压力容积导管系统评价卒中易感性自发性高血压大鼠左心室功能的意义

目的 采用压力容积导管研究慢性压力超负荷对高血压大鼠左心室(LV)血流动力学的影响.方法 10只6月龄雄性卒中易感性自发性高血压大鼠(SHR-SPs)和10只同月龄雄性Wistar-Kyoto(WKY)大鼠分别作为高血压组和对照组.对两组大鼠行在体LV血流动力学检测,大鼠麻醉后经右颈总动脉向LV内插入2F Millar压力容积导管(SPR-838),记录大鼠稳定状态和改变心脏前负荷时的压力-容积(P-V)变化.结果 与WKY大鼠比较,SHR-SPs LV收缩末压、LV收缩末容积和室内压最大上升速率( dP/dtmax)均增高,而射血分数、每搏输出量和心排血量均出现降低(P<0.05).在压力负荷的影响下,SHR-SPs LV收缩末压力容积曲线的斜率代偿性增高(P<0.05).SHR-SPs LV舒张末压、LV舒张末容积和LV压力衰退的时间常数均高于WKY大鼠(P<0.05),而室内压最大下降速率(-dP/dtmin)低于WKY大鼠(P<0.05).与WKY大鼠比较,SHR-SPs在体LV P-V曲线出现了明显的右移.结论 SHR-SPs发生了LV舒张功能障碍及收缩功能减低,并在此基础上伴有一定程度的LV扩张.压力容积导管能够客观准确地评价大鼠的心功能.     

压力-容积环评价压力负荷型慢性心力衰竭大鼠左心室功能的意义

目的采用压力-容积(P-V)环研究压力超负荷对大鼠左心室血流动力学的影响。方法 13只SD大鼠随机分为2组:假手术(Sham)组(n=7)和心力衰竭(HF)组(n=6)。HF组采用腹主动脉缩窄法制备模型,Sham组只穿线不缩窄。对两组大鼠进行血流动力学检测,大鼠麻醉后经右颈总动脉向左心室内插入Millar导管(SPR-838),记录两组大鼠的P-V变化。结果与Sham组相比,HF组大鼠的心脏(P0.01)和肺脏(P0.05)重量均显著增加。在稳定状态的P-V环中可以看到,和Sham组相比,在压力超负荷的影响下,HF组左心室P-V环明显增高、右移,P-V曲线斜率也明显高于Sham组,左心室收缩/舒张末期压力(P_(es)/P_(ed))、收缩/舒张末容积(V_(es)/V_(ed))、压力衰退的时间常数(Tau)均增高(P0.05),而室内压最大上升速率(dP/dt_(max))、左室压力最大下降速率(-dP/dt_(min))、射血分数(EF)和每搏输出量(SV)均出现降低(P0.05)。结论压力负荷型慢性HF大鼠左心室发生了舒张和收缩功能障碍,并且伴有一定程度的左心室肥大。P-V环能够准确地定性、定量评价大鼠的心功能。     

依普利酮对慢性心力衰竭大鼠血流动力学和运动能力的影响

目的探讨依普利酮对慢性心力衰竭大鼠血流动力学和运动能力的影响。方法将18只成年健康清洁级SD雄性大鼠随机分为空白组、心力衰竭组与依普利酮组,每组6只大鼠。心力衰竭组与依普利酮组均采用结扎左冠状动脉前降支建立心力衰竭模型,依普利酮组在心力衰竭模型建立后2周给予依普利酮20 mg/(kg·d)灌胃,连续应用4周。记录大鼠不同时间点的血流动力学和运动能力。结果所有大鼠都成活,心力衰竭组与依普利酮组实验2周、6周的收缩压与舒张压均明显高于空白组(P0.05),依普利酮组实验6周的收缩压与舒张压均明显低于心力衰竭组(P0.05)。实验6周,心力衰竭组与依普利酮组左室收缩末期内径(LVESD)明显高于空白组(P0.05),依普利酮组LVESD低于心力衰竭组(P0.05)。实验6周心力衰竭组与依普利酮组左室内压最大上升速率(+dp/dt_(max))和左室内压最大下降速率(-dp/dt_(max))值均低于空白组(P0.05),依普利酮组+dp/dt_(max)、-dp/dt_(max)均高于心力衰竭组(P0.05)。结论采用结扎左冠状动脉前降支建立心力衰竭模型能反映大鼠的心力衰竭状况,依普利酮可改善慢性心力衰竭大鼠血流动力学状况,提高心功能与运动能力。     

