Changes of fibronectin in the right and left ventricles of rats exposed to chronic normobaric hypoxia.

Changes of fibronectin (FN) in the right and left ventricles of adult rats exposed to chronic normobaric hypoxia were observed by a peroxidase immunohistochemical stain technique and analyzed quantitatively by a point counting method. Fifty-six rats were randomly divided into control groups of day 0 (immediately prior to the experiment), day 5, day 15, and day 30 and hypoxia groups of day 5, day 15, and day 30. Rats of the hypoxia groups were put into a normobaric hypoxia chamber with oxygen concentration adjusted to 10 percent. The rats of the control groups breathed room air. From day 5 on, the ratio of the weight of the right ventricle (RV) to that of the left ventricle (LV) plus interventricular septum (SP), RV/(LV+SP), and the ratio of the weight of the right ventricle (RV) to the body weight (BW), RV/BW, in the hypoxia groups increased significantly as compared with those of the control groups. The amount of immunoreactive FN in the right ventricle increased significantly in the hypoxia groups after exposure to hypoxia environment for 15 days (10.31% +/- 2.15%, mean +/- S.D.) and for 30 days (9.55% +/- 1.65%) as compared with those in the day 0 control group (3.05% +/- 1.15%, p < 0.01), the day 15 control group (3.26% +/- 0.83%, p < 0.01), and the day 30 control group (3.19% +/- 0.51%, p < 0.01). However, there were no significant changes in the amount of immunoreactive FN in the left ventricle of the hypoxia groups as compared with the control groups. These results suggest that chronic hypoxia may lead to an increase of FN in the hypertrophied right ventricle but not in the left ventricle, which indicates that pulmonary hypertension induced by chronic hypoxia rather than chronic hypoxia itself is a major cause for the increase of FN in the myocardium. The increased FN in the right ventricle may accelerate the accumulation of collagen and, in turn, contribute to the increase of the myocardial stiffness and eventually to the diastolic dysfunction of the hypertrophied right ventricle induced by chronic hypoxia.     

Effect of hemodialysis on left ventricular function. Dissociation of changes in filling volume and in contractile state

Prior studies of the effect of hemodialysis on left ventricular function have not distinguished between the removal of uremic toxins and the change in cardiac filling volume. To separate these effects, left ventricular function was examined by serial echocardiography in five stable hemodialysis patients before and after three different dialysis procedures: (a) hemodialysis with volume Loss, (b) ultrafiltration (volume loss only), and (c) hemodialysis without volume loss. The patients were similarly studied under control conditions and after increased (5 degrees of head-down tilt for 90 min) and decreased (lower body negative pressure) cardiac filling volume. After hemodialysis with volume loss, end-diastolic volume (EDV) decreased from 167 to 128 ml (P less than 0.001) and end-systolic volume (ESV) decreased from 97 to 51 ml (P less than 0.001) without a change in stroke volume (SV). Ejection fraction increased from 42 to 52% (P less than 0.001) and mean velocity of circumferential fiber shortening (VCF) increased from 0.61 to 1.04 circumferences (circ)/s (P less than 0.001). After ultrafiltration, EDV decreased from 167 ml to 124 ml (P less than 0.001) and SV from 73 ml to 39 ml (P less than 0.001), without significant changes in ESV or VCF. In contrast to the maneuvers in which volume loss occurred, after hemodialysis without volume loss ESV decreased from 95 to 66 ml (P less than 0.001) and SV increased from 74 ml to 97 ml (P less than 0.001) without changes in EDV. EF increased from 44 to 59% (P less than 0.001) and VCF increased from 0.64 to 1.26 circ/s (P less than 0.001). Ventricular function curves plotted from data obtained under conditions of altered cardiac filling volume before and after the three dialysis maneuvers demonstrate that ultrafiltration produced a pure Frank-Starling effect, while hemodialysis with or without volume loss produced a shift in the ventricular function curves, which demonstrated an increase in the contractile state of the left ventricle. The changes in left ventricular function produced by regular hemodialysis are the combined effects of a decrease in EDV and an increase in the contractile state of the left ventricle.     

