自发性高血压大鼠心肌胶原与血管紧张素Ⅱ的关系

目的　观察成年 (16周龄 )自发性高血压大鼠 (spontaneouslyhypertensiverat,SHR)与同龄对照组 (WKY)大鼠之间细胞外基质成分的差异及血管紧张素Ⅱ (AngiotensinⅡ ,AngⅡ )在SHR大鼠左室肥厚形成过程的作用。方法　用尾袖法间接测定大鼠血压 ;检测左心室组织及血浆中的血管紧张素转化酶 (angiotensinconvertingenzyme ,ACE)活性 (紫外分光光度法 ) ;放免法测定左室心肌AngⅡ含量。免疫组化测定左室心肌胶原含量 ,用3H -Proline掺入量测定体外培养心肌成纤维细胞 (cardiacfibroblast,CFB)胶原的合成率。结果　 (1) 16周龄SHR大鼠血压明显高于对照组 (WKY)大鼠 ,分别为 (2 7.6 3± 2 .6 7)kPa和 (16 39± 0 54)kPa ,P <0 .0 5;(2 )SHR大鼠左室心肌AngⅡ含量明显高于WKY组 ,分别为 (2 6 6± 75)pg/ 10 0mg和 (134± 4 1)pg/ 10 0mg ,P <0 .0 5;(3)左室重量 (Leftventricalarmass,LVM)SHR明显高于WKY组 ,分别为 (10 14.3± 6 2 .1)mg和 (895.7± 86 .4 )mg ,P <0 .0 5;(4 )心体比 (Letventricrlarmass/bodyeight,LVM/BW )SHR明显高于WKY组 ,分别为 (3.4 4± 0 .15)mg/g和 (2 .17± 0 .11)mg/g ,P <0 .0 5;(5)体外细胞培养的心肌成纤维细胞3H -Proline掺入量随着AngⅡ浓度升高而增加 ,1μmol/L的AngⅡ使SH     

链霉素对颈动脉窦压力感受器反射的抑制作用

在 2 3只隔离灌流颈动脉窦区的麻醉大鼠 ,观察了链霉素对颈动脉窦压力感受器反射的影响。结果如下 :(1)以链霉素 (10 0 μmol/L)隔离灌流大鼠左侧颈动脉窦区时 ,压力感受器反射机能曲线向左下方移位 ,曲线最大斜率 (PS)由 0 40± 0 0 1kPa降至 0 33± 0 0 1kPa (P <0 0 0 1) ,血压反射性下降 (reflexdecrease ,RD)幅度由 6 2 2±0 13kPa降至 5 0 2± 0 11kPa (P <0 0 0 1) ,阈压 (TP)、平衡压 (EP)和饱和压 (SP)则分别从 8 2 7± 0 2 5 ,12 71± 0 2 1和 2 4 41± 0 14kPa增至 10 33± 0 32 (P <0 0 1) ,13 33± 0 30 (P <0 0 1)和 2 6 11± 0 2 8kPa (P <0 0 1)。其中RD ,PS和TP的变化呈明显的剂量依赖性。 (2 )应用腺苷隔离灌流大鼠颈动脉窦区 ,引起颈动脉窦压力感受器反射的易化 ;在用链霉素预处理后 ,此易化效应不仅完全被阻断 ,且可使反射效应小于应用腺苷前的对照值。以上结果表明 ,链霉素对大鼠颈动脉窦压力感受器反射有明显的抑制作用。     