β3肾上腺素能受体阻断剂对扩张型心肌病大鼠心功能的影响

目的研究选择性β_3肾上腺素能受体(β_3-AR)阻断剂SR59230A对扩张型心肌病大鼠心功能的影响。方法雄性Wistar大鼠72只,随机取14只分为对照组(Nor-C)和用药组(Nor-T),每组7只。其余大鼠应用异丙基肾上腺素制备心力衰竭(简称心衰)模型后,存活大鼠随机分为心衰组(HF-C,8只)和心衰用药组(HF-T,9只)。Nor-T组与HF-T组给予2 mmol/L的SR59230A 0.3 ml尾静脉注射,Nor-C组与HF-C组给予同等剂量生理盐水。血流动力学指标测定后,留取左心室心肌组织,测定内皮源性一氧化氮合酶(eNOS)mRNA、β_3-AR蛋白表达以及cGMP水平。结果Nor-T组与Nor-C组比较,大鼠左心室压力最大上升速率(dp/dt_(max))及左心室压力最大下降速率(dp/dt_(min))绝对值显著增高(P<0.05);左心室收缩末期压力(P_(ES))有上升趋势,左心室舒张末期压力(P_(ED))有下降趋势,但差异无统计学意义(P>0.05);左心室等容舒张时间常数(Tc)显著缩短(P<0.05)。HF-T组较HF-C组dp/dt_(max)、dp/dt_(min)绝对值及P_(ES)显著升高(P<0.05或<0.01);而P_(ED)、Tc则明显减低(P<0.05)。HF-C组与Nor-C组比较,eNOS mRNA及β_3-AR蛋白表达显著增加(P<0.01);而Nor-T组与Nor-C组、HF-T组与HF-C组间差异无统计学意义(P>0.05)。HF-C组较Nor-C组心肌cGMP水平显著增加(P<0.01);Nor-T组与HF-T组cGMP水平分别低于Nor-C组与HF-C组(P<0.05或<0.01)。结论①β_3-AR阻断剂SR59230A可以改善大鼠心功能,尤其以心衰大鼠为著;②心衰时β_3-AR、eNOS表达增加,心肌cGMP水平增高;③β_3-AR阻断剂改善心功能的作用机制主要是通过抑制cGMP水平实现的。     

应用压力-容积环评价曲美他嗪对大鼠心肌顿抑的影响

目的应用压力-容积环评价曲美他嗪对大鼠心肌顿抑的影响及可能机制。方法 30只雄性SD大鼠,随机等分成3组:对照组、心肌顿抑组(生理盐水2 mL)和曲美他嗪组(曲美他嗪片3 mg/kg)。结扎冠状动脉左前降支20 min再灌注120 min,制作大鼠心肌顿抑模型(对照组只穿线不结扎)。用压力-容积系统动态观察心率、左心室收缩期末压、收缩期末压力容积、左心室舒张期末压及舒张期末压力容积等血流动力学变量以及压力-容积环变化,并应用软件PowerLab系统离线分析;再灌注结束后测定大鼠心肌组织中ATP含量、ATP酶活性及磷酸果糖激酶活性,并应用体视学方法定量分析大鼠心肌线粒体的变化。结果与心肌顿抑组相比,曲美他嗪组舒张期末压、收缩期末容积、前负荷补充搏功均显著降低(P<0.01),舒张期末压力-容积也降低(P<0.05);舒张期末容积、收缩期末压力容积均显著升高(P<0.01),ATP含量及ATP酶(Ca2+-Mg2+ATPase和Na+-K+ATPase)活性增加(P<0.05);磷酸果糖激酶活性显著增加(P<0.01);心肌线粒体损伤显著减轻(P<0.01)。结论曲美他嗪可以通过改善能量代谢降低心肌顿抑的发生,压力-容积环能准确敏感地评价心功能。     

