冠状动脉病变程度对左心室舒张末压的影响

目的 :探讨冠状动脉病变不同严重程度对左心室舒张末压的影响。　方法 :连续性冠状动脉造影 6 83例 ,分别按冠状动脉病变支数、狭窄程度和狭窄总积分分组 ,测定左心室造影前及造影后左心室舒张末压 (LVEDP)。结果 :与各自正常对照组比较 ,冠状动脉病变为单支病变、2 5 %～ 5 0 %狭窄或狭窄总积分 1～ 3分时LVEDP略有下降 ;双支病变、5 0 %～ 99%狭窄或狭窄总积分 4～ 9分时LVEDP稍有升高 ,超过 15mmHg ,但均无统计学意义 ;三支病变、10 0 %完全闭塞、狭窄总积分≥ 10分时LVEDP有显著意义升高 (P 0 .0 1或P 0 .0 5 )。造影后LVEDP与造影前比较 ,各组均有显著升高 (P 0 .0 1) ,但LVEDP上升幅度组间比较均无统计学意义。　结论 :在冠状动脉病变严重时 ,出现心室顺应性下降和LVEDP升高     

老年前期冠心病患者左心室舒张功能障碍诊断方法的评价及其相关关系

目的　探讨临床心功能NYHA诊断、有创与无创检查方法对老年前期冠心病患者左心室舒张功能障碍的诊断价值及其相关关系。方法　对 5 0例老年前期冠心病患者进行多普勒超声心动图、核素心室造影及X线心室造影检查 ,比较年龄、超声E/A、EF斜率及核素左室高峰充盈率 (PFR)和X线心室造影左心室舒张末压(LVEDP) ,并进行相关分析。结果　心功能Ⅱ ,Ⅲ级组的年龄大于Ⅰ级组 (P <0 0 5 ) ;心功能Ⅰ ,Ⅱ ,Ⅲ级组的LVEDP值组间各自比较均有差异 (P <0 0 1) ;而心功能Ⅲ级组超声的E/A、EF斜率及核素PFR均低于心功能Ⅰ级组 (P <0 0 1) ,心功能Ⅱ级组的EF斜率及核素PFR也低于心功能Ⅰ级组 (P <0 0 1)。心功能分级与超声E/A、EF斜率、核素PFR、LVEDP及年龄的相关系数 (r)分别为 - 0 4 0 3,- 0 5 72 ,- 0 5 6 6 ,0 773和 0 5 6 3;年龄与E/A、EF斜率及LVEDP的r分别为 - 0 36 6 ,- 0 4 73和 0 4 77;LVEDP与E/A、EF斜率、PFR的r分别为 - 0 2 88,- 0 5 2 2和- 0 380 ;PFR与E/A、EF斜率的r分别为 0 4 4 0和 0 5 2 6 (以上P值均 <0 0 5或 <0 .0 1)。结论　对于老年前期冠心病患者 ,临床心功能分级、超声、核素及X线造影之间的舒张功能指标具有一定的相关性 ,超声及核素对左心室舒张功能障碍的诊断价值较大     

RNA干扰血管紧张素Ⅱ1a型受体对肾血管性高血压大鼠血压及心肌肥厚的影响

目的用RNA干扰技术下调血管紧张素Ⅱ1a型受体(AT1a)表达,观察其对肾血管性高血压及其心肌肥厚重构的影响。方法构建两肾一夹(two-kidney,one-clip:2K1C)高血压大鼠模型,用携带U6启动子和AT1a特异短发夹RNA(shRNA)编码序列的质粒pAT1a-shRNA1,pAT1a-shRNA2单次尾静脉注射给药,以含非特异性shRNA编码序列的无关质粒pGenesil-Con(pCon)、选择性AT1受体拮抗剂缬沙坦每日灌胃给药干预3周,无干预为对照,检测尾动脉压变化和颈动脉压水平、左心室重量与体重之比(LV/BW),并用Western-blot分析组织AT1受体表达情况。结果尾动脉压(与干预前比较):Blank组及pCon组继续升高25mmHg左右,pAT1a-shRNA1、pAT1a-shRNA2组下降15~16mmHg,缬沙坦组下降约30mmHg;颈动脉压和左室/体重之比:pAT1a-shRNA1(194mmHg±5mmHg;2·27±0·37)、pAT1a-shRNA2(200mmHg±5mmHg;2·31±0·26)、缬沙坦组(164mmHg±5mmHg;2·26±0·39)显著低于对照组(234mmHg±10mmHg;3·24±0·38)及pCon组(232mmHg±7mmHg;2·94±0·06);与对照组相比,pAT1a-shRNA1、pAT1a-shRNA2组左心室(分别下降53·3%和47·8%)和主动脉(分别下降58·7%和49·3%)组织内AT1受体表达显著减少。结论RNA干扰AT1a受体有效地抑制了肾血管性高血压进展及其心肌肥厚重构。RNA干扰技术可能成为高血压病基因治疗的一种新策略。     

