经皮腔内冠脉介入术对冠脉循环中肾上腺髓质素及肿瘤坏死因子的影响

目的 探讨经皮腔内冠脉介入术对冠脉循环中肾上腺髓质素(ADM)及肿瘤坏死因子α(TNF-α)水平的影响。方法 33例冠心病患者分别于冠脉造影前后即刻、球囊扩张(PTCA)后即刻、支架置入后即刻、术后10 min采集冠状静脉窦血,同时采集股动脉血,采用放免法测定ADM、TNF-α浓度。结果 冠脉造影前后ADM及TNF-α无明显变化(P>0.05);PTCA后即刻冠状窦内ADM和TNF-α明显升高(P<0.01);支架后即刻ADM有上升趋势(P>0.05);术后10 min ADM降至术前水平。结论 冠脉造影对冠脉循环血管活性物质基本不影响;PTCA及支架术后冠脉循环中ADM和TNF-α升高,可能与球囊损伤内皮、支架对管壁的机械压迫及刺激有关,两者可能参与了PTCA及支架术后急性闭塞、再狭窄的调节。     

冠心病患者血浆尾加压素Ⅱ的临床研究

OBJECTIVE: To investigate the changes in plasma urotensin II(U II) expression levels in patients with coronary heart disease (CHD). METHODS: Plasma U II levels in 50 CHD patients with coronary stenosis indicated by coronary angiography and 20 healthy subjects were determined by radio immunoassay. RESULTS: Venous plasma U II levels were significantly lowered in CHD patients in comparison with the healthy subjects (1.61+/-1.02 pg/ml vs 3.70+/-1.30 pg/ml, P=0.000). In the CHD patient group, significantly differences were noted in the U II levels between patients with stable angina (2.62+/-1.20 pg/ml), unstable angina (1.39+/-0.80 pg/ml) and acute myocardial infarction (AMI, 1.04+/-0.45 pg/ml, P=0.004). CHD patients with coronary artery occlusion and those with only coronary stenosis had comparable venous plasma U II levels (1.29+/-1.02 pg/ml vs 1.76+/-1.00 pg/ml, P=0.131), whereas the patients with restenosis after percutaneous transluminal coronary angioplasty (PTCA) had higher U II levels than the other subjects in the CHD patient group (2.28+/-0.94 pg/ml vs 1.40+/-0.96 pg/ml, P=0.008), and the femoral plasma U II levels were significantly elevated after PTCT, increasing from 1.18+/-1.14 pg/ml to a postoperative level of 2.22+/-1.77 pg/ml (P=0.001). CONCLUSION: U II might play a role in the pathophysiological process of CHD and can be involved in the restenosis after angioplasty.     

ADM和ET-1在冠状动脉内皮损伤中的表达

①目的研究冠状动脉粥样硬化性心脏病(CHD)病人急慢性冠状动脉内皮损伤时肾上腺髓质素(ADM)、内皮素-1(ET-1)在不同易患因素累积、不同冠状动脉狭窄程度、不同内皮稳定状态以及急性内皮损伤(PTCA)时的水平变化,探讨血管活性物质与急慢性内皮损伤的关系及临床意义。②方法选择72例CHD病人作为慢性内皮损伤组,按冠心病易患因素分为A(0~1个因素)、B(2个因素)、C(≥3个因素)组;按病人临床表现分为稳定型心绞痛组(SAP)和不稳定型心绞痛(UAP)组;按冠状动脉狭窄程度分为轻度狭窄、中度狭窄和重度狭窄组。急性内皮损伤组为28例PTCA病人。两组均以冠状动脉造影者作为对照。用放射免疫法测定各组ADM、ET-1的含量。③结果除A组ADM值与正常对照组无差异外(t=1.051,P>0.05),研究组血浆ADM、ET-1含量均高于对照组(t=4.287~13.945,P<0.01)。研究组内ADM、ET-1在3组间均有显著意义(t=2.813~11.649,P<0.01)。随着冠状动脉狭窄程度加重,ADM、ET-1有增高趋势,中度狭窄和重度狭窄组与对照组比较有明显增高(t=2.627~10.098,P<0.01);轻、中、重度狭窄3组间比较差异有显著性(t=3.150~11.708,P<0.01)。SAP组ADM、ET-1与对照组比较无显著性差异(t=0.297、1.983,P>0.05),而UAP组显著高于SAP组和对照组(t=2.932~12.175,P<0.01)。PTCA急性损伤冠状动脉内皮后与治疗前比较血浆ADM、ET-1水平显著升高(t=3.48、11.17,P<0.01)。④结论CHD易患因素对内皮细胞慢性损伤有累积作用。血浆ADM、ET-1水平与冠状动脉狭窄程度有关,可以作为判断CHD病情及预后的参考指标。UAP病人血浆ADM、ET-1水平可以作为判定心绞痛稳定性的参考指标。PTCA造成冠状动脉内皮急性损伤,激活ADM、ET-1的内皮源性释放。保护CHD病人内皮功能,干预易患因素及内皮功能的改善治疗是防止介入术后再狭窄及慢性内皮损伤的重要环节及途径。     