辛伐他汀联合辅酶Q10对慢性心力衰竭大鼠心肌结缔组织生长因子表达的影响

目的探讨辛伐他汀联合辅酶Q10对慢性心力衰竭大鼠结缔组织生长因子(CTGF)表达的影响。方法利用腹主动脉缩窄法制作雄性SD大鼠慢性心力衰竭模型,随机分为模型组、辛伐他汀组、辅酶Q10组、联合用药组,另设假手术组,每组8只大鼠,观察各组大鼠血流动力学参数(左室舒张末压,左室内压上升、下降最大速率)和左心室心肌组织病理学改变,免疫组化检测各组大鼠左心室心肌中CTGF表达情况。结果与模型组相比,辛伐他汀组、辅酶Q10组和联合用药组左室舒张末压显著降低(P<0.01),最大收缩、舒张速率显著升高(P<0.01),左心室心肌CTGF阳性表达水平显著降低;联合用药组较辛伐他汀组、辅酶Q10组改变更为显著(P<0.01或P<0.05)。结论辛伐他汀与辅酶Q10联合应用较两药单独应用改善心力衰竭大鼠心功能、抑制心室重塑和减少CTGF表达作用明显。     

生脉注射液对慢性心力衰竭大鼠血流动力学的影响

目的探讨生脉注射液对慢性心力衰竭(CHF)大鼠血流动力学的影响。方法雄性Wistar大鼠60只随机分为假手术组(10只)和模型组(50只),分别行假腹主动脉缩窄术和腹主动脉缩窄术。8周后从每组选取10只进行血流动力学参数测定,若测定结果显示CHF大鼠模型制作成功,则将模型组余下大鼠随机分为对照组和生脉组,分别予以生理盐水和生脉注射液治疗,4周后进行血流动力学参数测定。结果生脉组大鼠的收缩压(SBP)、舒张压(DBP)、左室收缩压(LVSP)、左室内压上升最大速率( dP/dTmax)和左室内压下降最大速率(-dP/dTmax)大于对照组(P<0.01),心率(HR)和左室舒张末压(LVEDP)小于对照组(P<0.01)。结论生脉注射流能有效改善CHF大鼠的血流动力学状况。     

Notch3介导RhoA/ROCK/Hif1α轴对心肌梗死心功能的影响

目的 分析Notch3介导RhoA/ROCK/Hif1α轴对心肌梗死(MI)心功能的影响。方法 将45只雄性SD大鼠随机分为假手术组、模型组和Notch3过表达组三组,每组各15只。大鼠心肌注射Notch3慢病毒过表达后构建MI模型。术后12周检测心功能及心脏血流动力学指标,观察心肌组织结构,并检测心肌组织Notch3和RhoA/ROCK/Hif1α轴相关蛋白水平。结果 与假手术组比较,模型组大鼠心肌组织Notch3表达水平、左心室射血分数(LVEF)、左心室舒张末压(LVEDP)显著降低,左心室收缩末期内径(LVESD)、左心室舒张末期内径(LVEDD)、左心室收缩末压(LVESP)、左心室压力最大上升速率(LV+dp/dtmax)、左心室压力最大下降速率(LV-dp/dtmax)、心肌组织RhoA、ROCK1、ROCK2、Hif1α表达水平显著增加(P<0.05);Notch3过表达组大鼠LVESD和LVEDD显著小于模型组,心肌组织Notch3表达水平、LVEF、LVEDP显著高于模型组(P<0.05);LVESP、LV+dp/dtmax和LV-dp/dtmax、心肌...     

非诺贝特治疗大鼠左心室肥厚

目的研究非诺贝特逆转腹主动脉缩窄(AAC)大鼠左心室肥厚的作用,并初步探讨其对 Akt/GSK3β信号通路的影响。方法采用 AAC 法建立心肌肥厚模型。术前1周和术后4周灌胃给予非诺贝特[80 mg/(kg·d)],观察了其对血流动力学参数、超声参数、左室质量(LVM)/体质量(BM)、心肌超微结构的影响。同时检测了心肌组织中 Akt 和 GSK3β蛋白磷酸化的表达变化。结果 1)与假手术组相比,大鼠腹主动脉缩窄4周后,主动脉收缩压(AoSP)、主动脉舒张压(AoDP)、左室内压(LVESP、LVEDP)明显升高(P<0.05);室内压最大上升速率(+dp/dt_(max))和室内压最大下降速率(-dp/dt_(min))明显减少(P<0.05),而非诺贝特治疗后,+dp/dt_(max)、-dp/dt_(min)明显上升(P<0.05);AoSP、AoDP、LVESP 无明显变化(P>0.05)而 LVEDP 稍降(P<0.05)。2)手术后4周 AAC 大鼠呈现出明显的向心性肥厚,室间隔(IVSd 和 IVSs)及左室后壁厚度(PWTd 和 PWTs)(P<0.05)、LVM/BM[LVM:(2.94±0...     