不同剂量卡维地洛防治大鼠急性心肌梗死左室重构的研究

目的对比观察不同剂量卡维地洛对大鼠急性心肌梗死(AMI)左室重构(LVRM)的防治作用。方法雌性SD大鼠AMI术后成活142只,分为AMI对照组(n=35),和卡维地洛大剂量(10mg·kg-1·d-1,n=37),中剂量(1mg·kg-1·d-1,n=35),及小剂量(0.1mg·kg-1·d-1,n=35)四组。另设假手术组对照。直接灌胃给药4周后行血流动力学测定、心脏标本固定及病理分析。去除梗死面积＜35％或＞55％者,最终58只大鼠资料完整。结果AMI各组间梗死面积均无显著差异(44.5％～46.3％,P均＞0.05)。与假手术组相比,AMI组的左室舒张末压(LVEDP)、容积(LVV)、实际左心室重量(LVAW)及相对重量(LVRW)均显著增加(P均＜0.01),左室球形指数和左室内压最大上升和下降速率(±dp/dt)及其校正值(±dp/dt/LVSP)均显著降低(P均＜0.01)。与AMI组相比,卡维地洛大、中、小剂量组的LVEDP、LVV、LVAW和LVRW均呈剂量相关性显著降低(LVEDP7.7mmHg±1.9mmHg,12.1mmHg±2.0mmHg,14.5mmHg±4.6mmHg对24.5mmHg±5.3mmHg;LVV0.72ml±0.10ml,0.79ml±0.08ml,0.82ml±0.10ml对0.92ml±0.11ml;LVAW589mg±57mg,622mg±70mg,666mg±57mg对730mg±79mg;P＜0.05～0.001),±dp/dt及±dp/dt/LVSP均显著增加(P＜0.05～0.01),但各剂量组间均无显著差异,左室球形指数仅在大剂量组显著改善(P＜0.05)。结论卡维地洛大、中、小剂量均能有效地防止大鼠AMI左室重构,改善血流动力学和左室功能;小剂量有效,大剂量更好。     

精神因素对肠易激综合征患者内脏敏感性的影响

目的　探讨肠易激综合征 (IBS)患者选择性关注的特征及心理暗示对患者内脏敏感性的影响。方法　将改编后的抑郁症病人选择性关注调查卡用于IBS(符合罗马Ⅱ诊断标准 )患者选择性关注特征调查 ,随后观察IBS患者在不同暗示刺激下直肠气囊扩张的各种阈值与正常对照者的差异。结果　 36例IBS患者在看过调查卡片内容 30min后 ,回忆起的胃肠疾病相关的术语超过 50 % ,而对照组不超过 30 % (P <0 0 0 1 )。IBS患者直肠气囊扩张诱发的初始感觉 (2 1mmHg± 5mmHg)、排便感 (36mmHg± 9mmHg)、排便紧迫感 (51mmHg± 1 4mmHg)及最大耐受的阈值 (67mmHg± 1 7mmHg)均低于 2 6例健康对照组 (P <0 0 0 1 )。诱导IBS患者转移对胃肠刺激的注意力所需时间 (1 0min±4min)长于健康对照组 (2 8min± 1 2min) (P <0 0 0 1 ) ,转移注意力后两组受试者内脏敏感性阈值均比相应基线值增加 (P <0 0 5) ,但IBS患者初始感觉值增加更显著 (P <0 0 1 )。恶性视听暗示刺激能降低IBS患者组的各项内脏敏感性观察指标 (P <0 0 5) ,对健康对照组影响不显著。结论　对胃肠道症状及其刺激的选择性关注是IBS患者认知 行为的重要特征 ,转移注意力可明显减低患者对胃肠道刺激的反应。研究结果说明采用心理方法治疗IBS的合理性     