冠心病患者血浆尾加压素Ⅱ的临床研究

目的 探讨血管活性物质尾加压素Ⅱ(UⅡ)在冠心病患者体内的表达及其变化。方法 采用放射免疫法测定50例冠心病患者及20例健康体检者的血浆UⅡ的水平。结果 (1)健康对照组静脉血浆UⅡ含量为3.70±1.30 pg/ml,冠心病患者的血浆UⅡ含量为1.61±1.02 pg/ml,两者有统计学差异(P=0.000)。冠心病患者中稳定性心绞痛者血浆UⅡ含量为2.62±1.20 pg/ml,不稳定心绞痛者UⅡ含量为1.39±0.80 pg/ml,急性心肌梗死者UⅡ含量为1.04±0.45 pg/ml,3组之间有显著性差异(P=0.004)。(2)冠心病患者中冠脉血管有闭塞组静脉血浆UⅡ含量为1.29±1.02 pg/ml,单纯狭窄组UⅡ含量为1.76±1.00 pg/ml,两者无统计学差异(P=0.131)。(3)经皮腔内冠状动脉成型术(PTCA)及支架植入术后,出现再狭窄患者组血浆UⅡ含量为2.28±0.94 pg/ml,而其他病人的血浆UⅡ含量为1.40±0.96 pg/ml,两者有统计学差异(P=0.008)。(4) PTCA治疗前后,股动脉血浆UⅡ的含量分别为1.18±1.14、2.22±1.77 pg/ml,两者有统计学差异(P=0.001)。结论 UⅡ可能参与了冠心病的发病;在PTCA治疗后出现支架内再狭窄中可能起作用。     

冠心病患者PTCA后冠脉循环TNF-α水平的改变及其临床意义

目的 :观察经皮穿刺冠状动脉腔内成形术 (PTCA )对冠脉循环肿瘤坏死因子α(TNF-α)水平的影响。 方法 :采用生物活性法检测 PTCA前后冠状窦 (CS)及股动脉 (AO)血浆 TNF-α水平。 结果 :与 PTCA前相比 ,术后即刻 AO血浆 TNF-α水平升高 [(15 .86± 3.75 ) U / ml对 (4 1.32± 4.36 ) U / ml,P<0 .0 1],而术后即刻 CS血浆 TNF-α水平升高更为显著 [(16 .72± 4.14) U/ ml对 (96 5 .6 1± 6 .2 5 ) U / ml,P<0 .0 1]。术后 2 4h AO血浆 TNF-α[(18.32± 5 .12 ) U / ml]与术前比较无显著差异(P>0 .0 5 )。结论 :术后血浆 TNF-α活性增高可能与 PTCA时冠状动脉内膜损伤有关 ,TNF-α是否参与了 PTCA后冠状动脉闭塞和再狭窄过程还有待进一步研究     

经皮腔内冠状动脉成形术对冠心病患者循环血内皮素水平的影响

来研究观察PTCA后股动脉血ET浓度的变化以探讨PTCA对ET释放的影响。14例行PTCA患者分别于术前、术后即刻及术后1小时取股动脉血,20例单纯行冠状动脉造影(CAG)的患者分别于术前及术后即刻取股动脉血,用放射免疫分析法测血浆ET浓度。结果:PTCA术后早期股动脉血ET水平明显升高(从69.87±31.74pg/ml到79.09±31.18pg/ml,P<0.05),术后1小时继续升高(83.65±39.69pg/ml)。术后血ET浓度升高值与球囊扩张后直径比被扩张动脉直径之比(B/A)呈正相关(R=0.589,P<0.05)。CAG术后血浆ET浓度较术前无变化(分别为59.36±22.57pg/ml和54.20±18.70pg/m1,P>0.05)。结论:PTCA使循环ET水平升高,内皮损伤可能是引起ET释放和合成的主要因素。     

