Effects of pressure overload, left ventricular hypertrophy on beta-adrenergic receptors, and responsiveness to catecholamines.

Pressure overload left ventricular (LV) hypertrophy was produced by banding the ascending aorta of puppies and allowing them to grow to adulthood. LV free wall weight per body weight increased by 87% from a normal value of 3.23 +/- 0.19 g/kg. Hemodynamic studies of conscious dogs with LV hypertrophy and of normal, conscious dogs without LV hypertrophy showed similar base-line values for mean arterial pressure, heart rate, and LV end-diastolic pressure and diameter. LV systolic pressure was significantly greater, P less than 0.01, and LV stroke shortening was significantly lss, P less than 0.01, in the LV hypertrophy group. In both normal and LV hypertrophy groups, increasing bolus doses of norepinephrine or isoproterenol produced equivalent changes in LV dP/dt. beta-adrenergic receptor binding studies with [3H]-dihydroalprenolol ( [3H]DHA) indicated that the density of binding sites was significantly elevated, P less than 0.01, in the hypertrophied LV plasma membranes (111 +/- 8.8, n = 8), as compared with normal LV (61 +/- 5.6 fmol/mg protein, n = 11). The receptor affinity decreased, i.e., disassociation constant (KD) increased, selectively in the LV of the hypertrophy group; the KD in the normal LV was 6.8 +/- 0.7 nM compared with 10.7 +/- 1.8 nM in the hypertrophied LV. These effects were observed only in the LV of the LV hypertrophy group and not in the right ventricles from the same dogs. The plasma membrane marker, 5' -nucleotidase activity, was slightly lower per milligram protein in the LV hypertrophy group, indicating that the differences in beta-adrenergic receptor binding and affinity were not due to an increase in plasma membrane protein in the LV hypertrophy group. The EC50 for isoproterenol-stimulated adenylate cyclase activity was similar in both the right and left ventricles and in the two groups. However, maximal-stimulated adenylate cyclase was lower in the hypertrophied left ventricle. Plasma catecholamines were similar in the normal and hypertrophied groups, but myocardial norepinephrine was depressed in the dogs with LV hypertrophy (163 +/- 48 pg/mg) compared with normal dogs (835 +/- 166 pg/mg). Thus, severe, but compensated LV hypertrophy, induced by aortic banding in puppies, is characterized by essentially normal hemodynamics in adult dogs studied at rest and in response to catecholamines in the conscious state. At the cellular level, reduced affinity and increased beta-adrenergic receptor number characterized the LV hypertrophy group, while the EC50 for isoproterenol-stimulated adenylate cyclase activity was normal. By these mechanisms, adequate responsiveness to catecholamines is retained in conscious dogs with severe LV hypertrophy.     

超声评价血管紧张素转换酶抑制剂及血管紧张素受体拮抗剂对高血压左室肥厚患者冠状动脉血流动力学的影响

目的应用超声技术评价血管紧张素转换酶抑制剂雷米普利和血管紧张素受体拮抗剂氯沙坦及联合用药对高血压左室肥厚患者冠状动脉血流动力学的影响.方法将60例高血压合并左室肥厚的患者随机分入雷米普利、氯沙坦单用和二者联合用药组,治疗6个月后复查,采用多平面经食管超声心动图和动态三维超声心动图评价用药前后左室质量(LVM)和冠状动脉血流动力学的变化.结果最终共50例患者完成了全部检查.治疗6个月后,雷米普利组、氯沙坦组及联合用药组收缩压、舒张压均显著下降,LVM明显减轻(P均《0.01);雷米普利组、氯沙坦组和联合用药组均见冠状动脉前降支近端经LVM校正的舒张期血流流速积分(DVic)较用药前显著增高,收缩期血流流速积分(SVic)降低(P均《0.01);静脉注射双嘧达莫后,经LVM校正后的SVic、DVic在雷米普利组、氯沙坦组和联合用药组均见治疗后较治疗前显著增高(P《0.05～0.01);氯沙坦组和联合用药组冠状动脉血流储备(CFR)指标显著增加(P《0.05),经LVM校正后的上述指标增加程度更为显著(P《0.05～0.01),且联合用药组CFR高于雷米普利组(P《0.05),雷米普利组仅见经LVM校正后的CFR指标较治疗前显著增加(P《0.05).结论雷米普利和氯沙坦联合用药与单一用药在降压、消退LVH方面同样有效,在改善CFR方面联合用药优于雷米普利单用.     