血小板活性因子及其拮抗剂对大鼠肝硬化门脉高压的影响

目的探讨肝硬化时肝脏和血循环中血小板活性因子(PAF)的变化以及其对门脉高压的影响。方法CCl4腹腔注射8周(0·15ml/kg,2次/周)诱导大鼠肝硬化,快速3H-PAF液闪检测肝及循环中PAF水平;受体饱和结合实验分析肝组织PAF结合能力;监测外源性PAF及其拮抗剂BN52021对门脉压和系统动脉压的影响。结果与对照组相比,肝硬化时肝内PAF、肝脏输出PAF及肝内生PAF水平明显升高,分别4·0ng/g±0·4ng/gvs2·7ng/g±0·5ng/g(P<0·01)、6·3ng/ml±0·6ng/mlvs3·4ng/ml±0·6ng/ml(P<0·01)、1·0ng/ml±0·6ng/mlvs-0·3ng/ml±0·5ng/ml(P<0·01);肝组织PAF结合能力Bmax明显升高(2·8±0·21)fmol/μg膜蛋白vs(0·9±0·06)fmol/μg膜蛋白,P<0·01,而受体亲和力Kd差异无统计学意义(8·0nmol/L±1·3nmol/Lvs5·8nmol/L±1·0nmol/L,P>0·05)。肝硬化组基础门脉压升高(12·2mmHg±0·7mmHgvs5·3mmHg±0·6mmHg,P<0·01),系统动脉压降低(82mmHg±10mmHgvs114mmHg±9mmHg,P<0·01)。门脉注入PAF(1μg/kg)后,肝硬化组门脉压提高了32%(12·1mmHg±0·6mmHgvs16·0mmHg±0·7mmHg,P<0·01),升高幅度约为对照组的227%(4·1mmHg±1·0mmHgvs1·8mmHg±0·3mmHg,P<0·01),而系统动脉压在两组均下降(肝硬化组由82mmHg±10mmHg降至48mmHg±4mmHg,P<0·01;对照组由114mmHg±9mmHg降至52mmHg±4mmHg,P<0·01)。门脉注入BN52021(5mg/kg),肝硬化组门脉压降低了16%(14·6mmHg±1·6mmHgvs12·3mmHg±0·8mmHg,P<0·05),而系统动脉压在肝硬化组和对照组均无明显变化(P>0·05)。结论肝硬化时肝脏合成PAF明显增加是循环血PAF升高的重要来源,并上调节肝的血流动力学影响门脉高压形成,其作用可被其拮抗剂BN52021部分逆转。     

肾上腺素预处理对大鼠离体心脏缺血再灌注的保护作用

目的　研究肾上腺素预处理对大鼠离体心脏缺血再灌注损伤的保护作用 ,并探索其与剂量的关系。方法　大鼠随机分为 3组 ,每组 8只。A组 :即对照组 ,予静脉输注生理盐水 1ml/kg ,持续 3min ;B组 :静脉输注较低剂量肾上腺素 2 μg/kg ,持续 3min ;C组 :静脉输注较高剂量肾上腺素 2 0 μg/kg ,持续 3min。大鼠心脏稳定后 ,结扎冠状动脉左前降支 ,在Langendorff灌流模型下缺血 40min、再灌注 90min。 结果　B组缺血后心脏功能恢复良好 ,左心室压差为 ( 82 .96± 5 .60 )mmHg ,左室舒张末压为 ( 4.95± 0 .96)mmHg ,A组心脏功能恢复较差 ,左心室压差为 ( 70 .16± 5 .0 7)mmHg ,左室舒张末压为 ( 6.60± 1.0 4)mmHg ,B组较A组明显增高 (P <0 .0 5 ) ;B组灌注流出液中肌酸激酶值较低 ,B组梗死面积为 ( 2 8.70± 3 .41) % ,较A组的 ( 3 7.90± 6.2 9) %明显下降 (P <0 .0 5 )。结论　低剂量肾上腺素预处理在心肌缺血再灌注损伤中具有心肌保护作用     