血小板源生长因子受体介导的信号转导在自发性高血压大鼠心肌肥大中的作用

为了探索血小板源生长因子 (platelet derivedgrowthfactor,PDGF)受体介导的信号转导在自发性高血压大鼠(spontaneouslyhypertensiverats,SHR)心肌肥大中的作用 ,实验采用Westernblot法检测SHR及其对照WKY大鼠心肌PDGF受体β和细胞外信号调节激酶 (extracellularsignal regulatedkinase1/ 2 ,ERK 1/ 2 )的蛋白表达和ERK 1/ 2磷酸化水平的变化。结果显示 :4周龄SHR的收缩压、舒张压、±dp/dtmax和心肌肥大指数与同龄WKY大鼠相比均无明显差异 ,而 12周龄SHR上述指标与同龄WKY大鼠相比均明显升高 ,表明 12周SHR已发生高血压 ,心脏收缩功能代偿性增强 ,并出现心肌肥大。 4周龄SHR心肌PDGF受体 β和ERK1/ 2的磷酸化水平以及ERK 1/ 2的蛋白表达水平与同龄对照相比均无明显变化 ,12周时SHR心肌PDGF受体 β的蛋白表达较同龄WKY增加 32 77% (P <　　　　　　　　　 0 0 5 ) ,PDGF受体介导的信号转导通路的下游信号分子ERK 1/ 2的磷酸化水平较同龄WKY升高 19 6 % (P =0 0 1) ,表明ERK 1/ 2的活化增加 ,但ERK 1/ 2的蛋白表达水平尚无变化。为进一步明确PDGF受体 β在心肌细胞生长中的作用及其与ERK 1/ 2活性的关系 ,采用PDGF BB刺激培养的乳鼠心肌细胞 ,发现 [3 H]亮氨酸掺入量明显增加 ,ERK 1/ 2的磷酸化水平明     

K_(ATP)通道开放剂对颈动脉窦压力感受器反射的易化作用

在 30只隔离灌流颈动脉窦区的麻醉大鼠 ,观察了KATP通道开放剂 (cromakalim ,Cro)对颈动脉窦压力感受器反射的影响。结果如下 :( 1)以Cro ( 10 μmol/L)隔离灌流大鼠左侧颈动脉窦区时 ,压力感受器机能曲线向左下方移位 ,曲线最大斜率 (PS)由 0 36± 0 0 1增至 0 48± 0 0 1kPa/kPa (P <0 0 0 1) ,反射性血压下降幅度 (RD)由 5 78± 0 14增至 7 87± 0 12kPa (P <0 0 0 1) ;阈压 (TP)、平衡压 (EP)和饱和压 (SP)则分别从 8 34± 0 35 ,12 71± 0 2 5和 2 4 89±0 2 5下降至 6 41± 0 0 9kPa,11 78± 0 2 4kPa ,2 2 5 6± 0 16kPa (P <0 0 1～ 0 0 0 1)。其中RD ,PS和TP的变化呈明显的剂量依赖性。 ( 2 )用KATP通道阻断剂格列苯脲 (glibenclamide,10 μmol/L)预处理后 ,Cro的上述反射效应即被阻断。( 3)先给予腺苷 (adenosine,12 5 μmol/L)则可以加强Cro对压力感受器反射的影响。以上结果表明 ,KATP通道开放剂Cro对大鼠颈动脉窦压力感受器反射有易化作用 ,此作用是由KATP通道开放剂引起窦壁扩张而牵张压力感受器所致     

Amiloride和Ni2+抑制缺血/复灌引起的大鼠心肌细胞内钙的增加

本文旨在研究Na+/H+交换以及Na+/Ca2 +交换对模拟缺血 /复灌引起的大鼠心肌细胞内游离钙水平变化的调节作用。分别利用模拟缺血液和正常台氏液对大鼠心肌细胞进行缺血 /复灌处理 ,在缺血期间分别应用Na+/H+交换抑制剂阿米洛利 (amiloride)、Na+/Ca2 +交换抑制剂NiCl2 以及无钙液 ,观察它们对细胞内游离Ca2 +浓度变化的影响。利用Zeiss LSM 5 10激光共聚焦显微镜检测、采集细胞内游离Ca2 +的指示剂Fluo 3 AM的荧光信号 ,计算出相对于正常(缺血前 )的相对荧光强度 ,以表示胞内游离Ca2 +浓度的变化。结果显示 ,模拟缺血引起大鼠心肌细胞内游离Ca2 +持续上升 ,缺血前的相对荧光强度值为 10 0 % ,模拟缺血 5min后为 140 3± 13 0 % (P <0 0 5 ) ,复灌 15min后为 142 8±15 5 % (P <0 0 5 )。经 10 0 μmol/Lamiloride、5mmol/LNiCl2 和无钙液分别预处理 ,模拟缺血 5min后的相对荧光强度分别为 10 1 4± 16 3 % (P <0 0 5 )、110 4± 11 1% (P <0 0 5 )和 10 7 1± 10 8(P <0 0 5 ) ;复灌 15min后则分别为 97 8±14 3 % (P <0 0 5 )、10 6 2± 14 5 % (P <0 0 5 )和 10 6 6± 15 7(P <0 0 5 )。另外 ,与对照组细胞相比 ,再灌注期间NiCl2和无钙液处理的细胞钙振荡的产生幅度明显减弱 ,amilorid     