microRNA-497在麝香保心丸调控急性心肌梗死心室重构中作用机制的实验研究

目的探讨microRNA-497(miRNA-497)在麝香保心丸调控急性心肌梗死心室重构中的作用机制。方法将75只SD大鼠随机分为A组、B组、C组、D组、E组,每组15只。A组为空白对照组,B组、C组、D组、E组采用结扎左冠状动脉前降支法建立急性心肌梗死模型。C组给予miRNA-497激动剂和麝香保心丸干预,D组给予miRNA-497抑制剂和麝香保心丸干预,E组给予麝香保心丸干预,B组给予等量生理盐水。6周后,比较各组大鼠一般情况、心功能指标[左室收缩末压(LVESP)、左室内压最大上升速率(LV+dp/dt_(max))、左室舒张末压(LVEDP)、左室内压最大下降速率(LV-dp/dt_(max))]、急性心肌梗死面积、心肌细胞凋亡率、心肌组织形态学变化、miRNA-497表达量。结果与B组比较,C组大鼠一般情况及心肌组织病理学改变无明显改善,D组、E组大鼠一般情况及心肌组织病理学改变有改善,且D组较E组改善更明显。D组、E组大鼠LVEDP、急性心肌梗死面积、心肌细胞凋亡率明显低于B组、C组(P0.05),且D组大鼠LVEDP、急性心肌梗死面积、心肌细胞凋亡率明显低于E组(P0.05);D组、E组大鼠LV+dp/dt_(max)、LVESP、LV-dp/dt_(max)明显高于B组、C组(P0.05),且D组大鼠LV+dp/dt_(max)、LVESP、LV-dp/dt_(max)明显高于E组(P0.05);C组大鼠LVEDP、LV+dp/dt_(max)、LVESP、LV-dp/dt_(max)、急性心肌梗死面积、心肌细胞凋亡率与B组比较,差异均无统计学意义(P0.05)。B组、C组、D组、E组大鼠心肌组织中miRNA-497表达量明显高于A组(P0.05);C组大鼠心肌组织中miRNA-497表达量明显高于B组(P0.05);D组、E组大鼠心肌组织中miRNA-497表达量明显低于B组、C组(P0.05),D组大鼠心肌组织中miRNA-497表达量低于E组(P0.05)。结论 miRNA-497是麝香保心丸改善急性心肌梗死后心室重构中的关键分子,这为急性心肌梗死后心室重构提供了新的研究方向。     

Endothelin-A Receptor Antagonism during Acute Myocardial Infarction in Rats

Endothelin levels are increased in rats with experimentally induced myocardial infarction. The purpose of this study was to determine whether endothelin-A (ET_A) receptor antagonism alters ventricular remodeling and the development of heart failure after myocardial infarction (MI). We administered 10 mg/kg/day of A-127722 to rats post-MI for 6 weeks. A hemodynamic study was performed and passive pressure-volume curves obtained. In rats without infarcts, ET_A receptor antagonist (n=8; vehicle, n = 5) had no effect. However, in rats with infarcts ET_A antagonism (n = 14, MI = 35%; vehicle: n = 19, MI = 32%) reduced systemic arterial and LV systolic (but not end-diastolic) pressures and shifted the pressure-volume relationship to the right. Because LV mass was not changed, the volume-to-mass ratio was increased and was correlated inversely with the ability of the LV to maximally develop pressure. This increase in volume at low distending pressures was also coupled with a tendency (P < 0.06) for reduced scar thickness, suggesting that early initiation of an ET_A receptor antagonism increased infarct expansion. The reduction in blood pressure offset the increase in volume such that wall stresses were unchanged, as was LV mass. The early use of ET_A receptor antagonism in the rat model of myocardial infarction did not beneficially alter LV remodeling.     