Effects of angiotensin converting enzyme inhibitor and angiotensin II receptor blocker on ventricular defibrillation threshold

BACKGROUND: Angiotensin converting enzyme (ACE) inhibitors and Angiotensin II (AII) receptor blockers have previously been shown to be beneficial in treating patients with not only hypertension but also with cardiovascular diseases. Therefore, such drugs may potentially be used in patients with an implantable cardioverter defibrillator (ICD) who show cardiac dysfunctions. OBJECTIVE: This study aimed to determine effects of short-term administration of the ACE inhibitor (CV-3317) and the AII receptor blocker (CV-11974, an active form of candesartan) on internal defibrillation threshold (DFT) in anesthetized canine hearts. Methods: DFTs were evaluated using a "hot can" defibrillation lead system in: (a) seven dogs following three intravenous administrations of 20 cc saline; (b) 11 dogs that received intravenous CV-3317 doses of 1 mg/kg, 10 mg/kg, and 50 mg/kg; and in (c) 10 dogs that were intravenously given 0.1 mg/kg, 1 mg/kg, and 10 mg/kg CV-11974. DFTs were determined using a "down-up down-up" protocol. RESULTS: Mean DFT delivered energies at baseline and following three consecutive intravenous saline injections were 16.4 +/- 9.3 J, 15.3 +/- 7.5 J, 15.9 +/- 7.1 J, and 15.5 +/- 5.6 J, respectively. Those at baseline and following 1 mg/kg, 10 mg/kg, and 50 mg/kg intravenous CV-3317 were 12.9 +/- 6.4 J, 12.2 +/- 6.4 J, 11.0 +/- 6.6 J, and 11.9 +/- 6.6 J, respectively. Similarly, those at baseline and after 0.1 mg/kg, 1 mg/kg, and 10 mg/kg CV-11974 were 13 +/- 6.6 J, 12.5 +/- 6 J, 12.9 +/- 5.8 J, and 13.2 +/- 6.6 J, respectively. There were no significant differences between DFT at baseline and the others in each treatment group. CONCLUSIONS: Since an ACE inhibitor and an AII receptor blocker did not alter DFT, such drugs may be useful in ICD patients without a decrease in safety margins.     

Cardiac β-adrenoceptors and adenylyl cyclase activity in human left ventricular hypertrophy due to pressure overload

Summary— The effect of left ventricular hypertrophy (LVH) due to chronic pressure overload on right atrial (RA) and left ventricular (LV) myocardial β-adrenergic receptor (β-AR) density and subtypes, adenylyl cyclase (AC) activity and ADP-pertussis toxin ribosylated proteins was investigated in humans with LVH due to aortic stenosis and in patients without LVH undergoing heart surgery for mitral stenosis or coronary artery disease taken as controls. Both groups presented normal systolic function or plasma catecholamine levels. In LVH and controls, β-AR density was similar in RA (62 ± 6 vs 77 ± 12 fmol·mg^?1 protein) and LV (39 ± 7 vs 32 ± 2 fmol·mg^?1 protein). In LVH, β₁-AR percentage was < than in controls in LV (35 ± 11 vs 73 ± 5%, P < 0.05) but not in RA (79 ± 5 vs 73 ± 8%). Basal AC activity in RA (19 ± 4 vs 21 ± 6 pmol·;mg^?1 protein) and LV (22 ± 5 vs 27 ± 3 pmol·mg^?1 protein) was similar in LVH and in controls. Isoprenaline-induced stimulation of AC in RA was similar in LVH and in controls (51 ± 18 vs 36 ± 18%) but < in LV of LVH (7 ± 6 vs 45 ± 6%, P < 0.05). In the presence of ICI-118,551 (a β₂-adrenoceptor antagonist), isoprenaline failed to induce any increase in cAMP in LVH. The quantification of ADP-pertussis toxin ribosylated proteins indicated a lower concentration of substrates in LV myocardial membranes from LVH. These data indicate that in LVH due to pressure overload, there is a down-regulation of β₁-AR and an increase in β₂-AR density. This is associated with alterations of the transmembrane signalling marked by a decreased capacity of isoprenaline to stimulate AC and an impaired expression of Gi proteins.     

