cardiomyopathy (DCM) patients with chronic heart failure (CHF) and normal QRS wave width, by pulsed-wave Doppler tissue imaging (PW-DTI), and study its relation with left ventricular systolic function, ventricular remodeling, and functional mitral regurgitation (FMR). METHODS: The time to peak systolic velocity (Ts) in 12 left ventricular segments was evaluated by PW-DTI, from which the standard deviation (SD) of Ts in the 12 segments (Ts-SD) and maximum Ts difference (Ts-maxD) were calculated. RESULTS: Ts-SD and Ts-maxD in the 12 LV segments of the DCM patients with CHF were significantly higher than those of the healthy controls (P<0.01). In DCM patients with CHF and normal QRS wave width, the incidence of LV-SD was 29.8% (14/47) and the inferior wall was the most frequent distribution site of contraction delay. Linear regression analysis revealed a negative correlation between Ts-SD, Ts-maxD, and left ventricular ejection fraction (LVEF) (P<0.01), but a positive correlation between Ts-SD, Ts-maxD and left ventricular end-diastolic volume (LVEDV), lefe ventricular end-systolic volume (LVESV), New York Heart Association (NYHA) cardiac function, FMR (P<0.01) in DCM patients with CHF. CONCLUSION: LV-SD exists in DCM patients with normal QRS width. LV-SD aggravates the LV systolic function damage, which is closely associated with left ventricular remodeling. LV-SD may contribute to the FMR in DCM patients.

High levels of glucose induce apoptosis in cardiomyocyte via epigenetic regulation of the insulin-like growth factor receptor.

Diabetic hyperglycemia result in cardiovascular complications, but the mechanisms by which high levels of glucose (HG) cause diabetic cardiomyopathy are not known. We investigate whether HG-induced repression of insulin-like growth factor 1 receptor (IGF-1R) mediated by epigenetic modifications is one potential mechanism. We found that HG resulted in decreased IGF-1 receptor (IGF-1R) mRNA levels, and IGF-1R protein when compared with H9C2 rat cardiomyocyte cells incubated in normal glucose. HG also induced apoptosis of H9C2 cells. The effects of HG on reduced expression of IGF-1R and increased apoptosis were blocked by silencing p53 with small interference RNA but not by non-targeting scrambled siRNA. Moreover, HG negatively regulated IGF-1R promoter activity as determined by ChIP analysis, which was dependent on p53 since siRNA-p53 attenuated the effects of HG on IGF-1R promoter activity. HG also increased the association of p53 with histone deacetylase 1 (HDAC1), and decreased the association of acetylated histone-4 with the IGF-1R promoter. Furthermore, HDAC inhibitor relieved the repression of IGF-1R following HG state. These results suggest that HG-induced repression of IGF-1R is mediated by the association of p53 with the IGF-1R promoter, and by the subsequent enhanced recruitment of chromatin-modifying proteins, such as HDAC1, to the IGF-1R promoter-p53 complex. In conclusion, our data demonstrate that HG decreases expression of IGF-1R and decreases the association of acetylated histone-4 with the IGF-1R promoter. These studies may help delineate the complex pathways regulating diabetic cardiomyopathy, and have implications for the development of novel therapeutic strategies to prevent diabetic cardiomyopathy by epigenetic regulation of IGF-1R.

[Induction of IL-8 by Chlamydia trachomatis through MAPK pathway rather than NF-kappaB pathway].

OBJECTIVE: To determine the signaling pathway required for Chlamydial induction of IL-8 expression in epithelial cells. METHODS: The production and localization of IL-8 in Chlamydia-infected Hela 229 cells were monitored using Western blot, immunoflourescence, and ELISA. Activation of MAPK and NF-kappaB signaling pathways were detected by Western blot and immunoflourescence. The effect of different signaling pathways on Chlamydia-induced Il-8 was measured by experiments of chemical inhibitors. RESULTS: IL-8 was induced by Chlamydia and was time-dependant. Chlamydial infection activated MAPK/ERK and MAPK/p38 pathways but not NF-kappaB pathway. Chlamydial induction of IL-8 was blocked by small molecule inhibitors targeting the ERK and p38 pathways. CONCLUSION: Chlamydia-induced IL-8 in cervical epithelial cells, the natural target cell type of Chlamydia trachomatis infection, is dependent on MAPK pathway but not NF-kappaB pathway, which provides important information for further understanding the molecular mechanism of Chlamydia-induced inflammatory pathologies.

[Characteristics of spectra of superior vena cava flow Doppler velocities in pulmonary arterial hypertension].

OBJECTIVE: To explore and evaluate the characteristics of spectra wave shapes and parameters of the superior vena cava (SVC) Doppler flow patterns in patients with pulmonary arterial hypertension(PAH) by echocardiography. METHODS: Forty-nine patients with PAH as the PAH group and the paired healthy subjects as the control group were included in this study. Transthoracic echocardiography was used, and the spectra of SVC flow Doppler velocities in the right supraclavicular fossa view were examined and recorded. Peak velocity and velocity time integral (VTI) were measured. RESULTS: The spectra wave shapes of SVC flow velocity in the PAH group were distinguished from those of the control. The peak velocity and VTI of S waves during inspiration and the rate of respiratory changes of peak velocity of SVC flow Doppler velocity in moderate and severe PAH groups were significantly lower than those of the control (P<0.05).The peak velocity and VTI of D waves of SVC flow Doppler velocity in the PAH groups were significantly lower than those of the control (P<0.05). The rate of respiratory changes of peak velocity of D waves in the PAH groups was significantly lower than those of the control (P<0.05). The peak velocity and VTI of AR, and VR waves of SVC flow Doppler velocity in the PAH groups were significantly higher than those of the control (P<0.05). Linear regression analysis revealed a significant correlation between pulmonary arterial systolic pressure(PASP) and the Vexp/Vins ratio (r=0.760, P<0.001). CONCLUSION: The spectra wave shapes of SVC flow velocity in the PAH groups were distinguished from those of the control which may have some diagnostic value for PAH.The peak velocities and VTI of S waves during inspiration, D waves, AR waves and VR waves of SVC flow Doppler in the PAH groups are different from the control. The ratio of Vexp/Vins of S wave may be a non-invasive quantitative index to detect PAH.