自发性高血压大鼠肥厚左室心肌组织微小RNA-1与内向整流钾通道2.1表达的改变及其意义

目的观察自发性高血压大鼠(SHR)肥厚的左室心肌组织微小RNA-1、内向整流钾通道2.1(Kir2.1)表达的变化及其关系,以探讨高血压左心室肥厚(LVH)发生室性心律失常的分子机制。方法取10只17周龄雄性SHR为LVH组,10只8周龄雄性SHR为阳性对照组,10只17周龄雄性WKY大鼠作为空白对照组,通过HE染色、心肌细胞横径测量、实时荧光定量聚合酶链反应(qRT-PCR)、免疫组织化学法及Western blot检测等方法,检测大鼠左室心肌组织病理学改变、微小RNA-1表达、Kir2.1蛋白表达水平的改变。结果①与空白对照组比较,LVH组和阳性对照组的收缩压、舒张压明显升高(分别P<0.01,P<0.05);②与两对照组相比,LVH组的左室质量指数及心肌细胞横径均明显增大(均P<0.05),左室心肌细胞明显肥大,心肌间质增多,伴随着微小RNA-1表达水平明显升高,Kir2.1蛋白表达水平显著降低(P<0.05);③LVH组大鼠左室心肌组织微小RNA-1与Kir2.1蛋白的表达水平呈负相关(r=-0.720,P<0.05)。结论SHR肥厚左室心肌组织微小RNA-1表达上调,并伴随Kir2.1表达下调。     

Continuous measurement of left ventricular volume in rabbit,using a two-electrode catheter

Summary We developed a device for monitoring instantaneous left ventricular (LV) volume using an alternating-current excitation two-electrode conductance catheter. Instantaneous conductance between a pair of electrodes was amplified by a noninverting circuit. The level of conductance was linearly related to changes in blood volume from 0.8 to 2.0ml in a latex balloon (r ² = 0.95), and to changes in blood volume from 0.4 to 2.2ml in a post-mortem rabbit left ventricle (r ² = 0.99). The difference between the maximal and minimal conductance of the LV in situ during a cardiac cycle was closely correlated with changes in stroke volume, measured by an electromagnetic flow probe (r ² = 0.97). The endsystolic pressure-conductance relation (ESPCR) was highly linear (r ² = 0.92). Changes of the slope (Ees) of the ESPCR correlated directionally with changes of the time derivative of LV pressure (LVdP/dt) during intravenous infusions of dobutamine and propranolol. Accordingly, the two-electrode conductance catheter was useful in vivo in rabbits for continuously assessing changes in the LV volume.     

Left ventricular volume determination in dogs: a comparison between conductance technique and angiocardiography

Left ventricular (LV) volume was determined simultaneously bymonoplane cineangiocardiography and conductivity using a multielectrodeconductance catheter at rest and during pressure loading inseven mongrel dogs (mean body weight 22 kg). LV volumes werecalculated frame-by-frame (75 frames s^–1) by angiocardiographyand matched with instantaneous volumes obtained by conductivity.There was an excellent correlation between the two techniquesat rest (correlation coefficient, r = 0.96) and during pressureloading (r = 0.92) when the data of each dog were pooled. Thestandard error of estimate of the mean angiographic volume was4%. The slope of the regression analysis showed a small butsignificant (P <0.01) decrease from 0.365 at rest to 0.289during pressure loading, whereas the intercept remained unchanged(24 versus 26 ml). Since no calibration for parallel conductivityof the surrounding tissue was performed, LV end-systolic volumewas significantly over- and LV ejection fraction significantlyunderestimated whereas LV end-diastolic volume was estimatedcorrectly by the conductance technique. It is concluded that LV end-diastolic volume can be determinedaccurately by the conductance technique in dogs. However, LVend-systolic volume is significantly over- and ejection fractionsignificantly under-estimated. Since there is a good correlationbetween angiocardiography and conductivity, exact determinationOf LV volumes and ejection fraction is feasible using a correctionfactor. The change is slope of the regression equation betweenangiocardiography and conductivity suggests a change in conductivityof the surrounding tissue during pressure loading which limitsthe application of the conductance catheter to stable haemodynamicsituations or calls for repeated calibrations by an independenttechnique during acute interventions.     