普伐他汀降脂治疗对冠心病血管内皮舒张功能的影响

目的 :研究普伐他汀对冠心病高胆固醇血症患者血管内皮依赖性舒张功能的影响。方法 :采用高分辨超声技术 ,对 70例冠心病高胆固醇血症患者普伐他汀降脂前后和 70例正常对照者的血管内皮依赖性舒张功能进行检测。结果 :高胆固醇血症组肱动脉血流介导性舒张较正常对照组明显减弱 ((3.5± 2 .8) %和 (14 .5± 3.4 ) % ,P<0 .0 0 1) ,而 2组对硝酸甘油的反应差异无统计学意义 ((2 0 .5± 7.2 ) %和 (2 2 .9± 4 .3) % ,P >0 .0 5 )。 70例冠心病高胆固醇血症患者服用普伐他汀 10mg治疗 (3.8± 0 .8)个月后 ,血浆总胆固醇从 (6 .31± 0 .70 )mmol/L降至 (5 .0 6±0 .6 3)mmol/L ,同时肱动脉内皮依赖性舒张较治疗前明显改善 ((10 .0± 3.2 ) %和 (3.5± 2 .8) % ,P <0 .0 0 1) ,而治疗前后肱动脉对硝酸甘油的反应无明显改变。结论 :冠心病高胆固醇血症患者存在血管内皮依赖性舒张功能障碍 ;经普伐他汀降胆固醇治疗后 ,受损的血管内皮依赖性舒张功能得到明显改善     

vWF基因19内含子MspI多态性、循环水平与中国人冠心病关系的研究

目的　探讨vWF基因 19内含子MspⅠ多态性在中国人冠心病发病中的作用。 方法　收集冠心病患者 (冠心病组 ) 10 9例和中国汉族健康人 (正常对照组 ) 10 4名的资料 ,冠心病组进一步分为心肌梗死和心绞痛亚组。采用PCR技术结合MspⅠ酶切分析等测定vWF基因 19内含子MspⅠ限制性片段长度多态性 ;同时采用ELISA法测定循环vWF水平。结果　①正常对照组中M+/M+、M+/M-和M-/M-基因型频率分别为0 .0 2 0、0 .490和 0 .490 ;心肌梗死、心绞痛亚组的MspⅠ多态性基因型分布与正常对照组相比 ,差异有显著性 (P<0 .0 5 ) ,其M-/M-型频率分别为 0 .64 9和 0 .712 ,均显著高于正常对照组 (P值均 <0 .0 5 ) ;②冠心病心功能Ⅰ～Ⅱ级及Ⅲ～Ⅳ级患者的M-/M-基因型频率分别为 0 .667和 0 .70 6,低射血分数 (EF)和正常EF分别为 0 .744和 0 .5 89,差异均无显著性 (P >0 .0 5 ) ;③经冠状动脉造影确诊的冠心病患者M-/M-基因型频率在单支、双支和多支病变分别为 0 .778、0 .667和 0 .5 84;④冠心病组、心肌梗死、心绞痛亚组和正常对照组循环vWF水平分别为 ( 185 .0 7± 80 .5 7) %、( 2 11.2 2± 85 .85 ) %、( 15 6.3 2± 63 .60 ) %和 ( 117.0 1± 5 5 .5 2 ) % ,各疾病组与正常对照组相比 ,差异均有显著性 (P <0 .0 5 ) ;冠心     

