实时心肌造影结合斑点追踪技术评价不同顿抑状态犬心肌微循环与收缩功能变化

目的:应用实时心肌造影技术(RT-MCE)和斑点追踪技术(STI),研究不同顿抑状态心肌的收缩功能和微循环的变化及相互关系,从影像可视化角度探讨顿抑心肌的生物学特征.方法:制作冠状动脉左前降支阻断后再灌注犬心肌顿抑模型,分为短顿抑组(阻断15 min)、长顿抑组(阻断45 min)和假手术组(不阻断),分别于阻断前、再灌注即刻、再灌注10、30、60、90、120 min进行MCE和STI检查.实验结束后,心肌标本行透射电镜检查.结果:再灌注即刻,长顿抑组和短顿抑组缺血心肌的径向应变和A·β均低于基础状态及假手术组,差异具有统计学意义(P＜0.01);随再灌注时间的延长,长顿抑组和短顿抑组缺血心肌A·β值较再灌注即刻时增高;至再灌注后30 min,径向应变峰值进一步降低,再灌注60、90、120 min,径向应变峰值有所恢复.再灌注120 min时缺血心肌A·β值和径向应变峰值仍低于基础状态和假手术组.缺血心肌血流量(Y)与径向应变(X)呈线性关系,可拟合直线方程,其回归方程与相关系数为Y=0.443+49.64X,r=0.80,R2=0.64,P=0.031(长顿抑组);Y=-2.184+65.88X,r=0.78,R2 =0.60,P=0.039(短顿抑组).结论:STI能够反映心肌微循环血流情况.STI结合MCE能反映顿抑心肌生物学特征的动态变化     

中药川芎嗪对慢性压力超负荷大鼠心肌纤维化的干预作用

目的为验证中药川芎嗪对心肌肥大心功能不全时改善心肌生物力学方面的功能。观察中药川芎嗪对压力超负荷大鼠心肌纤维化动态改变的影响。方法采用缩窄腹主动脉造成大鼠压力负荷模型。将63只大鼠SPSS软件采用随机分为3组:假手术组(shamoperatedgroups,SOG)、手术组(operatedgroups,OG)和手术+川芎嗪干预组(OG+川芎嗪)。每组分为术后1,2,4,7,14,21,30d7个时间点。采用组织病理学和计算机图像分析技术对在各时间点大鼠心肌纤维化进行形态学和形态计量法上的比较。结果(1)OG组光镜下显示出反应性纤维化和修复性纤维化阶段,OG+川芎嗪组心肌纤维化程度明显比OG组减轻,未见修复性纤维化出现。(2)OG组心肌血管周围纤维化(perivascularcollagenarea,PVCA)在术后1d(2.09±0.45)就已显著高于SOG组(0.83±0.06),以后平稳上升,而与此同时OG+川芎嗪组PVCA(1.16±0.06)显著低于OG组;OG组心肌胶原容积分数(collagenvol-umefraction,CVF)在术后2d(3.08±0.56)已显著高于SOG组(2.78±0.64),从术后21d始呈现迅速上升的趋势,而OG+川芎嗪组CVF从术后21d(4.69±0.85)开始显著低于OG组(7.56±0.88),P均<0.05。结论川芎嗪可减缓压力超负荷大鼠心肌胶原的沉积,具有心脏保护作用。     

Clinical characteristics and outcomes of neurogenic stress cadiomyopathy in aneurysmal subarachnoid hemorrhage

Background

Aneurysmal subarachnoid hemorrhage (aSAH) is an often devastating form of stroke. Aside from the initial hemorrhage, cardiac complications can occur resulting in neurogenic stress cardiomyopathy (NCM), leading to impaired cardiac function. We investigated whether aSAH patients with NCM had poorer long term functional outcomes than patients without NCM. Mortality, vasospasm, and delayed ischemic complications were also evaluated.

Methods

A retrospective study of all patients admitted for aneurysmal subarachnoid hemorrhage (aSAH) from January 2006 to June 2011 (n = 299) was conducted. Those patients who underwent an echocardiogram were identified (n = 120) and were assigned to the NCM (n = 49) category based on echocardiographic findings defined by a depressed ejection fraction (EF%) along with a regional wall motion abnormality (RWMA) in a non-vascular pattern. Primary outcome measures included in-hospital mortality and functional outcomes as measured by the Modified Barthel Index (mBI) at 3 months and one year. Secondary analysis determined if there was an association between NCM, cerebral vasospasm and delayed cerebral ischemia.