牵张所致心室不应性变化的频率依赖现象及其机制

本文旨在探讨牵张所致麻醉兔心室不应性变化的频率依赖现象及其机制。采用部分夹闭兔主动脉根部以增加左室后负荷的在体心脏模型 ,观察不同起搏周长时左室后负荷增加后心室有效不应期 (effectiverefractoryperi od ,ERP)的变化及链霉素对此的影响。结果显示 ,当起搏周长为 10 0 0和 5 0 0ms时 ,左室收缩期内压增加后的心室ERP较主动脉夹闭前略有缩短 ( 10 0 0ms,3± 2ms,1 5 % ;5 0 0ms,7± 3ms,4 0 % .P >0 0 5 ) ,而起搏周长 3 0 0和 2 0 0ms时则明显缩短 ( 3 0 0ms,2 1± 5ms ,17 0 % ;2 0 0ms,19± 3ms,18 8% P <0 0 1) ;( 2 )链霉素可有效消除基本驱动周长 3 0 0和 2 0 0ms时左心室后负荷增加对ERP的影响 (P >0 0 5 ,组内比较 )。结果提示 ,牵张所致心室ERP变化具有快频率依赖性 ,且链霉素通过抑制牵张激活性离子通道的活化而消除这种电生理效应     

慢性捆绑紧张致大鼠记忆受损及海马神经元NOS和Tau5的变化——组织化学与免疫组织化学研究

目的　探讨慢性捆绑紧张对大鼠学习与记忆的影响及其可能的神经生物学机制。方法　选雄性 SD大鼠 18只 ,其中 10只为实验组 ,8只为对照组。对实验组采用捆绑器每天捆绑 6 h,2 1天后用 Y迷宫对两组大鼠进行行为检测 ,并用酶组织化学和免疫组织化学方法观察海马内一氧化氮合酶 (NOS)阳性神经元及 Tau蛋白 (Tau5 )免疫反应的变化。结果　 1实验组大鼠学会躲避电击的次数为 35 .7± 7.5次 ,对照组为 2 5 .2± 2 .8次 ,P<0 .0 1;2海马右侧 CA1 区 NOS阳性神经元数目 ,对照组 2 7.2± 4.8个 ,实验组 38.9± 6 .4个 ,P<0 .0 5 ;NOS阳性神经元胞质平均灰度 ,对照组 170 .7± 11.8,实验组 16 2 .5± 12 .6 ,P<0 .0 5 ;3海马右侧 CA3 区 Tau5免疫阳性产物的平均灰度 ,对照组 16 1.7± 12 .8,实验组 145 .8± 13.8,P<0 .0 5。结论　一氧化氮产生过多而导致的神经毒性作用可能是慢性捆绑紧张导致动物学习与记忆功能受损的部分神经生物学机制 ,而海马 CA3 区神经元内所有的 Tau蛋白 (磷酸化及非磷酸化的 Tau)的总量增多说明 Tau蛋白的变化可能在此过程中起一定的作用。     