非控制性出血性休克低压复苏治疗效果的研究

目的　应用大鼠脾损伤非控制性出血性休克模型探讨低压及低压扩容复苏治疗非控制性出血性休克的可行性。方法　雄性Wistar大鼠 5 0只 ,在大鼠脾损伤模型复制成功后随机等分为 5组 ,组 1 :假手术组 ;组 2 :休克未处理组 ;组 3:常压复苏组 (急救期控制MAP在 80mmHg以上 ) ;组 4 :低压复苏组 (急救期控制MAP在 6 0mmHg±5mmHg) ;组 5 :低压扩容复苏组 (急救期输入硝普钠 5 μg·kg- 1 ·min- 1 ,同时输液控制MAP在 6 0mmHg± 5mmHg)。结果　 1～ 5组平均存活时间 (min)分别为 1 80、73.5 0± 8.0 4、1 1 4 .30± 31 .33、1 4 6 .70± 2 8.0 7和 1 71 .6 0± 1 5 .74 ,除组1、组 5外 (P =0 .0 6 71 ) ,其余各组间比较均有统计学意义 (P <0 .0 5 ) ;2～ 5组的急救期出血量 (ml·kg- 1 )分别为 :3.79± 1 .39、1 7.4 1± 8.88、8.6 7± 4 .5 9、1 0 .33± 4 .31 ,其中组 3出血量明显高于其他各组 (P <0 .0 1 ) ;组 4、组 5与组 2比较出血量明显增多 (P <0 .0 5 )。结论　在非控制性出血性休克治疗中 ,低压及低压复合适量硝普钠扩容复苏方法可改善组织代谢 ,提高生存时间 ,是更为理想的复苏方法     

卡维地洛与倍他乐克防治大鼠AMI左室重构作用的比较

目的对比卡维地洛及倍他乐克对大鼠急性心肌梗死(AMI)左室重构(LVRM)的防治作用.方法 105只AMI术后成活的雌性SD大鼠随机分成AMI对照(n=35)、卡维地洛1 mg/(kg@d)(n=35)和倍他乐克2 mg/(kg@d)(n=35)三组.另设假手术组.给药4周后行血流动力学测定和病理分析.去除死亡及梗死面积＜35%或＞55%者,最终46只大鼠资料完整,在以上各组分别为11,12,11和12只.结果与假手术组相比,AMI组的左室舒张末压(LVEDP)、容积(LVV)、重量(LVW)显著增加(P＜0.05～0.111),左室内压最大上升和下降速率(±dp/dt)及其校正值(±dp/dt/LVSP)显著降低(P＜0.01～0.001).与AMI组相比,卡维地洛和倍他乐克组的LVEDP及LVV均显著降低(P均＜0.001),±dp/dt及±dp/dt/LVSP均显著升高(P＜0.05～0.001),而LVW和RVW仅在卡维地洛组显著减轻(P均＜0.05～0.01).结论 1、卡维地洛能有效抑制大鼠AMI左室重构并改善血流动力学和左室功能,2、倍他乐克与卡维地洛的作用相似,但对心室肥厚似无抑制作用.     

COMPARISON OF THE EFFECTS OF LOSARTAN，ENALAPRIL AND THEIR COMBINATION IN THE PREVENTION OF LEFT VENTRICULAR REMODELING AFTER ACUTE MYOCARDIAL INFARCTION IN THE RAT

Objectives. To compare the effects of losartan, enalapril and their combination in the prevention of left ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in the rat.Methods. AMI model was induced in female SD rats by ligating left coronary artery. Forty-eight hours after the procedure, 83 surviving rats were randomized into one of the following 4 groups : 1) AMI control group (n = 19), 2) losartan group (n =22, 3 mg · kg-1 · d-1), 3) enalapril group (n =20, 1mg · kg-1· d-1), 4) losartan - enalapril combinative group (n = 22, 3 and 1mg · kg-1 · d-1 respectively). 5) sham-operated group (n = 10) and 6) normal rats group (n = 10) were selected randomly to serve as non-infarction controls. Losartan and enalapril were delivered by direct gastric gavage. After 4 weeks of medical therapy, hemodynamic studies were performed in each group, then the rat hearts were fixed with 10% formalin and pathologic analysis on them was performed. Complete experimental data was obtained in 56 rats,     

Hemodynamic observation and treatment approach for patients with angina decubitus.