冠心病患者介入治疗后血浆新型气体信号分子硫化氢及一氧化氮变化的临床研究

目的研究新型气体信号分子硫化氢(H2S)及一氧化氮(NO)在冠心病患者和冠脉造影正常者血浆中含量的差异及介入治疗对其的影响,探讨其在冠心病发病及介入治疗中的病理生理意义。方法冠心病组40例,造影正常组17例,采用硫敏感法测定术前血浆H2S含量并用Greiss法测定血浆中NO含量,动态监测冠心病患者冠状动脉造影前后、介入治疗后即刻、术后24h和72h血浆H2S、NO含量,分析冠心病组和造影正常组患者血浆H2S、NO含量的差异及介入治疗后血浆H2S和NO的变化。结果冠心病患者血浆H2S、NO含量远低于造影正常组(P均<0.01);冠脉双支和多支病变组血浆H2S含量差异无统计学意义(P>0.05),但均明显低于单支病变组(P<0.05和P<0.01)。不同支数病变冠心病患者血浆NO含量差异无统计学意义。冠脉血管有闭塞组其血浆H2S、NO含量明显低于单纯狭窄组(P均<0.05);支架植入术后复查狭窄者NO含量明显低于无狭窄者(P<0.05),H2S含量也低于无狭窄者,但差异无统计学意义(P>0.05)。冠状动脉造影术对血浆H2S、NO含量无影响,但PCI治疗术后即刻H2S、NO含量显著降低;H2S含量术后24h恢复至术前水平,NO含量术后24h降至最低水平,72h仍未恢复至术前水平。结论 H2S和NO可能参与了冠心病的发病过程及介入治疗后急性血管闭塞及再狭窄的发生,血浆H2S含量的高低与冠脉血管病变严重程度相关。     

肾上腺髓质素及尾加压素Ⅱ在先天性心脏病肺动脉高压中作用的研究

目的探讨先天性心脏病(CHD)合并肺动脉高压(PH)患者手术前后血浆肾上腺髓质素(ADM)及尾加压素Ⅱ(UⅡ)变化的临床意义。方法将52例患者按肺动脉收缩压分为3组:无PH组(<30 mm Hg)17例,轻度PH组(30~49 mm Hg)18例,中重度PH组(≥50 mm Hg)17例。测定3组术前、术后即刻及术后7 d ADM及UⅡ含量,并比较手术前后的变化;分析两者及其与肺动脉压(PAP)间的相互关系。结果(1)3组患者肺动脉压(PAP)与血浆ADM浓度呈正相关(术前r=0.8012,P<0.01;术后即刻r=0.6325,P<0.01;术后7 dr=0.7126,P<0.01)。(2)3组患者UⅡ浓度则与PAP无相关性(均P>0.05)。(3)无PH组术前ADM浓度为33 pg/m l±5 pg/m l、术后即刻为29 pg/m l±4 pg/m l、术后7 d为20 pg/m l±3 pg/m l;轻度PH组术前ADM浓度为44 pg/m l±8 pg/m l、术后即刻40 pg/m l±6 pg/m l、术后7 d为34 pg/m l±4 pg/m l;中重度PH组术前ADM浓度为60 pg/m l±10 pg/m l、术后即刻58 pg/m l±8 pg/m l、术后7 d为38 pg/m l±4 pg/m l。各组术后ADM浓度呈下降趋势,但只有术后7 d与术前比较差异有统计学意义(无PH组q=5.41,P<0.01;轻度PH组q=4.76,P<0.01;中重度PH组q=6.32,P<0.01)。(4)无PH组术前UⅡ浓度为2.2 pmol/L±0.5pmol/L、术后即刻为2.2 pmol/L±0.44 pmol/L、术后7 d为2.2 pmol/L±0.6 pmol/L;轻度PH组术前UⅡ浓度为2.7 pmol/L±0.6 pmol/L、术后即刻2.6 pmol/L±0.6 pmol/L、术后7 d为2.6 pmol/L±0.5pmol/L;中重度PH组术前UⅡ浓度为2.9 pmol/L±0.6 pmol/L、术后即刻2.6 pmol/L±0.7 pmol/L、术后7 d为2.8 pmol/L±0.4 pmol/L。3组患者手术前后UⅡ浓度差异无统计学意义(均P>0.05)。结论(1)ADM在PH形成和血管重建中发挥重要的作用。(2)UⅡ与PAP无相关性,但是不能排除UⅡ在PH形成和血管重建中有重要的作用。(3)血浆ADM水平可作为判断PH严重程度的指标之一。     

Effect of aspirin plus clopidogrel on inflammatory markers in patients with non-ST-segment elevation acute coronary syndrome