延髓腹外侧头端区注射肾上腺髓质素对大鼠血压、心率和肾交感神经活动的影响

本研究在 3 4只麻醉Sprague Dawley大鼠观察了延髓腹外侧头端区内微量注射肾上腺髓质素 ( 10μmol/L ,2 0 0nl)对平均动脉压 (MAP)、心率 (HR)和肾交感神经放电 (RSNA)的影响。实验结果如下 :( 1)延髓腹外侧头端区内微量注射肾上腺髓质素可引起MAP、HR、和RSNA明显增加 ,分别由 99 0 9± 3 3 2mmHg ,3 70 78± 7 84bpm和 10 0± 0 %增至 113 5 7± 3 64mmHg (P <0 0 0 1) ,3 83 2 8± 7 3 8bpm (P <0 0 0 1)和 12 3 72±2 74% (P <0 0 0 1) ;( 2 )降钙素基因相关肽受体阻断剂CGRP8 3 7( 10 0 μmol/L ,2 0 0nl)不能阻断肾上腺髓质素的上述效应 ;( 3 )静脉注射NO前体L 精氨酸 ( 10 0mg/kg ,0 2ml)可消除肾上腺髓质素的上述效应。以上结果提示 ,肾上腺髓质素作用于延髓腹外侧头端区可产生显著的心血管作用 ,此作用不是由降钙素基因相关肽受体介导 ,但可被NO所阻断     

肾上腺髓质素对大鼠损伤性心肌肌浆网功能的改善

通过观察下述五个指标,评价肾上腺髓质素(adrenomedullin,Adm)对大鼠损伤性心肌肌浆网功能的改善程度左心室压力最大变化速率(±dp/dtmax)、肌浆网钙摄取和释放及钙泵活性.皮下注射异丙肾上腺素(isoproterenol,ISO,69μmol/kg体重)制备大鼠心肌损伤坏死模型.摘取心脏后用Adm灌流,观察左心室压力最大变化速率(±dp/dtmax);制备并提纯心肌肌浆网(sarcoplasmicreticulum,SR)膜,测定SRCa2+摄取和释放速率、SR钙泵活性和钙通道蛋白～3H-ryanodine受体的最大结合量.结果发现,5×10-5mol/LAdm灌流能使ISO损伤的大鼠心脏左室±dp/dtmax分别增加16.9%(2?135±281vs1?980±302)和29.2%(1?375±267vs1?064±355,均P<0.05);SRCa2+摄取和释放率分别增加23.0%(15.0±1.4vs12.2±1.2)和43.5%(6.6±1.0vs4.6±0.6,均P<0.01);SRCa2+-ATPase活性和～3H-ryanodine受体最大结合量(Bmax)分别增加24.2%(P<0.01)和42.2%(P<0.05).提示Adm对ISO诱导的大鼠心肌损伤具有保护作用,其机制可能与Adm增加SRCa2+-ATPase活性、增加～3H-ryanodine所致SRCa2+摄取和释放升高有关.外源性给予Adm对损伤心肌可能具有临床治疗作用.     

马麝生理生化正常值的测定

对甘肃兴隆山国家级自然保护区人工养麝场的马麝 3项临床指标、6项血液生理指标和 1 3项血清生化指标进行了测定。结果表明 ,成麝体温为 ( 39 94± 0 87)℃ ,呼吸 ( 1 2 4 67± 1 7 2 9)次 min ,心率( 1 2 4 67± 1 7 2 9)次 min;红细胞 ( 2 0 1 9± 4 95 )× 1 0 12 L ,白细胞计数 ( 1 2 4 76± 5 4 96)× 1 0 9 L ,PCV 0 5 78±0 0 3;血糖 ( 8 2 64± 2 0 5 6)mmol L ,K( 4 4 85± 0 2 4 3)mmol L ,Na ( 1 38 2± 1 6 64)mmol L ,Ca ( 2 75 8± 0 31 )mmol L ,总蛋白 ( 74 70 5± 8 1 5 9)g L ,白蛋白 ( 5 2 77± 2 2 32 )g L ,球蛋白 ( 2 1 4 8± 7 2 76)g L等。     

Differential change in expression of pulmonary ET-1 and eNOS in rats after chronic left ventricular pressure overload