In order to investigate the mechanism and treatment of angina decubitus, 20 patients (18 men and 2 women aged 36-70 years) were studied during hospitalization. All patients were found to have an increased heart rate x systolic blood pressure product before the onset of angina decubitus, indicating that this type of angina pectoris belongs to the category of effort angina. Of the 11 patients investigated by continuous hemodynamic monitoring, 3 had significant progressive increases in pulmonary artery systolic pressure (PASP) and pulmonary artery diastolic pressure (PADP) before onset: their episodes of angina could not be completely controlled by digoxin and diuretics, but quickly subsided after beta blockers were added. Among the other 8 patients, PADP increased slightly in 5 and remained unchanged in 3 cases before onset: these patients had no manifestations of LV dysfunction, and beta blockers combined with coronary vasodilators produced satisfactory effects. These results indicate that LV failure is not a major factor in the pathogenesis of angina decubitus. The LV diastolic dysfunction seen in 8/11 cases may have been related to LV hypertrophy caused by long-term hypertension or chronic persistent ischemia.     

Beneficial effects of early coronary reperfusion on left ventricular remodeling and systolic function in patients with acute myocardial infarction.

OBJECTIVE: To evaluate the beneficial effects of early coronary reperfusion on left ventricular remodeling (LVRM) and systolic function in patients with acute myocardial infarction (AMI). METHODS: Eighty-one patients with first AMI in the convalescent stage and having undergone left ventriculography (LVG) and coronary arteriography (CAG) were divided into four groups: the anterolateral wall (ALW) myocardial infarction (MI) non-reperfusion (n = 20) and reperfusion (n = 21), and inferoposterial wall (IPW) MI non-reperfusion (n = 20) and reperfusion (n = 20), according to infarct location and early treatment with or without successful coronary reperfusion therapy within 6 hours after onset of symptoms. By LVG, the parameters of LVRM and systolic function in the four MI groups were analyzed and compared with those in normal group (n = 25) and between the two reperfusion and non-reperfusion MI groups. RESULTS: In both ALW and IPW MI non-reperfusion groups, the left ventricular (LV) end-diastolic volume (EDV), circumference (EDC), short-axis dimension (EDD), short to long axis ratio (ED-D/L), sphericity index (ED-SI) and end-systolic volume (ESV) were all significantly increased (P < 0.01-0.001), while LV ejection fractions (LVEF) were significantly decreased (both P < 0.001) when compared with those of normal group; and the increase in ESV and decrease in LVEF were both significantly greater in ALW than in IPW MI groups (both P < 0.01). In both ALW and IPW MI reperfusion groups, however, the EDV, EDD, ESV, as well as the extent and severity of regional wall motion abnormality (RW-MA) were significantly smaller (P < 0.05-0.001), while LVEF were significantly higher (P < 0.01-0.001) when compared with those in the two non-reperfusion MI groups respectively. There were no longer significant differences in LVEF and ESV between ALW and IPW MI groups (both P > 0.05). The EDC in IPW MI reperfusion group and the ED-D/L and ED-SI in ALW MI reperfusion group were also significantly reduced compared with those in the two non-reperfusion MI groups respectively (P < 0.05-0.001). All the above parameters in the two reperfusion MI group were decreased to the normal in comparison with normal group except ESV and LVEF, and ED-D/L and ED-SI in IPW MI group. CONCLUSION: It was indicated that in both ALW and IPW MI non-reperfusion groups, LVRM had occurred in convalescent stage of AMI with an increase in EDV and EDC, spherical change in LV shape, and accompanying reduction in LV systolic function; and early coronary reperfusion in AMI could reduce the extent and severity of RWMA, prevent from LV enlargement and remodeling, and preserve or improve LV systolic function with more prominence in ALW MI.     