黄芪多糖对压力超负荷诱导的大鼠心肌肥大的影响

目的:探讨黄芪多糖(astragalus polysaccharides,APS)对压力超负荷所致大鼠心肌肥大的抑制作用。方法:SD大鼠随机分为5组:假手术手组、模型组、APS低剂量组(AP1)、APS高剂量组(AP2)和卡托普利组。给药8周后,分别进行心脏超声和HE染色检测心脏肥大指数及形态学改变。结果:超声检测发现,与假手术组相比,模型组左右心室质量比明显增加,舒张期左心室容量、左心室射血分数和左心室短轴缩短速率均明显降低;AP2组与模型组相比,以上指标均有显著性改善,而AP1组和模型组比较无明显差异。HE染色显示,模型组肌细胞排列疏松、肥大,AP1组和AP2组细胞排列整齐,有少量肥大细胞夹杂。结论:高剂量APS对压力超负荷大鼠的心肌肥大有明显保护作用。     

Effects of angiotensin II generated by an angiotensin converting enzyme-independent pathway on left ventricular performance in the conscious baboon.

Human chymase is a serine proteinase that converts angiotensin (Ang) I to Ang II independent of angiotensin converting enzyme (ACE) in vitro. The effects of chymase on systemic hemodynamics and left ventricular function in vivo were studied in nine conscious baboons instrumented with a LV micromanometer and LV minor axis and wall thickness sonomicrometer crystal pairs. Measurements were made at baseline and after [Pro11DAla12] Ang I, a specific substrate for human chymase, was given in consecutive fashion as a 0.1 mg bolus, an hour-long intravenous infusion of 5 mg, a 3 mg bolus, and after 5 mg of an Ang II receptor antagonist. [Pro11DAla12]Ang I significantly increased LV systolic and diastolic pressure, LV end-diastolic and end systolic dimensions and the time constant of LV relaxation and significantly decreased LV fractional shortening and wall thickening. Administration of a specific Ang II receptor antagonist reversed all the hemodynamic changes. In separate studies, similar results were obtained in six of the baboons with ACE blockade (20 mg, intravenous captopril). Post-mortem studies indicated that chymase-like activity was widely distributed in multiple tissues. Thus, in primates, Ang I is converted into Ang II by an enzyme with chymase-like activity. This study provides the first in vivo evidence of an ACE-independent pathway for Ang II production.     

Quantitative analysis of cardiac hypertrophy due to pressure load in reference to the relations of blood pressure, left ventricular weight and left ventricular capacity.

In almost all of the cases of cardiac hypertrophy due to sustained hypertension, left ventricular capacity is increased in proportion to increased left ventricular weight, even in the absence of manifest cardiac insufficiency. The condition is regarded as the general expression of cardiac response to pressure load, and the concept of "isomorphic hypertrophy" is proposed. Concentric hypertrophy of the current concept is observed only on rare special occasions, and its role in cardiac adaptation to pressure load is obscure. The increase in myocardial mass is sufficient to maintain the work done by a unit myocardial volume at a normal level. However, the calculation on pertinent models demonstrates that hypertrophied hearts of any type expel the normal stroke volume with smaller shortening of muscle fibers under larger stress, which is further elevated with the progress of cardiac contraction. Because the maximum force generated by muscle fibers declines with advancing cardiac contraction, hypertrophied hearts harbor a latent risk of mechanical insufficiency. Even under pressure load, ventricular dilation seems to precede the re-inforcement of ventricular wall in the development of cardiac hypertrophy. A common mechanism may be therefore assumed underlying the development and performance of all types of hypertrophied hearts, regardless of the difference in the character of physical loads.     

脉压与冠心病患者左室功能及左室肥厚的关系

目的:比较分析合并与未合并糖尿病、高血压冠心病患者脉压与心功能指标及左室肥厚的关系。方法:①选择2001-01/12上海交通大学附属第一人民医院心内科住院冠心病患者105例,男70例,女35例。其中仅合并高血压者29例(合并高血压组),同时合并高血压及糖尿病者27例(合并高血压及糖尿病组),合并糖尿病者32例(合并糖尿病组),无高血压及糖尿病者(无高血压及糖尿病组)17例。患者均知情同意。②在行冠状动脉造影术过程中测定主动脉内收缩压、舒张压,计算脉压值。超声心动描记法为M型模式下测定舒张末期左室腔直径、左室后壁厚度及室间隔厚度及左室射血分数。根据公式:左室质量=1.04[(室间隔厚度+舒张末期左室腔直径+左室后壁厚度)3-舒张末期左室腔直径3]-13.6计算左室质量。根据公式:相对室壁厚度=(室间隔厚度+左室后壁厚度)/舒张末期左室腔直径计算相对室壁厚度。③分别以脉压、左室质量、左室射血分数及相对室壁厚度为变量,以年龄、性别、伴有高血压、伴有糖尿病、同时伴有高血压及糖尿病为控制变量,进行偏相关分析。组间分析采用方差分析。结果:冠心病105例均进入结果分析。①各组脉压无明显差别。合并高血压及糖尿病组左室质量、相对室壁厚度大于其他3组(P<0.05),心功能指标左室射血分数明显低于其他3组(P<0.05)。②各组脉压均与左室质量呈显著正相关(r=0.35～0.47,P<0.05～0.01)。合并高血压组、合并高血压及糖尿病组脉压与左室射血分数呈显著正相关(r=0.33,0.41P<0.05)。合并高血压及糖尿病组脉压与相对室壁厚度呈显著正相关(r=0.51,P<0.01)。结论:脉压是一独立于高血压之外的,与左室肥厚有关的独立指标;同时合并高血压及糖尿病,为影响冠心病患者左室肥厚,左室收缩功能的重要因素。     