Pressure overload in the left ventricle of the heart follows a chronic and progressive course, resulting in eventual left heart failure and pulmonary hypertension (PH). The purpose of this research was to determine whether a differential pulmonary gene change of endothelin (ET)-1 and endothelial nitric oxide synthase (eNOS) occurred in adult rats with left ventricular overload. Eight groups of eight rats each were used (four rats with banding and four rats with sham operations). The rats underwent ascending aortic banding for 1 day, 2 weeks, 4 weeks, and 12 weeks before sacrifice. Significant medial hypertrophy of the pulmonary arterioles developed in two groups (4 and 12 weeks). Increased pulmonary arterial pressures were noted in three groups (1 day, 4 weeks, and 12 weeks). The aortic banding led to significant increases in pulmonary preproET-1 messenger RNA (mRNA) at 1 day and 12 weeks, and in pulmonary eNOS mRNA at 1 day and 12 weeks. In addition, there was increased pulmonary eNOS content at 1 day and 12 weeks in the banded rats, and increased lung cGMP levels were observed at 1 day. Increased lung ET-1 levels were also noted at 1 day (banded, 310 +/- 12 ng/g protein; sham, 201 +/- 12 ng/g protein; P < 0.01), 4 weeks (banded, 232 +/- 12 ng/g protein; sham, 201 +/- 12 ng/g protein; P < 0.01) and 12 weeks (banded, 242 +/- 12 ng/g protein; sham, 202 +/- 12 ng/g protein; P < 0.01). This indicates that the upregulated expression of ET-1 developed at least 4 weeks before eNOS expression in the course of PH, and, thus, medication against ET-1 could play a crucial role in treating PH with cardiac dysfunction secondary to aortic banding.     

Acute effects of methoxamine on left ventricular-arterial coupling in streptozotocin-diabetic rats: a pressure-volume analysis

We determined the acute effects of methoxamine, a specific alpha1-selective adrenoceptor agonist, on the left ventricular-arterial coupling in streptozotocin (STZ)-diabetic rats, using the end-systolic pressure-stroke volume relationships. Rats given STZ 65 mg x kg(-1) iv (n = 8) were compared with untreated age-matched controls (n = 8). A high-fidelity pressure sensor and an electromagnetic flow probe measured left ventricular (LV) pressure and ascending aortic flow, respectively. Both LV end-systolic elastance E(LV,ES) and effective arterial elastance Ea were estimated from the pressure-ejected volume loop. The optimal afterload Q(load) determined by the ratio of Ea to E(LV,ES) was used to measure the optimality of energy transmission from the left ventricle to the arterial system. In comparison with controls, diabetic rats had decreased LV end-systolic elastance E(LV,ES), at 513 +/- 30 vs. 613 +/- 29 mmHg x mL(-1), decreased effective arterial elastance Ea, at 296 +/- 20 vs. 572 +/- 48 mmHg x mL(-1), and decreased optimal afterload Q(load), at 0.938 +/- 0.007 vs. 0.985 +/- 0.009. Methoxamine administration to STZ-diabetic rats significantly increased LV end-systolic elastance E(LV,ES), from 513 +/- 30 to 602 +/- 38 mmHg x mL(-1), and effective arterial elastance Ea, from 296 +/- 20 to 371 +/- 28 mmHg x mL(-1), but did not change optimal afterload Q(load). We conclude that diabetes worsens not only the contractile function of the left ventricle, but also the matching condition for the left ventricular-arterial coupling. In STZ-diabetic rats, administration of methoxamine improves the contractile status of the ventricle and arteries, but not the optimality of energy transmission from the left ventricle to the arterial system.     