Background Aspirin can inhibit inflammatory reactions and platelet aggregation, but little is known about the effects of the combination of aspirin plus clopidogrel, a new antiplatelet agent, on inflammation. The purpose of this study was to determine whether aspirin plus clopidogrel can further suppress inflammation in patients with non-ST-segment elevation acute coronary syndrome (NSTEACS) . Methods One hundred and fifteen patients with NSTEACS were randomized into two groups: group A (aspirin alone, n =58) and group B (aspirin plus clopidogrel, n =57). Patients in group A received a loading dose of 300 mg aspirin, then 100 mg per day. The patients in group B received a loading dose of 300 mg aspirin and 300 mg clopidogrel, then 100 mg aspirin and 75 mg clopidogrel per day. Serum high sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor - α (TNF- α ) were measured in all patients at baseline prior to any drug treatment after admission, and at 7 and 30 days after beginning drug treatment. Thirty healthy volunteers on no medications were enrolled as controls (group C). Results Baseline levels of hs-CRP and TNF- α in group A and group B were significantly higher than those in group C. Seven days after administration, the levels of hs-CRP in both group A and group B decreased significantly [Group A: ( 6.15 ± 1.39) mg/L vs (9.18 ± 1.62) mg/L, P &lt;0.01; Group B:(4.99 ± 1.62) mg/L vs (10.29 ± 1.47) mg/L, P &lt;0.01] . Similarly, levels of TNF- α in both groups decreased at 7 days compared to baseline [Group A: ( 90.99 ± 28.91) pg/ml vs (117.20 ± 37.13) pg/ml, P &lt;0.01; Group B: (74.32 ± 21.83) pg/ml vs (115.27 ± 32.11) pg/ml, P &lt;0.01 ]. Thirty days after administration, the levels of hs-CRP in both group A and group B decreased further to ( 3.49 ± 1.53) mg/L, and (2.40 ± 1.17) mg/L respectively ( P &lt;0.01 for both comparisons) . Levels of TNF- α in groups A and B also decreased significantly between 7 and 30 days, to 63.28 ± 29.01 pg/ml (group A) and (43.95 ± 17.10) pg/ml (group B; P &lt;0.01 for both comparisons) . Significantly lower levels of hs-CRP and TNF- α were observed in group B compared to Group A at thirty days after initiating drug treatment (P &lt;0.05). Conclusions A spirin plus clopidogrel treatment reduced levels of serum hs-CRP and TNF- α in patients with NSTEACS significantly more than aspirin alone. Because both aspirin and clopidogrel produce important anti-inflammatory effects, these results suggest the possibility that long-term treatment with aspirin plus clopidogrel may produce greater clinical benefits compared to treatment with aspirin alone.     

Changes of plasma adrenomedullin and proadrenomedullin N-terminal 20 peptide concentrations in patients with heart failure.

OBJECTIVE: To study the changes in plasma adrenomedullin (ADM) and proadrenomedullin N-terminal 20 peptide (PAMP) concentrations and their clinical significance in the pathological process of congestive heart failure (CHF). METHODS: Plasma ADM and PAMP concentrations in 45 patients with CHF (according to the functional classification of New York Heart Association, NYHA) and 20 control subjects were measured by specific radioimmunoassay. RESULTS: Plasma ADM concentrations were 51.464+/-.52 pg/ml and 70.39+/-3.22 pg/ml respectively in patients of NYHA class II and class III, which were significantly higher than those in control subjects (24.12+/-1.59 pg/ml, P<0.05 for both comparisons), while significant differences in plasma PAMP concentrations were not identified in the 2 groups of patients (6.24+/-1.71 pg/ml and 7.38+/-1.28 pg/ml, respectively) in comparison with the control level(8.56+/-2.44 pg/ml, P>0.05 for both comparisons). Patients of NYHA class IV, when compared with the 2 groups of patients mentioned above, had significantly decreased plasma ADM and PAMP concentrations (36.33+/-2.17 pg/ml and 2.79+/-0.89 pg/ml respectively, P<0.05 in both cases), but had higher plasma ADM and lower PAMP concentrations when compared with the control subjects, (P<0.05 respectively). CONCLUSION: The changes of plasma ADM and PAMP concentrations at different stages of CHF indicate intramolecular regulation disturbances of vasodilator peptides of proadrenomedullin, and ADM may play a more important role in the development of CHF.     