Results

16% of aSAH patients developed NCM. Mortality was higher (p < .001) in the NCM group (n = 23[46.9%]) than in the non-CM group (n = 28[11.2%]). Patients with NCM had poorer functional outcomes as measured by the mBI at both 3 months (p = .002) and 12 months (p = .014). The Hunt–Hess score was predictive of functional outcome as measured by the mBI at both 3 months (p = .002) as well as at 1 year (p = .014). NCM was associated with both death (p = .047 CI, 1.012–7.288) and vasospasm (p = .008 CI, 1.34–6.66) after correction for Hunt–Hess grade. Tobacco use (p < .001) and a history of diabetes mellitus (p < .009) were also associated with vasospasm. NCM was associated with higher in-hospital mortality (p = .047) in multivariate analysis.

Conclusion

NCM is seen in a substantial number of aSAH patients and when present, it is associated with higher mortality and poorer long-term functional outcomes. This finding may guide further prospective studies in order to determine if early recognition of NCM as well as optimization of cardiac output would improve mortality.     

银杏叶提取物对糖尿病大鼠心肌线粒体的保护作用

目的观察银杏叶提取物(EGb)对糖尿病大鼠心肌线粒体的保护作用。方法40只SD大鼠随机分为正常对照组、糖尿病组和EGb治疗组，观察各组大鼠心肌线粒体超微结构，检测心肌线粒体琥珀酸脱氢酶(SDH)、超氧化物歧化酶(SOD)、一氧化氮合酶(NOS)的活性，以及一氧化氮(NO)、丙二醛(MDA)的含量。结果糖尿病大鼠心肌线粒体主要表现为肿胀，嵴变短，空泡化；SDH、SOD活性下降，NOS活性及MDA、NO含量增高。EGb治疗组病变较糖尿病组明显减轻，心肌线粒体SDH、SOD活性升高，NOS活性及NO、MDA含量下降。结论EGb能保护自由基和过量一氧化氮对心肌线粒体的损伤，提高SDH活性，从而对糖尿病大鼠心肌起保护作用。     

二氮嗪介导的延迟预处理对未成熟心肌的保护机制研究

目的研究二氮嗪(DZX)介导的延迟预处理对缺血缺氧环境中未成熟心肌的保护作用机制。方法分离培养新生鼠心肌细胞随机分为:①缺氧组;②DZX组:细胞缺氧培养前24 h放入含100μmol/L的DZX的培养液15 min;③DZX+PDTC组:细胞缺氧培养前24 h放入含100μmol/L DZX和500μmol/L二硫代氨基甲酸吡咯烷(PDTC)的培养液15 min;④对照组。前3组细胞在缺氧模型中培养16 h,对照组一直有氧培养。采用Hoechst染色、Annexin V/PI流式检测凋亡细胞,Western Blot检测心肌细胞Bax和Bcl-2的表达。结果①流式检测示DZX组较缺氧组细胞凋亡明显降低(P<0.01),Hoechst染色心肌凋亡细胞也减少;②与DZX组比较,加入PDTC后,流式检测显示细胞凋亡显著增多(P<0.01),Hoechst染色心肌细胞凋亡增多,Western blot检测显示Bcl-2表达减少,Bax表达增加。结论线粒体钾通道开放剂二氮嗪介导的延迟预处理对心肌有明显的保护作用;位于下游的NF-κB通过调控促凋亡蛋白Bax和抗凋亡蛋白Bcl-2的的表达在未成熟心肌的延迟预处理中起着关键作用。     