Effect of losartan on the Na+/Ca2+ exchanger in left ventricle of the insulin resistant and hypertensive hHTg rat

As the Na+/Ca2+ exchanger plays an important role in the regulation of myocyte contractility, it has been suggested that alterations in this system might be involved in the development of insulin resistance and/or diabetes-induced myocardial alterations. Moreover, gene expression and function of the Na+/Ca2+ exchanger in states of combined hypertension and insulin resistance is of a special interest. Thus, we used hereditary hypertriglyceridemic (hHTg) rat (a model of genetically induced insulin resistance and hypertension) to study the effect of losartan, the blocker of type 1 angiotensin receptors, on the Na+/Ca2+ exchanger in the rat heart. We found that gene expression, but not activity of the Na+/Ca2+ exchanger was decreased in the left ventricle of hHTg rats when compared to their normotensive mates. No changes were observed in the right ventricle. In addition, losartan decreased mRNA levels of the Na+/Ca2+ exchanger in the left, but not in the right ventricle of normotensive rats. In hHTg rats, losartan had no effect on the gene expression of this transporter. Our results point to different modulatory pathways of Na+/Ca2+ exchanger in normotensive and hHTg rats.     

Blood flow measurements by the reference sample method with microsphere injection in to the aorta: an accurate and easy approach.

The validity of hemodynamic measurements by the reference sample method with microspheres injection into the aorta, via a carotid artery catheter, was evaluated in rats and compared with the results obtained after left ventricle injection. In the aorta injection group, a good mix of microspheres was observed in 83% of the animals. Moreover, a symmetrical distribution of microspheres was observed in 10 out of 12 rats (83%). An excellent correlation between right and left kidney-testes blood flows was observed (r = 0.93 and 0.96, respectively; P less than 0.01). Mean arterial pressure was not modified during microspheres injection into the aorta. Cardiac output (104 +/- 26 vs 101 +/- 23 ml/min, NS) and portal blood flow (14.2 +/- 3.3 vs 13.5 +/- 2.2 ml/min, NS) were similar after aorta and left ventricle injections series, respectively. Our results indicate that the injection of microspheres into the aorta is an adequate and easy approach to systemic and splanchnic hemodynamic measurements. This approach could be a good alternative to left ventricle injection of microspheres in experimental studies in rats.     

Myocardial perfusion abnormalities in patients with active acromegaly.

Cardiomyopathy is often seen in patients with a long history of acromegaly. In order to screen for perfusion abnormalities, patients with active acromegaly without evidence for coronary heart disease were examined by single photon emission computed tomography (SPECT). The study included a group of 11 strictly selected patients with active acromegaly (7 males and 4 females; age 51 +/- 12 y [mean +/- S.D.]) with elevated age-adjusted IGF-I levels (IGF-I 569 +/- 193 micro g/l; GH 31.2 +/- 56.3 micro g/l) compared to an age- and sex-matched non-acromegalic control group with comparable muscle mass index of the left ventricle (126 +/- 41 active vs. 122 +/- 33 g/m 2 control group) and body mass index (26.6 +/- 2.7 vs. 27.0 +/- 5.0 kg/m 2). To address this issue, myocardial perfusion was investigated by single photon emission computed tomography (SPECT) using a triple head gamma-camera. 70 MBq 201TlCl was injected, and post-stress (from bicycle ergometer) images were obtained. Images were interpreted quantitatively by bull's eye polary map (16 regions of the left ventricle) and were compared to the control group. In the patients with active acromegaly, the mean nuclide uptake of the 16 regions of the left ventricle after bicycle stress examination was lower than in the control group (82.99 +/- 2.85 active vs 85.48 +/- 1.29 control group, p < 0.01). Non-homogeneity of nuclide uptake was defined as the standard deviations of the 16 regions and was higher in patients with active acromegaly (11.11 +/- 2.35 active vs. 8.77 +/- 1.39 control group, p < 0.01). In conclusion, myocardial perfusion is impaired in patients with active acromegaly, thus representing an early stage of cardiac involvement in acromegaly that may be directly mediated by growth hormone excess.     