Synthesis and secretion of atrial natriuretic factor during chronic hypoxia: a study in the conscious instrumented rat

1. To investigate the mechanisms leading to enhanced synthesis and release of atrial natriuretic factor during chronic hypoxia, we measured immunoreactive plasma atrial natriuretic factor, blood gases, packed cell volume, pulmonary artery pressure and systemic artery pressure in male Sprague-Dawley rats exposed to 1, 2 or 3 weeks of normobaric hypoxia. Rats were implanted with pulmonary and carotid artery catheters and studied conscious, 23 h after return to hypoxia. 2. The concentration of atrial natriuretic factor messenger RNA was measured in the right and left ventricular free walls of rats exposed to 3 weeks of hypoxia and in normoxic control rats. 3. There was a trend for plasma atrial natriuretic factor to increase with the duration of exposure to hypoxia but only the 3-week hypoxic rats had a significantly higher level (1080 +/- 193 pg/ml) than the normoxic control rats (318 +/- 46 pg/ml, P less than 0.05, mean +/- SEM). When all the data from normoxic and hypoxic rats were considered together, plasma atrial natriuretic factor was positively correlated with packed cell volume (r = 0.66, P less than 0.001), pulmonary artery pressure (r = 0.68, P less than 0.002), and the index of right ventricular hypertrophy (r = 0.54, P less than 0.01), but after analysis of partial correlation, packed cell volume was the only independent contributing factor to the variance in the level of plasma atrial natriuretic factor (r2 = 0.24).(ABSTRACT TRUNCATED AT 250 WORDS)     

应用速度向量显像技术评价正常人及肥厚型心肌病患者的心肌扭转

目的 应用速度向量显像技术研究正常人和肥厚型心肌病(HCM)患者的左心室心肌扭转方式.方法 对25例健康志愿者(对照组)和41例HCM患者(HCM组)行常规超声心动图检查,采集二尖瓣水平短轴观、心尖水平短轴观、心尖四腔观及心尖二腔观二维图像,得到左室舒张末期容积、收缩末期容积、左室射血分数和室壁厚度.脱机分析得到收缩期心底部心内膜、心外膜和心尖部心内膜、心外膜的扭转速度峰值及扭转位移峰值,并分别计算心底部内外膜扭转速度/位移差值及心尖部内外膜扭转速度/位移差值.结果 收缩期心室扭转在心底部呈顺时针,在心尖部则呈逆时针,心尖部扭转幅度显著大于心底部(P＜0.05或P＜0.001),心内膜扭转显著大于心外膜(P＜0.01或P＜0.001).扭转速度-时间曲线由一个收缩期峰和两个舒张期峰组成,扭转位移- 时间曲线由一个舒张末期的小峰和一个收缩期的大峰组成.HCM组心底部呈不对称性肥厚,在显著肥厚的节段,HCM组心肌内外膜扭转速度/位移差值显著大于对照组(P＜0.01或P＜0.001).结论 速度向量显像技术能够简便准确地评价心室扭转,并能够发现HCM患者内外膜心肌扭转的不协调性.     

Beneficial effect of beta-adrenergic blockade on left ventricular function in haemodialysis patients

Congestive heart failure is a common and serious complication in patients undergoing chronic dialysis. However, there have been no studies on preferential medical therapies to improve left ventricular function in haemodialysis patients. Beta-blocker treatment is known to improve left ventricular function in patients with dilated cardiomyopathy; moreover, plasma levels of noradrenaline and natriuretic peptides are sensitive markers of left ventricular dysfunction. The present study investigated whether beta-blocker treatment could improve left ventricular function in haemodialysis patients with a dilated left ventricle. Our study group comprised 14 haemodialysis patients with a dilated left ventricle, who had undergone maintenance haemodialysis for a mean of 11 years. The following haemodynamic parameters were evaluated before and after 4 months of treatment with the beta-blocker metoprolol: left ventricular dimension at end-systole and end-diastole, and fractional shortening. Plasma levels of noradrenaline, atrial natriuretic peptide and brain natriuretic peptide were also determined. Dry body weight and haemoglobin concentration showed no significant change after compared with before treatment with metoprolol. Heart rate decreased significantly, from 79+/-9 beats/min to 69+/-9 beats/min, but systolic blood pressure remained unchanged. The left ventricular dimension both at end-systole and at end-diastole was decreased, and fractional shortening increased significantly. Plasma levels of noradrenaline did not change significantly, but those of atrial natriuretic peptide and brain natriuretic peptide decreased markedly [from 100+/-89 pg/ml to 46+/-29 pg/ml (P=0.0051) and from 549+/-516 pg/ml to 140+/-128 pg/ml (P=0.0035) respectively]. In conclusion, beta-blocker therapy with metoprolol can markedly attenuate left ventricular remodelling and decrease the plasma levels of natriuretic peptides in haemodialysis patients with a dilated left ventricle.     