美托洛尔对老年卧位型心绞痛患者左室舒张功能不全的作用

目的　观察美托洛尔对老年卧位型心绞痛患者左室舒张功能不全的作用。方法　用放射性核素心室显像检查 15例正常人和 9例老年卧位型心绞痛患者。结果　与正常对照组比较 ,老年卧位型心绞痛患者高峰充盈率 (PFR)、1/3充盈率 (1/3FR)、1/3充盈分数 (1/3FF)显著减少 (P <0 .0 1) ,而左室射血分数、1/3射血分数、高峰射血率无明显差异 (P >0 .0 5 )。与治疗前比较 ,老年卧位型心绞痛患者用美托洛尔治疗后PFR、1/3FR、1/3FF显著减少 (P <0 .0 1)。结论　老年卧位型心绞痛患者存在明显的舒张功能不全。美托洛尔能改善老年卧位型心绞痛患者的左室舒张功能不全。     

中药通心络对猪急性心肌梗死再灌注后无再流的影响

目的评价通心络防治猪急性心肌梗死(AMI)再灌注后无再流的作用。方法中华小型猪40只随机分成5组,每组8只:(1)AMI模型对照组(对照组),(2)通心络小剂量治疗组(0·05g·kg-1·d-1),(3)通心络中剂量治疗组(0·2g·kg-1·d-1),(4)通心络大剂量治疗组(0·5g·kg-1·d-1),(5)假手术组。通心络各组预给药3d后行冠状动脉结扎180min,松解60min制备AMI再灌注模型。AMI前、后和再灌注后均行血流动力学测定,心肌声学造影(MCE)检查和病理学分析。结果(1)与AMI前相比,对照组AMI后180min左室收缩压(LVSP)、心排量和左心室内压最大收缩和舒张变化速率(±dp/dtmax)均显著下降(P<0·05或P<0·01),左室舒张末压(LVEDP)显著升高(P<0·01);再灌注后60min仅LVSP显著恢复(P<0·05),然而±dp/dtmax继续显著下降(P<0·05)。小、中和大剂量通心络组AMI后180min各项指标变化与对照组相同;再灌注后60min仅大剂量通心络组LVEDP、±dp/dtmax和心排量均显著恢复(均P<0·05),且显著好于对照组(均P<0·05)。(2)对照组MCE和病理染色所测的冠脉结扎区心肌范围(LA)高度一致(P>0·05),再灌注后无再流区范围分别为78·5%和82·3%,心肌坏死面积占结扎区心肌面积的98·5%。3个通心络组LA与对照组相当(均P>0·05),但MCE和病理染色所测无再流范围在中及大剂量通心络组分别为41·1%、42·4%和24·1%、25·0%,坏死心肌范围分别为90·2%及81·2%,均显著小于对照组和小剂量组(P<0·05或P<0·01),大剂量组也显著小于中剂量组(P<0·05或P<0·01)。(3)对照组再灌注后即刻和再灌注后60min冠脉血流量仅占AMI前的45·8%和50·6%(均P<0·01),而大剂量通心络组冠脉血流量分别占AMI前的76·0%和73·5%,均显著高于对照组(均P<0·01)。结论通心络能有效地防治心肌梗死再灌注后无再流,缩小梗死面积;中剂量有效,大剂量更好。     

地尔硫卓对猪急性心肌梗死再灌注后无再流的影响

目的评价地尔硫卓防治猪急性心肌梗死(AMI)再灌注后无再流的作用。方法实验动物随机分成对照组、地尔硫卓组(2mg/min冠脉内)和假手术组。前两组行冠状动脉结扎3h,松解1h制备AMI再灌注模型。AMI前、后和再灌注后均行血流动力学测定和心肌声学造影(MCE)检查,最终行病理学分析。结果与AMI前相比,对照组AMI后3h、左室收缩压(LVSP)、心排量(CO)和左心室内压最大收缩和舒张变化速率(±dp/dtmax)均显著下降(均P<0.05,P<0.01),左室舒张末压(LVEDP)显著升高(P<0.01);再灌注后1h仅LVSP显著恢复(P<0.05),然而±dp/dtmax继续显著下降(P<0.05);而地尔硫卓组AMI后3h各项指标变化与对照组相同;但再灌注后1h LVEDP、±dp/dtmax和CO均显著恢复(均P<0.05),且比对照组更显著(均P<0.05)。对照组MCE和病理染色所测的冠脉结扎区心肌范围(LA)高度一致(P>0.05),再灌注后无再流范围(ANR)分别为78.5%和82.3%,心肌坏死范围(NA)占LA的98.5%;而地尔硫卓组两方法所测LA均与对照组相当(均P>0.05),但ANR仅分别为20.6%和19.9%,NA又与对照组差异无统计学意义(P>0.05)。对照组再灌注即刻和再灌注后1h冠脉血流量仅占AMI前的45.8%和50.6%(均P<0.01),而地尔硫卓组冠脉血流量分别提高到80.4%和79.3%,比对照组增加均有统计学意义(均P<0.01)。结论     