[Effect of Tongxinluo on endothelial function and hypersensitive C-reactive protein in acute coronary syndrome patients undergoing percutaneous coronary intervention].

OBJECTIVE: To determine the effect of Tongxinluo on the endothelial function and hypersensitive C-reactive protein (hs-CRP) in acute coronary syndrome patients undergoing percutaneous coronary intervention(PCI). METHODS: Thirty-three patients with unstable angina pectoris and 6 patients with acute myocardial infarction who underwent PCI for stenotic lesions of the coronary artery were enrolled. The patients were randomly assigned to a conventional group (n = 19) which took routine treatment or a tongxinluo group (n = 20) which took Tongxinluo(4 capsules once, 3 times per day) at the base of routine treatment after PCI. Nitric oxide synthase (NOS), nitric oxide (NO), endothelium-dependent vasodilation which was evaluated in the brachial artery flow mediated diameter(FMD) and hs-CRP were measured before the PCI and 24 hours and 3 months after the PCI. The correlation between NO and hs-CRP was analyzed. RESULTS: NOS, NO, and FMD in the 2 groups 24 hours after the PCI were significantly lower than those before the PCI(P < 0.05), but hs- CRP obviously increased (P < 0.05). NOS, NO, and FMD 3 months after the PCI in the 2 groups were significantly higher than those before the PCI (P < 0.05 or P < 0.01), but hs-CRP obviously decreased (P < 0.01).All indexes mentioned above in the Tongxinluo group showed greater changes than those of the conventional group(P < 0.05). NO was negatively correlated with hs-CRP (r = -0.3219, P<0.01). CONCLUSION: Tongxinluo capsules have obvious beneficial effect on endothelial function and anti-inflammation in acute coronary syndrome patients undergoing PCI, by directly acting on the endothelium and indirectly inhibiting inflammation.

[Protective effects of metformin on low-density lipoprotein-induced endothelial dysfunction in rats].

OBJECTIVE: To observe the protective effect of metformin on the endothelial function and the mechanisms in rats with low-density lipoprotein (LDL) injection. METHODS: A single dose (4 mg/kg) of natural LDL was injected through the sublingual vein of rats to induce vascular endothelial dysfunction. Blood samples were then collected from the rats to detect the concentrations of malondialdehyde (MDA) and nitric oxide (NO), activity of superoxide dismutase (SOD) and serum lipid levels. The thoracic aorta of rats was obtained to assay acetylcholine (ACh)-induced endothelium-dependent relaxation (EDR) and sodium nitroprusside (SNP)-induced endothelium-independent relaxation. The effects of metformin pretreatment on the endothelial functions in the rats were investigated. RESULTS: A single-dose LDL significantly inhibited ACh-induced EDR without affecting SNP-induced endothelial-independent relaxation. The injection decreased serum NO and elevated serum MDA level, but had no effect on serum lipid level. Metformin markedly attenuated LDL-induced inhibition of EDR, serum MDA elevation, and serum NO reduction without affecting the serum lipid levels. CONCLUSION: Metformin provides protection against vascular endothelial dysfunction induced by LDL in rats, the mechanism of which is probably associated with protection of endothelium-dependent relaxation factor and inhibition of the oxidative stress.

[Association of metabolic syndrome with serum interleukin-10 and high sensitive C reactive protein(hs-CRP) in old men].

OBJECTIVE: To explore the association of metabolic syndrome(MS) with serum interleukin-10 (IL-10) and high sensitive C reactive protein(hs-CRP) in old men with MS. METHODS: Seventy patients with MS and 30 age-matched controls were enrolled. Blood pressure, waist circumference(WC), weight, height, body mass index(BMI), lipid-profile, fasting plasma glucose(FPG), fasting plasma insulin (FINS), homeostasis model assessment of insulin resistance(HOMA-IR),the serum IL-10, and hs-CRP levels were measured. The concentration of serum IL-10 was measured by enzyme linked immunosorbent assay (ELISA), and serum hs-CRP level by the latex-enhanced immuno- turbidimetric assay. RESULTS: Compared with the control group, the serum IL-10 level in the MS group was significantly lower (P<0.05), and the concentration of hs-CRP was obviously higher (P<0.05). Using Pearson's correlation analysis, the serum IL-10 level was negatively related with HOMA-IR(r=-0.684,P=0.000)and FINS(r=-0.742,P=0.000); hs-CRP was positively related with BMI(r=0.372,P=0.002), HOMA-IR(r=0.276,P=0.021)and FINS(r=0.312,P=0.008)in the MS group. Stepwise regression analysis suggested that FINS might be the influencing factors of IL-10; BMI and FINS might be the influencing factors of hs-CRP in patients with MS. CONCLUSION: In old male patients with MS, the concentration of serum IL-10 decreases, and the serum hs-CRP level increases obviously. This suggests chronic inflammation.