脉压与冠心病患者左室功能及左室肥厚的关系

目的：比较分析合并与未合并糖尿病、高血压冠心病患者脉压与心功能指标及左室肥厚的关系.方法：[1]选择2001-01/12上海交通大学附属第一人民医院心内科住院冠心病患者105例,男70例,女35例.其中仅合并高血压者29例（合并高血压组）,同时合并高血压及糖尿病者27例（合并高血压及糖尿病组）,合并糖尿病者32例（合并糖尿病组）,无高血压及糖尿病者（无高血压及糖尿病组）17例.患者均知情同意.[2]在行冠状动脉造影术过程中测定主动脉内收缩压、舒张压,计算脉压值.超声心动描记法为M型模式下测定舒张末期左室腔直径、左室后壁厚度及室间隔厚度及左室射血分数.根据公式：左室质量=1.04[（室间隔厚度＋舒张末期左室腔直径＋左室后壁厚度）3-舒张末期左室腔直径3]-13.6计算左室质量.根据公式：相对室壁厚度=（室间隔厚度＋左室后壁厚度）/舒张末期左室腔直径计算相对室壁厚度.[3]分别以脉压、左室质量、左室射血分数及相对室壁厚度为变量,以年龄、性别、伴有高血压、伴有糖尿病、同时伴有高血压及糖尿病为控制变量,进行偏相关分析.组间分析采用方差分析.结果：冠心病105例均进入结果分析.[1]各组脉压无明显差别.合并高血压及糖尿病组左室质量、相对室壁厚度大于其他3组（P＜0.05）,心功能指标左室射血分数明显低于其他3组（P＜0.05）.[2]各组脉压均与左室质量呈显著正相关（r=0.35～0.47,P＜0.05～0.01）.合并高血压组、合并高血压及糖尿病组脉压与左室射血分数呈显著正相关（r=0.33,0.41,P＜0.05）.合并高血压及糖尿病组脉压与相对室壁厚度呈显著正相关（r=0.51,P＜0.01）.结论：脉压是一独立于高血压之外的,与左室肥厚有关的独立指标;同时合并高血压及糖尿病,为影响冠心病患者左室肥厚,左室收缩功能的重要因素.     

Effects of triiodothyronine and dexamethasone on plasma and tissue angiotensin converting enzyme in the rat

Summary— In order to identify tissue specific regulation of angiotensin converting enzyme (ACE), the effects of dexamethasone (0.04 mg sc per day for 7 days) and triiodothyronine (T3) (0.5 mg/kg sc per day for 10 days) on ACE activity were investigated in different tissues in male Wistar rats. ACE activity was measured by fluorimetry in the plasma, heart, lung and kidney. In the kidney, ACE activity was measured in the medulla, cortex and brush border of proximal tubular cells and ³H-ramiprilat binding was used to characterise the changes in brush border ACE activity. Dexamethasone elicited a significant increase in lung ACE activity and a significant decrease in plasma ACE activity, but did not alter enzyme activity in the other tissues studied. T3 produced a significant decrease in lung ACE activity and an increase in ACE activity in the plasma and heart. In the kidney, ACE activity was not modified in the medulla whereas in the cortex and brush border ACE activity was doubled. This increase in ACE activity corresponded to a similar increase in the maximum number of binding sites of ³H-ramiprilat, suggesting that the increase in activity corresponded to an increase in the ACE level. The increased heart and kidney ACE activity in response to T3 may contribute to the cardiovascular effects of thyroid hormones through increased local angiotensin II generation. These results show that under dexamethasone or T3, ACE activity can vary from one tissue to another, suggesting that the ACE regulatory mechanism acts differently in each tissue.     