Cardiopulmonary bypass impairs left ventricular function determined by conductance catheter measurement

OBJECTIVE: Postoperative cardiac depression is attributed to ischemia and the effects of cardiopulmonary bypass (CPB). To evaluate the effect of CPB alone on postoperative left ventricular (LV) dysfunction, we used a conductance catheter to determine the LV performance by pressure-volume relation before and after CPB. METHODS: Twenty-two 3-week-old piglets underwent sternotomy and normothermic CPB for one hour. A conductance catheter was placed in the LV cavity. End-systolic pressure-volume relationships (ESPVR), left ventricular end-diastolic pressure (LVEDP) and systemic vascular resistance (SVR) were measured under steady-state conditions before and 15 min after weaning from CPB in group A (n = 11). Group B included 11 piglets without CPB and served as control. RESULTS: There was no difference between groups before initiating CPB. As an indication of depressed LV function, the ESPVR slope (mmHg/ml) was significantly lower in group A after weaning from CPB than in group B (1.69 +/- 0.5 vs. 1.86 +/- 0.55; p = 0.008). In group A, peak dP/dt (max index) (mmHg/s/m (2)) decreased markedly (1596 +/- 339 vs. 2045 +/- 206; p = 0.03), while LVEDP (mmHg) was significantly increased (11.7 +/- 2.6 vs. 5.4 +/- 0.9; p < 0.0001). In addition, SVR (index) (dyn x s x cm (-5)/m (2)) in group A was significantly lower (1407 +/- 176 vs. 1677 +/- 313; p < 0.0001) than in group B. CONCLUSION: Using the very sensitive conductance catheter technique in a pig model, we could show that CPB leads to a significant depression of LV contractility and elastance even without ischemic arrest.     

Influence of cyclic variation of right ventricular volume on left ventricular mechanical parameters measured with conductance catheter

The conductance catheter is widely used for the continuous measurement of the left ventricular (LV) pressure-volume loops. Cyclical change of the right ventricular (RV) volume may alter the parallel conductance volume, thereby affecting the LV mechanical parameters. Using 8 open-chest adult mongrel dogs, multiple LV pressure-volume loops were obtained by 2 methods: first with a vena cava occlusion (VCO) method, which involved RV volume alteration, and second with a right-heart-bypass (RHB) preparation, which decompressed the right ventricle completely. The slope of the end-systolic pressure-volume relation (Ees), the end-systolic volume associated with the end-systolic pressure of 100 mmHg (V100,es), stiffness constant (beta), and the end-diastolic volume associated with the end-diastolic pressure of 9 mmHg (V9,ed) were calculated from each loop. There was minimal influence from RV volume alteration on systolic-phase indices [Ees (VCO method, 6.37 +/- 1.91 mmHg/ml; RHB preparation, 6.60 +/- 1.66mmHg/ml; p=0.356), and V100,es (VCO method, 18.4 +/- 9.3ml; RHB preparation, 17.8 +/- 9.0 ml; p=0.681)], but there was a significant influence on diastolic-phase indices [beta (VCO method, 0.0599 +/- 0.0152; RHB preparation, 0.0839 +/- 0.0150; p=0.007), and V9,ed (VCO method, 35.6 +/- 11.3 ml; RHB preparation, 31.9 +/- 12.3 ml; p=0.001)]. The increase in the RV volume in the diastolic phase increased the parallel conductance volume, causing overestimation of the LV diastolic volume measured by the conductance catheter.     

Conductance catheter for determining left ventricular volume and end-systolic pressure-volume relations: its clinical application]

In this study, the clinical usefulness of the conductance catheter technique was assessed. The end-systolic pressure-volume relations (ESPVR) measured with the increase and decrease in the preload were also compared. Fourteen patients with various heart diseases who underwent diagnostic cardiac catheterization were studied. Using a right atrial pacing catheter, 8 electrical stimuli delivered at a fixed rate of 800 msec were followed by a single early stimulus of 500 msec coupling interval, resulting in premature atrial contraction and post-extrasystolic potentiation (PESP). Left ventricular (LV) volume was measured by 2 methods; namely, the conductance catheter technique and single-plane left ventriculography (LVG). ESPVR was obtained either with the inferior vena cava occlusion induced by balloon inflation, or with the rapid transfusion of saline with electrical resistance identical to the blood volume in the right atrium. The LV volume obtained with the conductance catheter technique (VCON) was correlated with the LV volume as obtained by LVG (VLVG) (end-diastolic volume, VCON = 1.09VLVG - 4.66, r = 0.95; end-systolic volume, VCON = 1.42VLVG - 18.2, r = 0.89). There was correlation of the change in LV volume (delta V) induced by PESP between the 2 methods (end-diastolic volume, delta VCON = 0.52 delta VLVG + 0.94, r = 0.76; end-systolic volume, delta VCON = 0.42 delta VLVG - 4.78, r = 0.72), suggesting that the change in LV volume estimated by the conductance catheter technique was smaller than that estimated by LVG. The LV volume curves were similar.(ABSTRACT TRUNCATED AT 250 WORDS)     