糖尿病心肌病中转化生长因子β1相关的Smads信号通路的激活及缬沙坦的干预作用

目的探讨糖尿病心肌病（DCM）中转化生长因子β1（TGFβ1）相关的Smads信号通路的激活及缬沙坦的干预作用。方法雄性Wistar大鼠40只,随机分为3组：对照组（8只）,DCM组（16只）,缬沙坦组（16只）,采用高脂高热量饲料喂养加小剂量链脲佐菌素（STZ）注射制作DCM大鼠模型。成模后缬沙坦组给以缬沙坦（30mg／kg）干预治疗,实验末观察大鼠生化指标的变化,血流动力学观察大鼠心功能的变化,应用电子显微镜、Masson染色、实时定量逆转录（RT）-PCR和Western印迹技术,检测各组大鼠左室心肌组织胶原含量,TGFβ1、TGFβⅡR、Smad2、Smad3及Smad7 mRNA和蛋白质表达水平的变化。结果DCM组大鼠心功能明显低于对照组（P〈0．01）,左室心肌组织胶原含量明显高于对照组（17％±3％vs11％±3％,P〈0．01）,存在心肌间质纤维化;同时TGFβ1、TGFβⅡR、Smad2和Smad3mRNA表达水平均高于对照组（0．0054±0．0009vs0．0126±0．0057,0．0523±0．0218vs0．0877±0．0272,0．0413±0．0186vs0．0884±0．0146,0．0064±0．0021vs0．012±0．0048,P〈0．05-0．01）,Smad2／Smad7和Smad3／Smad7的mRNA的比值也明显高于对照组（P〈0．05）,TGFβ1、磷酸化（P）-Smad2和P-Smad3蛋白质表达水平明显高于对照组（103±18vs143±17,107±21vs212±43,89±17vs151±32,P〈0．01）,P-Smad2／Smad7和P-Smad3／Smad7蛋白质的比值也明显升高（P〈0．05）。应用缬沙坦干预治疗后,大鼠心功能明显好转,心肌间质胶原沉积减轻,同时上述分子异常均明显好转,Smad2、Smad3和Smad7之间的失平衡现象较DCM组减轻（均P〈0．05）。结论TGFβ1相关的Smads信号通路的激活及相关分子之间的平衡状态的改变可能是DCM心肌间质纤维化的机制之一,缬沙坦通过抑制这一信号途径,在一定程度上可逆转DCM心肌间质纤维化的发生和发展。     

Hemodynamic assessment of intravenous Isosorbidi Dinitras in coronary heart disease.

This study investigates the systemic hemodynamic effects of intravenous Isosorbidi Dinitras, Isoket (ISDN) in 20 patients with coronary arterial disease to test the validity of the hypothesis concerning the relief of myocardial ischemia. Patients were eligible for the study if they had angina with coronary angiographic records or if they were cases of post-myocardial infarction. Before and after ISDN infusion the following measurements were recorded or calculated: heart rate (HR); systolic, diastolic and mean aortic pressure (ASP, ADP, AP); systolic and mean pressure of the left ventricle (LVSP, LVP); end-diastolic pressure in the LV (LVEDP); left ventricular contractility (dp/dt max); the double products (DP, HR x LVSP) and myocardial perfusion pressure in the LV (LVPP). After ISDN the ASP, AP and LVEDP decreased while HR, ADP, dp/dt and DP showed no significant changes. However, LVEDP was significantly decreased from 20 +/- 7 to 12 +/- 5 mmHg (P less than 0.01) with increased LVPP from 49 +/- 12 to 56 +/- 13 mmHg (P less than 0.01), which may be favourable for the relief of myocardial ischemia. There was no significant change of dp/dt max with decreased LVEDP after ISDN. It is suggested that the left ventricle can maintain normal performance at lower intracardial volume (preload) in these patients.