冠心病患者血浆中新型气体信号分子硫化氢的变化

OBJECTIVE: To investigate the changes of plasma hydrogen sulfide (H(2)S) in patients with coronary heart disease (CHD). METHODS: Plasma H(2)S levels were measured in 40 patients with CHD and 17 angiographically normal patients by sulfide-sensitive electrodes, and the variation of plasma H(2)S levels was analyzed in different clinical types of CHD and in different types of coronary artery lesions. The association of plasma H(2)S levels with the risk factors of CHD was also analyzed. RESULTS: Plasma H(2)S levels were significantly lowered in CHD patients in comparison with that in angiographically normal control subjects (26.10+/-14.27 micromol/L vs 51.74+/-11.94 micromol/L, P<0.001). In CHD patients, plasma H(2)S levels in unstable angina patients (UAP, 23.60+/-14.41 micromol/L) and acute myocardial infarction patients (AMI, 19.98+/-7.516 micromol/L) were significantly lower than that in stable angina patients (SAP, 38.41+/-14.53 micromol/L, P<0.05). No significant difference in plasma H(2)S levels was found between CHD patients with double-vessel and multi-vessel lesions (16.91+/-7.98 vs 18.39+/-7.78 micromol/L, P>0.05), but the two groups of patients had significantly lower plasma H(2)S levels than patients with single-vessel involvement (33.04+/-15.01 micromol/L, P<0.05 and P<0.01, respectively). Plasma H(2)S level was significantly lower in CHD patients with coronary artery occlusion than in patients with simple stenosis (19.04+/-9.55 vs 28.24+/-14.85 micromol/L, P<0.05). Among the CHD patients, H(2)S levels were significantly lower in smokers than in non-smokers (27.54+/-10.37 vs 32.24+/-15.77 micromol/L, P<0.05), also lower in hypertensive patients than in normotensive patients (20.36+/-8.69 vs 33.77+/-15.86 micromol/L, P<0.01). Plasma H(2)S levels showed a significant inverse correlation with blood glucose (r=-0.493 6, P=0.001 6), but there were no significant correlations with sex, age, cholesterol, triglyeride, TC, low-density lipoprotein, high-density lipoprotein, or body mass index. CONCLUSION: Decreased plasma H(2)S levels may correlate with the severity of CHD and changes of the coronary artery, and may implicate the risk factors of CHD such as smoking, hypertension, and high blood glucose.     

脑梗死患者血清IL-6和sICAM-1变化及临床意义

目的： 分析急性脑梗死患者血清IL-6,sICAM-1变化及临床意义,探讨其在脑缺血炎性病理损伤中的可能作用机制。方法：选择发病3 d以内的符合试验入选标准的脑梗死患者32例,同时收集相匹配的同期体检者30例,分别用放射免疫法和酶联免疫吸附法测定血清IL-6和sICAM-1浓度。其中11例发病24 h内入院的患者进行血清IL-6和sICAM-1水平动态观察(发病第1 d,第3 d和第6 d)。所有脑梗死患者依据发病后48~72 h的CT检查结果计算脑梗死体积。结果： 发病3 d内［测定时间距发病时间平均为 (47.4±5.6) h］ 脑梗死患者血清IL-6浓度和sICAM-1浓度均显著高于正常对照组［(352.1±31.7) pg/ml vs. (135.4±18.3) pg/ml 和 (363.6±48.4) ng/ml vs. (227.2±30.1) ng/ml, P<0.01］。IL-6和 sICAM-1浓度随发病后时间的推移而逐渐下降;IL-6浓度在发病第1 d ［(364.5±29.7) pg/ml］ 与第3 d［［(345.7±28.9) pg/ml］ 比较无统计学意义(P>0.05),发病第6 d［(308.3±26.8) pg/ml］较第3 d明显降低 ( P<0.01);sICAM-1浓度在发病第1 d［(383.9±56.1) ng/ml］, 第3 d［(354.6±40.8) ng/ml］和第6 d ［(316.7±32.3) ng/ml］ 三个时间点两两比较差异显著(P<0.05);IL-6和sICAM-1浓度至第6 d时仍高于对照组 (P<0.01)。发病3 d内血清IL-6及sICAM-1水平均和脑梗死体积呈正相关 (r=0.368, P<0.05和 r=0.594,P<0.01),血清 IL-6浓度和sICAM-1浓度呈正相关 (r=0.453,P<0.05)。结论：急性脑梗死患者血清IL-6和sICAM-1水平升高,二者可能参与了脑缺血炎性病理损伤,sICAM-1的升高可能与IL-6升高有关,二者血清水平值可能能够反映脑缺血后炎性病理损伤的程度和脑梗死体积大小。     

Relation of pale tongue, purple tongue and TXA2-PGI2 regulation system

This paper analysed the relationship between pale tongue, purplish tongue and TXB2, 6-keto-PGF1 alpha levels in plasma of 70 cases with coronary heart disease (CHD) and 45 normal subjects. The results showed the following characteristics: The pale tongue group (217.76 +/- 30.5 pg/ml) showed no significant difference in TXB2 level compared with the normal group (164.49 +/- 10.85 pg/ml, P greater than 0.05), while both showed significant difference compared with the purplish tongue group (360.1 +/- 31.3 pg/ml) and that with purple spots (485.07 +/- 106.1 pg/ml, P less than 0.01). The pale tongue group (179.29 +/- 9.08 pg/ml) showed a significant difference in 6-keto-PGF1 alpha level compared with the normal group (244 +/- 19.31 pg/ml, P less than 0.01), but it showed no significant difference compared with the purplish tongue group (185.08 +/- 17.07 pg/ml) and that with purple spots (229.3 +/- 33.2 pg/ml, P greater than 0.05). The comparison between the groups of purplish tongue and that with purple spots and the normal group showed no significant difference (P greater than 0.05). The pale tongue group (1.33 +/- 0.18) showed a marked difference in TXB2/6-keto-PGF1 alpha ratio compared with the normal group (0.72 +/- 0.04, P less than 0.01), the purplish tongue group (2.12 +/- 0.22, P less than 0.01) and that with purple spots (2.25 +/- 0.55, P less than 0.05). The purplish tongue group and that with purple spots showed significant difference compared with the normal group (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