Interaction between neutral endopeptidase and angiotensin converting enzyme inhibition in rats with myocardial infarction: effects on cardiac hypertrophy and angiotensin and bradykinin peptide levels

Combined inhibition of neutral endopeptidase 24.11 (NEP) and angiotensin converting enzyme (ACE) is a candidate therapy for hypertension and cardiac failure. Given that NEP and ACE metabolize angiotensin (Ang) and bradykinin (BK) peptides, we investigated the effects of NEP inhibition and combined NEP and ACE inhibition on Ang and BK levels in rats with myocardial infarction. We administered the NEP inhibitor ecadotril (0, 0.1, 1, 10, and 100 mg/kg/day), either alone or together with the ACE inhibitor perindopril (0.2 mg/kg/day) by 12-hourly gavage from day 2 to 28 after infarction. Ecadotril increased urine cyclic GMP and BK-(1-9) excretion. Perindopril potentiated the effect of ecadotril on urine cyclic GMP excretion. Neither perindopril nor ecadotril reduced cardiac hypertrophy when administered separately, whereas the combination of perindopril and 10 or 100 mg/kg/day ecadotril reduced heart weight/body weight ratio by 10%. Administration of ecadotril to perindopril-treated rats decreased plasma Ang-(1-7) levels, increased cardiac BK-(1-9) levels, and increased Ang II levels in plasma, kidney, aorta, and lung. These data demonstrate interactions between the effects of NEP and ACE inhibition on remodeling of the infarcted heart and on Ang and BK peptide levels. Whereas increased cardiac BK-(1-9) levels may contribute to the reduction of cardiac hypertrophy, the reduction in plasma Ang-(1-7) levels and increase in Ang II levels in plasma and tissues may compromise the therapeutic effects of combined NEP/ACE inhibition.     

Increased adrenergic contractility and decreased mRNA expression of NOS III in aging rat urinary bladders

Our objective was to study age-related changes in adrenergic contractility and gene expression profile in the rat urinary bladder. Young (3-month old), adult (10-month old) and senescent (30-month old) male WAG/Rij rats were used. Gene expression profile in the rat urinary bladder was defined using Atlas microarray technology. In vitro contractile responses induced by KCl, phenylephrine (PHE) and norepinephrine (NE) were compared in isolated urinary bladders dissected from young, adult and senescent rats. Among a total of 1176 genes present on the arrays, 15 genes showed an increase in expression and 10 genes a decrease with age. Four genes related to nerve growth factor were upregulated whereas NOS type III was downregulated in aging rats. Intrinsic contractility of isolated rat urinary bladders was not changed between adult and aging rats as judged by the response curves to KCl. In contrast, an age-related increase in the maximal contractile responses to NE, but not PHE, was noticed (13 +/- 1, 48 +/- 2% and 59 +/- 2% at 3, 10 and 30 months, respectively). The alpha1D-adrenoceptor antagonist BMY7378 antagonized NE-induced contractions with low potency in both groups suggesting the involvement of the alpha1A-adrenoceptor subtype. This was confirmed by microarray, which demonstrated mRNA expression for the alpha1A-adrenoceptor subtype only. These results suggest that aging of the urinary bladder is associated with an increase in the maximal contractile response to NE which could be due to NO shortage resulting from downregulation of urothelial NOS III.     

Plasma concentrations of angiotensin II and aldosterone during acute left ventricular failure in the dog. Effect of converting enzyme inhibition

Acute left ventricular failure was induced in anesthetized dogs by left coronary embolization. Treatment with the converting enzyme inhibitor enalaprilat (MK-422) was then given. Hemodynamic registrations confirmed the development of left ventricular failure. Plasma concentrations of angiotensin II and aldosterone rose significantly. Treatment with enalaprilat was accompanied by significant reductions in heart preload and afterload and in plasma hormone concentrations.     

脉压与冠心病患者左室肥厚的关系探讨

目的 探讨冠心病患者左室肥厚与脉压的关系.方法 将本院收治的96例冠心病患者根据脉压大小分为3组:A组30例,脉压≤45 mmHg;B组35例,55 mmHg≥脉压＞45 mmHg;C组31例,脉压＞55 mmHg.采用彩色超声心脏诊断仪测定舒张期室间隔厚度(IVST)、左室后壁厚度(PWT)、左室舒张末期内径(LVD...     