氯通道阻滞剂尼氟灭酸对肥厚心肌心室有效不应期及心室颤动阈值的疗效

背景肥厚心肌离子通道的重塑容易发生恶性室性心律失常，钙激活氯通道的改变起着重要的作用，尼氟灭酸（NFA）是常用的钙激活氯通道的阻滞剂。目的不同剂量NFA对左室肥厚心肌心室有效不应期及心室颤动阈值的影响。方法32只10周龄雄性自发性高血压大鼠（SHR）随机分成非NFA处理组及3个NFA不同剂量（0．01，0．1，1．0μmol／kg．iv）处理组，每组8只，取8只雄性Wistar大鼠作为对照组，分别测定各组大鼠心率、动脉收缩压、心室有效不应期、心室颤动阈值及左室质量指数。结果1）SHR左室质量指数明显大于Wistar大鼠（P〈0．01）；2）NFA非处理组的心室颤动阈值明显小于对照组[（15．0&#177;1．2）mAVS（26．4&#177;1．5）mA，P〈0．01）；3）NFA浓度越大延长左室肥厚心肌的心室有效不应期越明显，提高左室肥厚心肌的心室颤动阈值越明显（P〈0．05），呈浓度依赖趋势；4）心室有效不应期与心室颤动阈值正相关，NFA的3个不同处理剂量与心室有效不应期或心室颤动阈值正相关。结论NFA可以延长左室肥厚心肌的心室有效不应期，提高左室肥厚心肌的心室颤动阈值。     

Echocardiographic assessment of left ventricular midwall mechanics in spontaneously hypertensive rats.

AIMS: The present study was attempted to determine whether LV midwall mechanics yielded different conclusions about LV systolic function than the assessment of endocardial LV mechanics by echocardiography in spontaneously hypertensive rats (SHR). METHODS AND RESULTS: Thirty-six (18 Wistar normotensive (W), 18 [SHR]) anesthetized rats were studied with two-dimensional directed M-mode echocardiogram to analyze LV structure (LV diameter, left ventricular wall thickness and LV mass [LVM]) and LV function (endocardial shortening [ES] and midwall shortening [MS]). Measurements were made from three consecutive cardiac cycles on the M-mode tracings. There was no significant difference in LV dimension. LVM was higher in SHR (SHR: 595 +/- 111 mg, W: 413 +/- 83 mg--p < 0.01). ES was higher in SHR (SHR: 64.1 +/- 6%, w: 58.2 +/- 4%--p < 0.01), whereas no significant difference was found in MS (SHR: 24 +/- 4%, W: 27.6 +/- 4%--ns). Twelve of 18 (66%) SHR showed endocardial shortening higher than normally predicted, compared with 3/18 (16%) with observed enhanced MS (p < 0.01). CONCLUSION: These results suggest that the analysis of midwall mechanics by echo allows us to better understand the LV performance in SHR and that the exaggerated endocardial motion could not represent a really supernormal systolic performance.     

Perioperative hemodynamic and geometric changes of the left ventricle during cardiomyoplasty in goats with dilated left ventricle

OBJECTIVE: Clinical data have suggested the occurrence of temporary short-term deterioration of the heart following cardiomyoplasty. The purpose of this study was to monitor the short-term hemodynamic effects of cardiomyoplasty in a goat model of a dilated left ventricle, using conductance catheters (ie, pressure-volume loops) and cardiac output measurements. METHODS: Eight female goats underwent acute cardiomyoplasty 8 to 12 weeks after left ventricular (LV) dilatation was induced by a carotid jugular arteriovenous shunt. The cardiomyoplasty procedure was monitored using a Swan-Ganz catheter for cardiac output measurements and a 12-electrode (dual-field) conductance catheter to LV pressure-volume loops. RESULTS: After wrapping the heart with the latissimus dorsi muscle, there was a significant reduction in both cardiac output and LV end-diastolic volume (LVEDV) at 10 min. Partial recovery was observed 45 min later. CONCLUSION: A decrease in both cardiac output and LVEDV was observed following myocardial wrapping. This may explain some of the perioperative and postoperative morbidity and mortality observed following cardiomyoplasty.