Alteration of collagen phenotypes in ischemic cardiomyopathy.

Ischemic cardiomyopathy refers to a significant impairment of left ventricular function, a condition resulting from atherosclerotic coronary artery disease. The left ventricular ejection fraction is usually 35% or less, and electron microscopy shows an increased deposition of collagen in the space between the capillaries and the myocytes. The present study shows the alteration in collagen concentration and phenotypes in ischemic cardiomyopathy, and the effect captopril treatment has on these parameters. In patients with ischemic cardiomyopathy, collagen concentration estimated from hydroxyproline increased from 7.96 +/- 1.24 mg/g to 13.9 +/- 1.30 mg/g, P less than 0.05. Ischemic cardiomyopathic patients given captopril therapy had a significantly lower collagen concentration of 10.03 +/- 1.46 mg/g, P less than 0.05. The collagen type I:III ratio decreased from 1.93 +/- 0.52 to 1.23 +/- 0.27 in patients with ischemic cardiomyopathy. Of these patients, those receiving captopril had a collagen type I:III ratio of 1.49 +/- 0.38, which did not differ significantly from the ratio of individuals with normal myocardium. There was no significant difference in type I collagen concentration in the myocardium of normal individuals, patients with ischemic cardiomyopathy, and patients with ischemic cardiomyopathy receiving captopril therapy. The type III collagen concentration increased significantly from 2.56 +/- 0.21 mg/g in normal myocardium to 6.10 +/- 0.58 mg/g in ischemic cardiomyopathic myocardium. Patients receiving captopril had a myocardial collagen type III concentration of 4.87 +/- 0.64 mg/g, which was significantly lower than that found in patients with ischemic cardiomyopathy. An increased deposition of type III collagen may be partly responsible for altering the compliance of the myocardium, resulting in dilatation of the heart and possibly leading to eventual heart failure.     

Biochemical evidence for an increased and progressive deposition of collagen in lungs of patients with pulmonary fibrosis

To assess the role of changes in lung collagen in pulmonary fibrosis, the content of this protein was measured in biopsy and autopsy lung from patients with cryptogenic fibrosing alveolitis (CFA), a fibrotic lung disorder of unknown cause. The collagen concentration was measured in lung samples from 21 patients with CFA (14 autopsy and seven open-lung biopsy) and 17 normal subjects; total lung collagen was determined in the right lung of 10 patients who died from CFA and the results were compared with those from 10 normal lungs. There was a wide variation in the collagen concentrations but the mean value (+/- SEM) for patients with CFA (217 +/- 13 mg/g dry weight) was significantly higher (P less than 0.02) than that of the controls (155 +/- 15 mg/g dry weight). The mean collagen concentration of the autopsy samples (243 +/- 20 mg/g dry weight) was significantly higher (P less than 0.05) than that of the biopsy samples (165 +/- 24 mg/g dry weight). The mean total collagen was markedly raised (P less than 0.001) in right lungs of patients with CFA (32.5 +/- 4.3 g) compared with normal lungs (14.0 +/- 1.1 g). When corrected for the predicted lung volume this difference in total lung collagen remained statistically significant (P less than 0.01, mean for patients 4.7 +/- 0.7 mg/ml, controls 2.3 +/- 0.2 mg/ml). These results demonstrate an increased deposition of lung collagen in this form of pulmonary fibrosis. They also suggest that there is a greater collagen concentration in lungs of patients with later disease, indicating a progressive deposition of collagen during the course of the disease.     