Effect of a fibrin-derived vasoactive peptide on pulmonary angiotensin converting enzyme activity and on pressure responses to bradykinin

Decreased angiotensin converting enzyme (ACE) activity is a common finding in patients with adult respiratory distress syndrome and in animal models of lung injury. The nature of this effect is unknown. Intravascular fibrin, also a common finding in lung injury, is degraded to small peptides by proteolytic enzymes. Peptide 6A, corresponding to amino acid residues 43 to 47 of the B beta chain of fibrin(ogen), is produced by plasmin degradation of fibrin and has been shown to inhibit ACE in vitro. We investigated the effect of this peptide on the pulmonary hydrolysis of a synthetic ACE substrate, benzoyl-phenylalanyl-alanyl-proline, in anesthetized rabbits and in isolated, perfused rabbit lungs. Peptide 6A caused a reversible, dose-dependent inhibition of benzoyl-phenylalanyl-alanyl-proline hydrolysis. It also potentiated the increase in pulmonary arterial pressure and the decrease in systemic arterial pressure due to bradykinin (BK), as well as the increase in pulmonary artery pressure due to BK in isolated lungs. The amount of BK needed to increase pulmonary arterial pressure was about 1000-fold larger in the isolated lung than in the intact animal. Peptides of this type might contribute to decreased ACE activity in patients with adult respiratory distress syndrome and may potentiate BK-mediated hemodynamic changes in these patients.     

Blood pressure and left ventricular hypertrophy in patients on different peritoneal dialysis regimens.

OBJECTIVE: To examine the relation between the results of ambulatory 24-hour blood pressure monitoring (ABPM) and left ventricular mass index (LVMI), then to find the independent determinant for left ventricular hypertrophy (LVH) in peritoneal dialysis (PD) patients. Finally, to evaluate the differences in the clinical and cardiovascular characteristics between patients on continuous ambulatory PD (CAPD) and continuous cyclic PD (CCPD). DESIGN: An open, nonrandomized, cross-sectional study. SETTING: Divisions of nephrology and cardiology in a medical center. PATIENTS: Thirty-two uremic patients on maintenance PD therapy (22 patients on CAPD, and 10 on CCPD) without anatomical heart disease or history of receiving long-term hemodialysis. INTERVENTIONS: Home blood pressure (BP) and office BP were measured using the Korotkoff sound technique by sphygmomanometer. ABPM was employed for continuous measurement of BP. Echocardiography was performed for measurement of cardiac parameters and calculation of LVMI. MAIN OUTCOME MEASURES: Multivariate logistic regression analysis was performed for independent determinant of LVH in PD patients. The differences in clinical and cardiovascular characteristics between CAPD and CCPD patients were compared. RESULTS: Simple regression analysis showed positive correlations between LVMI and the duration of hypertension, ambulatory nighttime BP/BP load/BP load > 30%, serum phosphate, calcium-phosphate product, ultrafiltration (UF) volume, and percentage of UF volume during the nighttime. A negative correlation was noted between LVMI and dipping. In multiple regression analysis, the duration of hypertension was the only variable linked to LVMI. In multivariate logistic regression analysis, only ambulatory nighttime systolic BP load > 30% had an independent association with LVH.There were correlations between office/home BP and ambulatory 24-hour BP. In addition, CCPD patients had higher LVMI, UF volume during the nighttime, and percentage of UF volume during the nighttime than those of CAPD patients. CONCLUSIONS: In this study, ambulatory nighttime systolic BP load > 30% had an independent association with LVH. Office and home BP measurements were correlated with ABPM in PD patients. The result that CCPD patients had a higher LVMI than CAPD patients may be due to a relative volume overload during the daytime in CCPD patients.     

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     

福辛普利和非络地平逆转原发性高血压左室肥厚的对比研究

目的 :对比研究福辛普利和非络地平逆转原发性高血压 (EH)左室肥厚的作用。方法 :将 10 4例EH伴左室肥厚的患者随机分为福辛普利组和非络地平组 ,于服药前及服药后 6个月、12个月、2 4个月分别测定左室舒张末内径 (LVDT)、舒张期室间隔厚度 (IVST)、左室后壁厚度 (LVPWT)、左室射血分数 (LVEF)、心排量 (CO)、A峰 /E峰比值 (A/E比值 )。结果 :两组治疗前后比较LVEF、CO均无变化 ,而A/E比值则明显降低 ;左室重量指数 (LVMI)、LVDd、IVST、LVPDWT在福辛普利组明显下降 ,而在非络地平组则无变化。结论 :福辛普利和非络地平均能明显改善左室舒张功能 ,但福辛普利能明显减轻左室肥厚。