Regulation of cardiac adrenomedullin-mRNA in different stages of experimental heart failure

Adrenomedullin (AM) is a peptide hormone with vasodilating and natriuretic properties. AM plasma concentrations are elevated in heart failure. Whether cardiac AM-mRNA synthesis is increased in heart failure is not known. We measured AM-mRNA/GAPDH-mRNA in all four heart chambers in compensated and overt heart failure in rats with two different sizes of aortocaval shunt. Left and right atrial AM-mRNA expressions were unchanged in both heart failure models. Similarly, left and right ventricular AM-mRNA expressions were unchanged in compensated heart failure. In overt heart failure, however, the AM-mRNA expression was significantly increased in the left ventricle (145+/-20 vs. 100+/-3% of control, p<0.05). The right ventricular AM-mRNA expression was significantly increased only in a subgroup of animals with pulmonary congestion (lung weight >2.0 g, 141+/-16 vs. 100+/-11% of control, p<0.05). Ventricular AM concentrations were elevated in both ventricles in overt heart failure. AM plasma concentrations were significantly higher in the subgroup with pulmonary congestion than in rats with compensated heart failure (496+/-95 vs. 143+/-7 pmol/l, p<0.01). These data indicate that ventricular AM-mRNA expression and AM concentrations were upregulated only in advanced stages of heart failure. However, the exact contribution of cardiac AM synthesis to the increased AM plasma levels remains to be established.     

Expression and localization of angiotensin subtype receptor proteins in the hypertensive rat heart

The cellular localization of the AT(2) receptor and the regulation of its expression in hypertrophied left ventricle are not well known. We compared the expression of the cardiac AT(1) and AT(2) receptor in spontaneously hypertensive rats/Izumo strain (SHR/Izm) and Wistar Kyoto rats/Izumo strain (WKY/Izm), ages 4, 12, and 20 wk, by means of immunohistochemistry and Western blot analysis. In SHR/Izm, compared with WKY/Izm, blood pressure (161 +/- 2 vs. 120 +/- 2 mmHg at 12 wk, P 相似文献   

Left ventricular rupture threshold during the healing phase after myocardial infarction in the dog

The mechanical resistance of the infarcted left ventricle to rupture, or rupture threshold, was measured by the balloon technique 1-42 days after left anterior descending coronary artery ligation in 70 dogs: 26 without infarction (18 sham, 8 with ligation) and 44 with infarction. Rupture threshold in noninfarcted hearts was higher than in infarcted hearts (1168 +/- 165 (SD) vs. 754 +/- 223 mmHg (1 mmHg = 133.32 Pa), p less than 0.001) and did not change over 6 weeks. In contrast, rupture threshold in infarcted hearts decreased (p less than or equal to 0.05) after 14 days, the average value for 21-42 days being less than that for 1-14 days: 577 +/- 140 vs. 867 +/- 191 mmHg, p less than 0.001. Passive left ventricular stiffness in infarcted hearts was higher than for noninfarcted hearts throughout the 6 weeks during early filling (11.1 +/- 3.9 vs. 7.1 +/- 1.4 mmHg/mL, p less than 0.001) but decreased (p less than or equal to 0.05) after 14 days during the prerupture phase (11.3 +/- 5.3 vs. 6.2 +/- 3.0 mmHg/mL, p less than 0.005). Between 7 and 42 days, the infarct zone showed marked increase in hydroxyproline (10.0 +/- 2.0 vs. 48.8 +/- 19.7 mg/g dry weight, p less than 0.001), shrinkage (infarct size, 25 +/- 9 vs. 9 +/- 5% of the left ventricle, p less than 0.005), and thinning (infarct to normal wall thickness ratio, 0.83 +/- 0.11 vs. 0.51 +/- 0.09, p less than 0.001) but little further stretching (expansion index or the ratio of lengths of infarcted and noninfarcted segments, 1.14 +/- 0.10 vs. 1.28 +/- 0.17, p less than 0.2). A mild decrease (p less than 0.05) in left atrial pressure and increase (p less than 0.05) in diastolic area and fractional change in area (two-dimensional echocardiography) were detected at 6 weeks. The late decrease in rupture threshold and prerupture stiffness of the infarcted left ventricle and thinning of the scar suggest a late decrease in mechanical strength and resistance of the infarcted left ventricle to distension.