肥厚型心肌病患者左心室舒张早期血流传播速度的变化及其临床价值

目的　检测肥厚型心肌病(HCM)左心室舒张早期血流传播速度(VP)的变化,探讨其临床价值。方法　选择HCM患者52例和健康志愿者 30 例,应用彩色 M型多普勒超声测量 VP。结果　与正常组比较,HCM组VP 显著减小( t=8.42,P<0.001),Spearman 等级相关分析显示VP 与左心室舒张功能分级之间存在良好相关性( r=-0.71,P<0.001)。结论　HCM患者VP 较正常人减小,且随着左心室舒张功能减低程度的加重而减小,为左心室舒张功能的评估提供了一个更好的途径。     

真武汤冲剂对压力负荷性心肌肥厚的影响

目的 观察真武汤冲剂对大鼠慢性压力负荷性心肌肥厚的影响.方法 租用广州呼吸疾病研究所实验室,将SD大鼠随机(随机数字法)分为3组,假手术组8只,手术组和中药组各15只.手术组和中药组行腹主动脉缩窄术,制作心肌肥厚模型.16周行心脏超声,确定术后心肌肥厚,中药组加用真武汤混合饲料喂养,24周时用高频超声测定各组心脏质量、结构和功能,以及心肌组织Mas-son染色,测定总胶原容积百分比(CVF-T)和无冠状动脉小血管视野胶原容积百分比(CVF-NV).各组数据采用SNK法进行两两比较.结果 手术组心脏质最增加,以左室增加为明显(P＜0.05),心脏增大,以舒张期室间隔(IVSd)和左室后壁(LVPWd)为明显(P＜0.01),心功能明显降低(P＜0.05);中药组相对于手术组,心脏质量减轻(P＜0.01),体积缩小,以IVSd和收缩期左室后壁(LVPWs)为明显(P＜0.01),心功能改善(P＜0.05).病理分析手术组间质和胶原增生明显,中药组有不同程度改善,CVF-T和CVF-NV较手术组组明显减少(P＜0.01),与假手术组相比,差异尤统计学意义(P＞0.05).结论 真武汤冲剂能够减少压力负荷性大鼠的心脏质量、体积,改善心功能,抑制胶原纤维增生,逆转心肌肥厚.     

步行运动训练对慢性充血性心衰患者左室结构和血浆B型脑利钠肽水平的影响

目的 观察步行运动训练对慢性充血性心衰(CHF)患者左心室结构和血浆B型脑利钠肽(BNP)水平的影响,探寻运动训练的意义.方法 将223例心功能分级Ⅱ～Ⅲ级的CHF患者分为处方康复组、非处方康复组和对照组,均给予基础药物治疗,处方康复组和非处方康复组按不同的要求进行康复训练.入选时及6个月随访时对各组进行血压测量、6 min步行距离测量和血浆BNP水平测定,并进行心脏超声检查观察左室射血分数(LVEF)和左室舒张末期内径(LVEDd)的变化.结果 入选时,各组血压、6 min步行距离、左室功能及血浆BNP水平比较,差异均无统计学意义.6个月随访时,处方康复组再次住院例次和其中因心功能恶化再次住院比率明显低于非处方康复组和对照组(P<0.05);与运动训练前及其他2组比较,血浆BNP水平明显下降,6 min步行距离和LVEF明显提高(P<0.01),LVEDd则无明显变化.结论 步行运动训练可改善CHF患者的运动耐力,降低血浆BNP水平,且安全性好,但短期内对左室的重构尚无积极影响.     

步行运动训练对慢性充血性心衰患者左室结构和血浆B型脑利钠肽水平的影响

目的 观察步行运动训练对慢性充血性心衰(CHF)患者左心室结构和血浆B型脑利钠肽(BNP)水平的影响,探寻运动训练的意义.方法 将223例心功能分级Ⅱ～Ⅲ级的CHF患者分为处方康复组、非处方康复组和对照组,均给予基础药物治疗,处方康复组和非处方康复组按不同的要求进行康复训练.入选时及6个月随访时对各组进行血压测量、6 min步行距离测量和血浆BNP水平测定,并进行心脏超声检查观察左室射血分数(LVEF)和左室舒张末期内径(LVEDd)的变化.结果 入选时,各组血压、6 min步行距离、左室功能及血浆BNP水平比较,差异均无统计学意义.6个月随访时,处方康复组再次住院例次和其中因心功能恶化再次住院比率明显低于非处方康复组和对照组(P<0.05);与运动训练前及其他2组比较,血浆BNP水平明显下降,6 min步行距离和LVEF明显提高(P<0.01),LVEDd则无明显变化.结论 步行运动训练可改善CHF患者的运动耐力,降低血浆BNP水平,且安全性好,但短期内对左室的重构尚无积极影响.     

