Objective:To observe the effect of chest pain center management model and emergency green channel on pre-hospital rescue rate of patients with acute ST-segment elevation myocardial infarction (STEMI).Methods:Patients with STEMI admitted in Yunnan Provincial Emergency Center between January 2017 and June 2019 were selected as the study subjects. 522 patients with STEMI sent by emergency center were included in the observation group (chest pain center management model of first-aid), while 326 patients with STEMI who came to the hospital by themselves were included in the control group (emergency green channel for first-aid). The pre-hospital and nosocomial first-aid related indexes, cardiac function (assessed by Killip grade), rescue rate, hospital stay and incidence of complications were compared between the two groups.Results:The response time of visit, time of initial electrocardiogram (ECG) completion and total time of first-aid in observation group [(1.04±0.11)min, (1.56±0.25)min, (10.63±2.26)min] were significantly shorter than those in control group [(2.82±0.26)min, (5.99±1.06)min, (18.65±2.98)min, P<0.05]. The grade of cardiac function in observation group was significantly better than that in control group ( P<0.05). Compared with the control group, the observation group had higher successful rescue rate, shorter hospital stay , lower total incidence of complications [94.25% vs 42.02%, (6.09±1.02)d vs (8.92±1.65)d, 13.01% vs 32.12%, P<0.05]. Conclusions:Compared with emergency green channel, chest pain center management model can not only shorten first-aid related time of STEMI patients, but also improve their successful rescue rate, reduce incidence of complications and improve prognosis.

Objective Angiotensin(AngⅡ)is an important proinflammatory mediator in the cardiovascular system.The present study is aimed at investigating the correlation between ceramide and p53 and apoptosis of human umbilical endothelial cells induced by AngⅡ.Methods Human umbilical endothelial cells were cultured in vitro and treated with AngⅡalone or in combination with Losartan(an in- hibitor of AT1),PD123319(an inhibitor of AT2),FB1(an inhibitor of ceramidase),PFT-?(an inhibitor of p53),respectively.The ap- optosis of cells was detected with TUNEL,and p53 expression at protein and mRNA was assessed with Western blotting and reverse tran- scription-polymerase chain reaction(RT-PCR).Results Compared to AngⅡgroup,PD123319 and FB1 could inhibit endothelial cells ap- optosis induced by AngⅡat 24h;hut Losartan and PFT-?could not.Compared to the control group,no statistical difference existed be- tween PD123319 and FB1,but it did exist between Losartan and PFT-?.FB1 and PFT-?down-regulated the p53 expression at the protein and mRNA levels.Conclusion In the process of apoptosis induced by AngⅡ,AngⅡcan induce the activation of ceramide by binding with AT2.AT2 and Ceramide play a key role in the endothelial cells apoptosis induced by AngⅡ.Ceramide may be situated in the upper stream of p53 and induce the apoptosis by p53 pathway.

Objective To investigate the expression changes of stromal interaction molecule 1 (STIM1) in vascular smooth muscle cells in balloon injury of carotid artery in rat in order to explore the proliferation mechanism of vascular smooth muscle cells. Methods A rat model of vascular restenosis induced by injury to the carotid arteries due to balloon dilatation was reproduced in present study. A total of 18 SD rats were randomly divided into 3 groups (6 each): control group, 7-day group and 14-day group after balloon injury to the carotid artery. The expression of STIM1 mRNA in vascular smooth muscle cells was assayed with reverse transcription polymerase chain reaction (RT-PCR), and the STIM1 protein was assessed by immunohistochemistry. The histopathology of the arteries was examined after by HE staining. Results Intima area/media area ratio (IA/MA) was significantly increased in 7-day group after balloon injury than in control group (P

Objective To explore the role of eNOS and NF-?B in the cultured endothelial cells apoptosis induced by TNF-? and Ang II.Methods The cultured endothelial cells were treated with TNF-? and Ang II in absence and presence of PDTC(an inhibitor of NF-?B);the mRNA of eNOS was measured by RT-PCR,the protein of eNOS and I?B? were assessed by Western-blot,the activity of NF-?B was evaluated by EMSA,and the apoptosis of cells was detected with Tunel.Results The mRNA and protein of eNOS were significantly decreased in the endothelial cells induced by TNF-? and AngII(P