DYNAMIC CHANGES OF SERUM VASCULAR ENDOTHELIAL GROWTH FACTOR LEVELS IN A RAT MYOCARDIAL INFARCTION MODEL

ＩＮＴＲＯＤＵＣＴＩＯＮ　　Ｖａｓｃｕｌａｒｅｎｄｏｔｈｅｌｉａｌｇｒｏｗｔｈｆａｃｔｏｒ(ＶＥＧＦ) ,ａｈｏｍｏｄ ｉｍｅｒｉｃ 34 ｔｏ 46 ｋＤａｈｅｐａｒｉｎ ｂｉｎｄｉｎｇｇｌｙｃｏｐｒｏｔｅｉｎ ,ｉｓａｐｏ ｔｅｎｔｓｔｉｍｕｌａｔｏｒｏｆｅｎｄｏｔｈｅｌｉａｌｃｅｌｌｒｅｐｌｉｃａｔｉｏｎａｎｄｉｓｒｅｇａｒｄｅｄａｓｏｎｅｏｆｔｈｅｍｏｓｔｓｐｅｃｉｆｉｃｏｆｔｈｅｋｎｏｗｎａｎｇｉｏｇｅｎｉｃｍｅｄｉａｔｏｒｓｂｅｃａｕｓｅｔｈｅｌｏｃａｌｉｚａｔｉｏｎｏｆｉｔｓｒｅｃｅｐｔｏｒｓｉ…     

经皮冠状动脉腔内成形及支架术对冠心病患者QT离散度的影响

目的 :探讨经皮冠状动脉腔内成形及支架术 (PTCA +Stent)对冠心病患者QT间期离散度 (QTd)的影响。方法 :对 42例成功进行PTCA +Stent的冠心病患者 ,进行术前、后 12导联同步心电图QTd及校正后QTd(QTcd)测定。结果 :术后QTd及QTcd均明显减少 (P <0 .0 1) ,单支病变与多支病变术前QTd及QTcd无明显差别 (P >0 .0 5 ) ,术后单支病变QTd及QTcd的降低程度显著大于多支病变 (P <0 .0 1)。 9例伴室性心律失常者术后该症状消失。结论 :冠心病患者QTd及QTcd在PTCA +Stent术后随着心肌缺血及心室复极不均一性的改善而降低 ,其降低程度可能与侧支循环建立开放有关。     

The role of serum leptin and tumor necrosis factor-α in malnutrition of male chronic obstructive pulmonary disease patients

Background Leptin is a protein mainly secreted by adipocytes, and the major function of leptin was its role in body weight regulation. It is suggested that increased levels of circulating leptin may contribute to anorexia in pathologic conditions including chronic obstructive pulmonary disease (COPD). Recent studies have provided evidence for a link between leptin and proinflammatory cytokines such as tumor necrosis factor-α (TNF-α). This study aimed to explore the role of serum leptin in the malnutrition of COPD patients, and to observe the changes of serum leptin levels during acute exacerbation, also to investigate relationship between leptin and TNF-α. Methods Seventy-two COPD patients and 34 control subjects participated in this study. Seventy-two COPD patients were divided into 3 groups: group COPD IA (patients without malnutrition during acute exacerbation, n=25), group COPD IB (patients without malnutrition during stable disease, n=29), group COPD II (patients with malnutrition during stable disease, n=18). To eliminate the effect of sex differences, all patients and controls were male. Body mass index (BMI), percent ideal body weight (IBW％), triceps skin-fold thickness (TSF), mid-upper arm circumference (MAC), mid-upper arm muscle circumference (MAMC), serum leptin and TNF-α levels, serum prealbumin (PA), serum transferrin (TF), serum albumin (Alb), total lymphocytes count (TLC), forced expiratory volume in one second (FEV(1)), maximal inspiration pressure (MIP) and maximal expiration pressure (MEP) were measured in all participants. Leptin levels were measured by radioimmunoassay. TNF-α levels were measured by ELISA. The between group difference and correlation of these parameters were analyzed. Results Serum leptin levels were significantly lower in group COPD II [(4.07±3.42) ng/ml] than in group COPD IB [(9.72±6.67) ng/ml] and controls [(8.21±5.41) ng/ml] (P&lt;0.05). There was no statistically significant difference in serum leptin levels between group COPD IA [(10.82±6.40) ng/ml], group COPD IB [(9.72±6.67) ng/ml] and controls [(8.21±5.41) ng/ml]. There was no statistically significant difference in serum TNF-α levels between group COPD II [(8.03±3.37) pg/ml], group COPD IA [(8.90±1.60) pg/ml], and group COPD IB [(7.25±2.08) pg/ml]. There was no significant correlation between leptin and TNF-α in any group. Conclusions Leptin was not involved in anorexia and weight loss of COPD patients. There was no statistically significant difference in serum leptin levels between COPD patients during stable stage and acute exacerbation, and there was no significant correlation between TNF-α and leptin during the regulation of the energy balance in COPD patients.     