Relationship Between Beat-to-Beat Changes in Hemodynamic State and Action Potential Duration of the Left Ventricle During Rapid Ventricular Pacing in Man

A relationship between beat-to-beat changes in hemodynamic state and action potential duration (APD) of the left ventricle was studied by pacing the right ventricle with a constant cycle length (400 msec) for 3 minutes and recording simultaneously the intraarterial pressure and left ventricular monophasic action potential in 16 patients (mean age 51 +/- 8 years) undergoing routine cardiac catheterization. The APD measured at the point of 90% repolarization (APD-90) shortened gradually from a baseline value of 305 +/- 25 msec to a minimum of 246 +/- 25 msec (P less than 0.001) by 160 +/- 10 seconds after the onset of pacing. After reaching the minimum duration, the APD and blood pressure were measured from 30 consecutive beats. The magnitude of beat-to-beat variation in the APD was directly correlated to variation in the mean arterial blood pressure (r = 0.65, P less than 0.01). Beat-to-beat changes in hemodynamic and electrical state were related in that an increase of at least 10 mmHg in the blood pressure of one beat was associated with an increase in the APD of the concomitant beat by at least 5 msec. In six patients with ventriculoatrial dissociation during the rapid ventricular pacing, the sequential ventriculoatrial pacing decreased the beat-to-beat variation of APD from 2.8% +/- 1.4% to 0.8% +/- 0.7% (P less than 0.01) and variation of blood pressure from 6.4% +/- 3.2% to 1.4% +/- 0.9% (P less than 0.01). The observed association between beat-to-beat changes in hemodynamic state and APD of the left ventricle demonstrates that an immediate force-interval relationship exists in the human left ventricle.     

左室中段室壁缩短率早期评价高血压患者左室舒张功能

目的　评价左室中段室壁缩短（ｍｉｄｗａｌｌｆｒａｃｔｉｏｎａｌｓｈｏｒｔｅｎｉｎｇ,ＭＦＳ） 率评价高血压患者左室舒张功能的临床价值。方法　对２９２ 例原发性高血压患者进行二维及多普勒超声心动图观察,比较常规测量左室射血分数（ＥＦ）,短轴缩短率（ＦＳ）及左室中段室壁缩短率与左室舒张功能的关系。结果　分别以左室肥厚和左室向心性重构分组,发现左室中段室壁缩短率在肥厚组（Ｐ＝０ ．０１１３） 和向心性重构（ Ｐ＝ ０．００００１） 组明显降低,与舒张功能的改变一致,ＥＦ,ＦＳ在分组比较中无显著差异。多元逐步回归分析结果显示：左室中段室壁缩短率ＭＦＳ较ＥＦ,ＦＳ与舒张功能的关系更为密切。结论　超声测量左室中段室壁缩短率对于早期评估高血压患者舒张功能降低具有重要价值。     

Possibilities of Doppler echocardiography application in a patient on program hemodialysis

The aim of the study was to investigate the significance of Doppler echocardiography (echoCG) for assessment of "dry weight" in hemodialysis patients. 43 dialysis patients (20 men and 23 women aged 49 +/- 11 years), receiving 4-hour bicarbonate hemodialysis (HD) 3 times a week, were studied prior to and after HD procedures. M-mode echoCG was performed and left ventricular mass index (LVMI) and ejection fraction (EF) were calculated. Transmitral flow was assessed by Doppler echoCG. Peak velocity of early (E) and late (A) filling, E/A ratio, isovolumic relaxation time (IVRT) and early deceleration time (DT) were detected. Left ventricular hypertrophy (LVH) was detected in 37 (86.0%) patients. EF was lower than 45% in 4 patients. There was significant positive correlation between the amount of ultrafiltration (evaluated in per cents of body mass after HD) and deltaE (r = 0.59; p = 0.001), and there was found no correlation between the amount of ultrafiltration and deltaA. Patients with intradialytic hypotension had substantially higher DT than patients without one (238.7 +/- 64.3 vs. 168.6 +/- 51.2 mc, respectively, p < 0.001). "Dry weight" is associated with increase of early DT over the level normal for the age in hemodialysis patients with left ventricular hypertrophy. Patients with increased early DT are exposed to the high risk of intradialytic hypotension development.     