Objective A retrospective analysis were conducted to identify the effect of bypassing the emergency department on 30-days outcomes of patients with acute myocardial infarction undergone primary percutaneous coronary intervention ( PPCI) . Methods From June 2014 to April 2015, 187 patients underwent PPCI in Kunming General Hospital were included. 13 patients were excluded owing to their incomplete follow-up data. The total 174 patients were divided into two groups: the control group (n =59) who did not bypass the emergency department, and the bypass group ( n = 115) who bypassed the emergency department and directly received PPCI. The data of all patients were collected and analyzed. Results There were no significant differences in baseline characteristics and PPCI related data (including percentage of thrombus aspiration catheter used, length or diameter of stents applied between two groups (all P ﹥ 0. 05) . The bypass group had shorter door-to-ballon ( D2B) than the control group [ (67. 7 ± 21. 5) min vs. (89. 4 ± 23. 6) min, P ﹤ 0. 001] . There were no significant differences in 30-days all-cause mortality, re-myocardial infacrtion and target ressel revascularization (TVR) between the two groups (P ﹥ 0. 05) . Total MACEs rate in the bypass group was lower than in the control group (10. 2% vs. 1. 7% , P = 0. 012) . Logistic regression analysis showed that age, diabetes, pain-to-door (PTD) time and CK peak value were the main influencing factors for 30-day MACEs rate of patients receiving PPCI ( P ﹤0. 05) . Conclusions Bypassing the emergency department can shorten D2B time and reduce 30-days MACEs post-PPCI, but reducing the total ischemic time will be more beneficial to patients with acute myocardial infarction.

Objectives To investigate clinic outcome of ticagrelor in treatment of patients with acute ST-segment elevation my ocardial infarction receiving primary percutaneous coronary intervention.Methods Sixty-two consecutive patients with ST segment elevation myocardial infarction (STEMI) receiving primary percutaneous coronary intervention (PCI) were included in this study.The clinic characteristics,thrombolysis in myocardial infarction (TIMI) refuse after PCI,clinical outcomes after 30 d of patients were compared between patients who were treated with ticagrelor (group A 30 cases) and clopidogrel (group B 32 cases).Results There was no difference in the age,proportion of women,hypertension,and diabetics (P ＞ 0.05).TIMI 3 refuse after PCI were significantly higher in group A than group B (96.7％ vs 87.5％,P ＜ 0.05).The 30 d re-angina pectoris was lower in group A than group B (3.3％ vs 12.5％,P ＜0.05).However,tiny bleeding of group A was higher than group B (13.3％ vs 3.1％,P ＜0.05).Conclusions Ticagrelortreatment can improve the prognosis of STEMI receiving primary PCI,but increase the risk of bleeding.

Objective To investigate the effects of B-type natriuretic peptides (BNP) on expression of monocyte chemoattractant protein-1(MCP-1) in rat peritoneal macrophages and to identify the inflammation-mediated effects of BNP in macrophages. Methods Peritoneal macrophages of primary culture were treated with BNP, BNP+HS-142-1, or BNP+TNF-?+HS-142-1. The protein expression of MCP-1 was measured by Western blot. Results BNP enhanced the MCP-1 protein expression in macrophages, and this effect could be abrogated by HS-142-1. In addition, BNP could inhibit TNF-? induced MCP-1 expression. Conclusion BNP can induce the MCP-1 protein expression in macrophages, suggesting BNP has a pro-inflammatory effect. However, BNP also can inhibit TNF-? induced MCP-1. These findings suggest that the effect of inflammation-mediated by BNP is biphasic though the mechanism is still unclear.

Objective To explore the mechanism by which urotensin Ⅱ induces hypertrophy of the cultured rat cardiomyocytes. Methods The cultured cardiomyocytes from neonatal SD rats were treated with urotensin Ⅱ, also with cyclosporine A for its blocking effect on urotensin Ⅱ induced cardiomyocytes hypertrophy. The mRNA and protein levels of ?-MHC and CaN were evaluated by real-time PCR and Western blotting, respectively. Results In the cells treated with 10-8 and 10-7 mol/L urotensin Ⅱ, the mRNA and protein levels of ?-MHC and CaN were significantly higher than that of control (P

Objective To study the effect of angiotensinⅡ(AngⅡ) on apoptosis in endothelial cells(EC). Methods Human umbilical endothelial cells were cultured in vitro and treated with AngⅡ in various concentrations alone and in combination with fumonisin B1(FB1, an inhibitor of ceramidase). TUNEL was employed to determine the apoptosis of the cultured EC. The bax mRNA and protein levels of EC were detected by RT-PCR and Western-blot techniques. Results The results showed that the number of apoptotic cells was significantly higher in AngⅡ-treated endothelium than in the control group(P0.05). Conclusion AngⅡ may induce apoptosis of endothelial cells via ceramide and up-regulating the bax mRNA and protein expression. Ceramide is the upper stream of bax and induces apoptosis by bax pathway.

AIM:The purpose of the present study was to investigate the effect of interleukin-10(IL-10)on the proliferation and calcineurin(CaN)activity in cultured cardiac fibroblasts(CFs)induced by arginine vasopressin(AVP).METHODS:The CFs of left ventricle in neonatal Sprague-Dawley rats were isolated and cultured by trypsin digestion and selective plating technique.Then the proliferation rates of cells were determined by using the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay(A490 value).Cell cycle distribution was determined with flowcytometry technique.The CaN activity was measured by ultra-violet spectrophotography.RESULTS:(1)MTT colorimetry showed that 10-7 mol/L AVP significantly increased A490 value of CFs in comparison with control group(P