高迁移率族蛋白1诱导内皮细胞释放细胞因子的作用及其与脂多糖对白细胞介素6释放的协同效应

目的观察高迁移率族蛋白1(HMGB1)对人脐静脉内皮细胞(HUVEC)释放细胞因子的影响及其对脂多糖(LPS)诱导细胞因子白细胞介素6(IL-6)表达的作用。方法用LiquiChip液相蛋白芯片系统检测重组HMGB1蛋白(15ng/ml)诱导HUVEC11种细胞因子/趋化因子的水平变化;检测不同浓度HMGB1(0~75ng/ml)刺激后不同时间点(0、1、3、6、12和24h)HUVEC分泌IL-6的水平以及HMGB1(15ng/ml)与LPS(10ng/ml)共同刺激对HUVEC分泌IL-6的影响。结果HMGB1刺激后HUVEC分泌粒细胞-巨噬细胞集落刺激因子(GM-CSF)、干扰素γ(IFN-γ)、IL-6、IL-8和单核细胞趋化蛋白1(MCP-1)的水平明显升高(均P<0.01),分别是对照(未加刺激)的5.7、4.2、27.8、12.8和5.4倍;HMGB1蛋白以时间和剂量依赖方式诱导IL-6的分泌,在刺激后3~6h,IL-6水平开始增加,在6h时IL-6由对照的32pg/ml±21pg/ml增加到75pg/ml±22pg/ml(P<0.01),12h(453pg/ml±78pg/ml)~24h(901pg/ml±184pg/ml)持续升高(P<0.01);随着HMGB1浓度的增加,IL-6的水平也明显增加,当HMGB1浓度为3、15、75ng/ml时,IL-6分别是155pg/ml±33pg/ml、901pg/ml±184pg/ml、1508pg/ml±378pg/ml,与基础值32pg/ml±21pg/ml相比,差异有统计学意义(P<0.01)。分别用LPS(10ng/ml)和HMGB1(15ng/ml)单独刺激HUVEC时,IL-6的含量从基础的32pg/ml±22pg/ml分别增加至289pg/ml±42pg/ml和901pg/ml±184pg/ml(均P<0.01);如果用二者共同刺激HUVEC,IL-6的生成量大大增加(2361pg/ml±299pg/ml),二者存在协同作用(F=69.405,P<0.01)。结论HMGB1蛋白可诱导HUVEC释放多种炎性细胞因子;HMGB1诱导IL-6的上调具有时效性和量效性关系,并可协同LPS刺激HUVEC释放IL-6,在脓毒症的发生和发展中起重要作用。     