实时三维超声心动图评价正常儿童左、右心室容积及收缩功能

目的应用实时三维超声心动图(RT-3DE)比较正常儿童左、右心室容积及收缩功能。方法以RT-3DE采集192名年龄2个月～13岁8个月正常儿童的左、右心室的全容积数据,并按年龄分为Ⅰ～Ⅴ组。应用TomTec LV-A-nalysis及RV-function软件分析左、右心室舒张末期容积(EDV)、收缩末期容积(ESV),每搏输出量(SV),心室射血分数(EF)及心室容积收缩峰值速率(PSVR),对各年龄组左、右心室上述指标进行比较;同时对EDV与年龄及体格指标进行相关性和曲线估计回归分析。结果各年龄组中,RT-3DE测量左、右心室EDV差异均无统计学意义(P均>0.05),左、右心室ESV、SV及PSVR在部分年龄组中差异无统计学意义(P均>0.05),而左心室EF高于右心室,其在5个年龄组中差异均有统计学意义(P均<0.05)。左、右心室EDV与年龄、身高、体质量、体表面积呈正相关(r均>0.85,P均<0.001),曲线估计回归分析表明其相关性均以幂模式拟合最佳,其中与体表面积拟合的曲线最佳,回归方程分别为左心室EDV=38.58BSA1.41(r2=0.89,P<0.001)、右心室EDV=37.46BSA1.29(r2=0.85,P<0.001)。结论RT-3DE测量正常儿童左、右心室舒张末期容积相近,两侧心室存在泵血功能平衡,心室容积随年龄增长呈指数模式增长。     

Tissue specific modulation of beta-adrenoceptor number in rats with chronic hypoxia with an attenuated response to down-regulation by salbutamol

The number of beta-adrenoceptors and their affinity for the radioligand 125I-labelled cyanopindolol (125I-CYP) were measured in crude membrane preparations of left ventricle, spleen and lung from Wistar rats exposed to 28 days continuous hypoxia. beta-Adrenoceptor density in the left ventricle was not significantly altered after exposure to chronic hypoxia (binding site maxima, Bmax.: normoxic control 36 SEM 5, hypoxic 24.8 SEM 2 fmol/mg of protein). There was no change in beta-adrenoceptor number in the spleen in response to chronic hypoxia (Bmax.: normoxic control 76 SEM 19 fmol/mg of protein, hypoxic 80 SEM 15 fmol/mg of protein). Chronic hypoxia resulted in a significant increase in beta-adrenoceptor number in lung tissue (binding site maxima, Bmax.: normoxic control 406 (SEM 31) fmol/mg of protein; hypoxic 535 (SEM 30) fmol/mg of protein, P less than 0.01 without change in the dissociation constant (KD) of the radioligand. beta-Adrenoceptor subtypes in lung homogenates were studied by establishing displacement curves for 125I-CYP by ICI 118551 (a selective beta 2-antagonist). A significant difference was seen in the proportion of beta 1-/beta 2-adrenoceptor subtypes after hypoxia (normoxic control 66 SEM 2.5%, hypoxic 79 SEM 2.4% beta 2-adrenoceptors, P less than 0.01). alpha 1-Adrenoceptor number in lung membranes was measured with 125I-labelled 2-[beta-(4-hydroxyphenyl)ethylaminomethyl]tetralone (125I-HEAT). No difference was seen in the number of alpha 1-receptors in normoxia and in chronic hypoxia [Bmax.: normoxic control 48 (SEM 3), hypoxic 48 (SEM 5) fmol/mg of protein].(ABSTRACT TRUNCATED AT 250 WORDS)     

Regional effects of propranolol on intraventricular conduction in coronary artery disease.