葛根素预处理对离体大鼠心肌缺血再灌注损伤的保护作用

目的通过建立大鼠离体心脏缺血再灌注模型,探讨葛根素预处理对大鼠心肌缺血再灌注损伤的保护作用及其可能机制。方法在langendǒrff离体心脏体外灌注模型复制基础上,采用随机对照方法将50只雄性SD大鼠平均分为5组:对照组、缺血再灌注组、缺血预处理组、小剂量葛根素预处理组、大剂量葛根素预处理组,记录每只大鼠平衡灌注15 min、再灌注153、0 min的心功能变化,包括心率(HR)、左室最高压(LVSP)、左室舒张末压(LVEDP)、左室压力升高速率(+dp/dtmax)、左室压力降低速率(-dp/dtmax)。并于平衡灌注15 min、复灌1、3、5、10、15、30 min测定冠脉流出液中肌酸激酶(CK)的含量。测定心肌丙二醛(MDA)、超氧化物歧化酶(SOD)、一氧化氮(NO)的含量,并作电镜检查。结果缺血再灌注组可引起HR、LVSP、+dp/dtmax、-dp/dtmax下降,LVEDP升高以及CK释放增加,心肌MDA产生增多、SOD及NO含量降低,与对照组相比有显著性差异。缺血预处理组及葛根素预处理组均能显著改善缺血再灌注引起的心功能损伤,降低CK的释放,减少心肌组织MDA的生成,并增加心肌组织中SOD和NO含量,减轻心肌细胞超微结构的病理改变。大剂量葛根素预处理组比小剂量葛根素预处理组对上述指标的改善更为显著。结论葛根素预处理能减少脂质过氧化,明显改善心功能,提高心肌组织对后续缺血的耐受性。这种保护作用存在量效关系,其产生与心肌中SOD增高减轻了氧自由基损伤和NO增高扩张冠脉有关。     

参麦冻干剂对猫心肌梗死的保护作用

目的:评价参麦冻干剂型用于心肌梗死猫心肌保护作用的有效性。方法:采用冠状动脉结扎法制备猫心肌梗死模型。随机将动物分为心肌梗死模型组(给予4ml/kg生理盐水)、参麦冻干剂大剂量组(1.76g/kg)、参麦冻干剂小剂量组(0.88g/kg)、参麦注射液组(0.88g/kg)和硝酸甘油组(0.44mg/kg)5组。观察各组动物平均动脉压(MAP)、6个胸前导联ST段抬高的总和(ΣST)、室性心律失常发生数、血清中肌酸激酶(CK)和乳酸脱氢酶(LDH)活性及心肌梗死范围的影响。结果:参麦冻干剂能增加心肌梗死猫的MAP,降低ΣST和心律失常发生数,缩减心肌梗死范围,降低CK和LDH活性,与心肌梗死模型组比较,上述各指标差异均有显著性(P<0.05或P<0.01);与参麦注射液和硝酸甘油组比较差异均无显著性。结论:参麦冻干剂能改善心肌梗死猫的心功能,对受损的心肌具有保护作用。     

Nitric oxide: not just a negative inotrope

Nitric oxide (NO) appears to play a role in modulating cardiac function in both health and disease. Early studies in isolated rodent cardiac myocytes demonstrated a depressant effect of NO supplied by NO donors (exogenous) as well as NO generated within myocytes (endogenous). There is increasing evidence for a functional NO generating system within the human myocardium, which appears upregulated in certain disease states. Induction of the high output nitric oxide synthase isoform (iNOS) has been demonstrated in the failing myocardium, though its functional significance remains unproven. More recently published data have contradicted the notion that NO acts solely as a negative inotrope demonstrating positive inotropy in both isolated rodent and human ventricular myocytes in response to a range of NO donors. Different NO donors have different NO release kinetics and generate a range of NO species (NO., NO+ and NO-) which may interact at a number of subcellular targets. The observed response of any cardiac preparation to an NO donor represents the net effect of activation of different effector targets and may explain the contradictory reported effects of NO. To realise the therapeutic potential of NO will require specific targeting at a subcellular level.     

1，6－二磷酸果糖对培养心肌细胞膜缺氧－再灌注损伤的保护作用

用培养的原代心肌细胞建立缺氧－再给氧方法，对缺氧６０分钟、１２０分钟及缺氧后再给氧３０及６０分钟时心肌细胞搏动、ＬＤＨ活性、（５１）￣Ｃｒ释放率、苔盼蓝摄取率、扫描电镜观察及１，６－二磷酸果糖对其影响进行了研究。结果显示：缺氧２小时可引起心肌细胞搏动频率减慢，再给氧后搏动频率加快；ＬＤＨ活性、（５１）￣Ｃｒ释放率和苔盼蓝摄取率增加，电镜显示心肌细胞膜受损。１，６－二磷酸果糖对心肌细胞膜具有保护作用。