针对Toll样受体4基因的小发夹结构RNA对RAW264.7细胞炎症因子分泌的抑制作用

目的构建针对Toll样受体(TLR)4 mRNA的小发夹结构RNA(shRNA)真核表达载体pEGFP-siRNA/TLR4,检测该shRNA诱导的RNA干扰(RNAi)对脂多糖刺激RAW264.7细胞分泌炎症因子的抑制作用,以探讨针对TLR4基因的RNAi对RAW264.7细胞炎症反应的抑制作用.方法构建携带增强型绿色荧光蛋白(EGFP)及shRNA克隆位点的质粒pEGFP-H1/siRNA,运用网络工具siRNA Wizard(http//www.simawizard.com/)设计针对TLR4 mRNA的寡核苷酸片段.将其克隆入pEGFP-H1/siRNA,构建表达EGFP及TLR4-shRNA的真核表达质粒pEGFP-H1/TLR4-siRNA.运用脂质体转染技术将pEGFP-H1/TLR4-siRNA转染至培养的小鼠巨噬细胞系RAW264.7,观察细胞系中荧光蛋白的表达强度;再运用脂多糖刺激转染的RAW264.7细胞,运用ELISA方法检测该细胞系分泌炎症因子水平的变化.结果质粒pEGFP-H1/siRNA及pEGFP-H1/TLR4-siRNA分别用Bbs Ⅰ和MluⅠ酶切电泳后,前者出现4.9 kb和340 bp的的条带,后者出现5.0 kb和220 bp的条带,与实验设计的质粒长度一致,且测序证实克隆序列正确.将pEGFP-H1/TLR4-siRNA转染至RAW264.7细胞后,EGFP的表达率为50%±8%.用脂多糖刺激后,TLR4-SiRNA转染组细胞培养液TNF-α水平(2 h825 pg/ml±136 pg/ml;8 h2190 pg/ml±359 pg/ml)明显低于对照siRNA转染组(2 h1179 pg/ml±240 pg/ml;8 h4720 pg/ml±227 pg/ml,均P＜0.01).结论针对TLR4 mRNA的shRNA可能通过RNAi机制对脂多糖诱导的RAW264.7细胞炎症因子的分泌有明显的抑制作用.     

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OBJECTIVE: To assess the effects of intracoronary diltiazem on no-reflow phenomenon of infarct-related artery (IRA) after emergent percutaneous transluminal coronary angioplasty or/and intracoronary stenting (PTCA/Stenting) in the patients with acute myocardial infarction (AMI). METHODS: We studied 34 AMI patients with no-reflow phenomenon of IRA after emergent PTCA/Stenting between January 1999 and August 2005. Urokinase-treated group (n=16) was given intracoronary urokinase 30,0000 - 50,0000 units within 15 - 30 minutes between January 1999 and April 2002 while diltiazem-treated group (n=18) was given intracoronary diltiazem 0.5 - 2 mg within 10 - 30 minutes between May 2002 and August 2005. Fifteen minutes later, coronary arteriography (CAG) was performed and the thrombolysis in myocardial infarction (TIMI) flow grade was measured. RESULTS: No apparent change of TIMI flow grade was found between pre-administration and post-administration of intracoronary urokinase, but TIMI flow grade was significantly improved after intracoronary diltiazem (P<0.01). TIMI flow grade of diltiazem-treated group was significantly higher than that of urokinase-treated group after the administration (P<0.05). The percentage of the patients who reached TIMI flow grade 3 after the intracoronary administration was higher in the diltiazem-treated group than that in the urokinase-treated group (P<0.01). CONCLUSION: The intracoronary administration of diltiazem 0.5~2mg can effectively improve the no-reflow phenomenon after emergent PTCA/Stenting in patients with AMI.     

磷酸肌酸钠对急性冠状动脉综合征患者经皮冠状动脉介入术后心肌的保护作用

目的近年来,经皮冠状动脉介入术(percutaneous coronary intervention,PCI)广泛应用于临床,如何有效减轻心肌再灌注损伤是一项需要解决的问题。文中旨在观察磷酸肌酸钠(creatine phosphate,CrP)对急性冠状动脉综合征(acute cor-onary syndrome,ACS)患者PCI术后的心肌保护作用。方法 180例ACS患者成功行PCI术后随机分为治疗组90例[男53例、女37例,平均年龄(63.6±12.4)岁]和对照组90例[男56例、女34例,平均年龄(65.3±12.6)岁]。对照组于PCI术前、术后只给予ACS常规药物治疗,治疗组在常规药物治疗基础上于PCI术后静脉应用CrP治疗5 d。监测所有患者术前及术后血清中磷酸肌酸激酶同工酶(creatine kinase isoenzyme,CK-MB)、乳酸脱氢酶(lactate dehydrogenase,LDH)、肌钙蛋白T(troporin T,cTnT)、超氧化物歧化酶(superoxide dismutase,SOD)、丙二醛(malondialdenyde,MDA)及一氧化氮(nitric oxide,NO)含量变化。结果治疗组术后血清中SOD含量明显高于对照组[41.2(10.3～168.2)pg/ml vs 32.4(10.5～96.8)pg/ml,P<0.01)];而血清MDA、LDH、CK-MB含量均明显低于对照组[3.22(1.00～7.84)pg/ml vs 3.67(0.58～9.82)pg/ml;156.2(84.0～703.5)U/L vs 176.5(94.0～983.7)U/L;11.0(5.0～104.0)U/L vs 14.5(5.0～196.5)U/L,P<0.01)];2组术后血清中cTnT及NO含量变化无明显差异[1.25(0.01～8.5)ng/ml vs 1.37(0.01～9.2)ng/ml;165.5(22.5～437.7)μmol/L vs159.6(20.3～414.4)μmol/L,P>0.05)]。结论 CrP对ACS患者PCI术后心肌具有一定保护作用。