In canines, propranolol slows conduction in acutely ischemic, but not in normal tissues. To determine propranolol effects on conduction in patients with coronary artery disease, we studied 7 patients after left anterior descending coronary artery bypass graft surgery. Bipolar electrodes were placed in the atrium, left ventricle (in the left anterior descending distribution), and right ventricle. On postoperative day 7, 3 mg propranolol were given intravenously. At a constant artrially paced rate, conduction intervals were measured from the earliest onset of the QRS in 3 simultaneously recorded surface electrocardiogram (ECG) leads to the major deflection of the electrogram recorded from each ventricle. Ten minutes after injection, conduction in the left ventricle was slowed by 4 +/- 0.3 msec (10 +/- 0.9%) and in the right ventricle by 0.4 +/- 0.3 msec (1 +/- 0.9%). QRS duration changed -1 msec (-0.8%). Stimulus to Q, a measure of propranol effect on A-V conduction, changed 16 +/- 2%. The difference in propranolol effects on left and right ventricles was significant (p less than 0.001). We suggest that in patients with coronary artery disease (1) propranolol has local anesthetic effects in slowing conduction; (2) the effects of propranolol vary with the region of ventricular myocardium; and (3) propranolol slows conduction more in the left than right ventricle. This difference may be due to potentiation of drug effects in left ventricular tissue that is abnormal due to chronic coronary artery disease.     

丹参对自发性高血压大鼠左室肥厚及心脏局部醛固酮的作用

目的　探究长期应用丹参对自发性高血压大鼠 (SHR)左室肥厚的预防作用及其可能机制———抑制心脏局部醛固酮的作用。方法　实验动物采用WKY大鼠及SHR ,部分SHR给予丹参注射液腹腔注射 12周。测量收缩压、左心室重量指数 ;左心室组织切片用HE染色和VanGieson染色 ,全自动图象分析系统进行分析。用放免法测定心脏局部醛固酮含量。各组指标进行显著性检验。结果　与WKY大鼠相比较 ,SHR有较高的血压 ,左室胶原含量及心脏局部醛固酮含量升高 (P <0 .0 5 )。而应用丹参后 ,除收缩压外各指标均有显著性下降 (P<0 .0 5 )。结论　丹参能预防自发性高血压大鼠左室肥厚 ,抑制左室胶原合成 ,其机制可能于抑制心脏局部醛固酮作用有关     

心脏声学造影对冠状动脉粥样硬化性心脏病并发症的诊断及心功能的评估

目的 通过左心声学造影(LVO)观察冠状动脉粥样硬化性心脏病(冠心病)患者室壁运动、左心室容量及并发症,综合讨论LVO在冠心病诊治中的应用价值.方法 回顾性研究2016年5月至2018年12月北京大学人民医院65例冠心病患者,采用双平面Simpson法测量收缩末期容积(ESV)、舒张末期容积(EDV)及左心室射血分数(...     

Left ventricular stiffness and chamber geometry in the pressure-overloaded hypertrophied heart.

Pressure-overloaded hypertrophy of the left ventricle (LV) was produced by coarctation of the ascending aorta in 7 dogs. The overall mean weight of the left ventricle (LVW) was 7.86 +/- 1.49 (S.D.) g/kg body weight; (normal, 5.99 +/- 0.70 g/kg: p less than 0.05). After potassium arrest, pressure-volume (P-V) relationships were examined with the left ventricles isolated from the normals and from the dogs of left ventricular hypertrophy (LVH-dogs). In both groups, the P-V relationships could be expressed by an equation deltaV=a-be-cP throughout the range of filling pressure of 2.5 to 35 cmH2O, where deltav was the actual volume change of LV, P intraventricular pressure, and a, b and c constants. A sensitive index of LV stiffness, the half-inflation pressure (h), was defined as 1n (2b/a)/c. In hypertrophied hearts, h was 10.5 +/- 0.7 cmH2O; (normal 8.0 +/- 0.4 cmH2O; P less than 0.001). The ratio of LVW to LVVp=h (the left ventricular volume at h) in hypertrophy, which was related to the LV chamber geometry, was 3.1 +/- 0.6 in contrast with the normal value of 2.0 +/- 0.3. The development of concentric hypertrophy was thus demonstrated. Moreover, h was closely correlated with LVW/LVVp=h in both the normals and the LVH-dogs (r=0.83; p less than 0.01). On the other hand, an index of LV wall stiffness h/LVW/LVVP=h was relatively constant. Therefore, the increase of LV stiffness in the LVH-dogs was attributed to the change in chamber geometry.