经食道心房调搏对病态窦房结综合征的诊断价值

经食道心房调搏是通过食道电极对右心房近窦房结处施加阈上刺激,以测定窦房结恢复时间和窦房传导时间的无创伤性窦房结功能检测方法。本文通过经食道心房调搏检测窦房结功能280例临床分析,探讨该方法对病态窦房结综合征的诊断价值。     

经食道调搏测定窦房结恢复时间评估窦房结功能不全的临床意义

目的 通过食道调搏(TEAP)测定窦房结恢复时间(SNRT)评估窦房结功能不全。方法36例经阿托品试验诊断为窦房结功能不全患者,经食道调搏方法测定窦房结恢复时间及矫正时间。结果 SNRT小于1500ms者4例。病窦综合征32例。结论 食道调搏是测定窦房结功能不全的有效方法。     

1例安装单腔起博器治疗病态窦房结综合征的护理

病态窦房结综合征是由于窦房结及其周围组织的器质性病变导致窦房结功能障碍，而产生多种心律失常的综合表现。病态窦房结综合征是危害人类身体健康和造成心脏猝死的重要疾病之一。药物治疗效果欠佳，安置永久性心脏起博器可有效控制病态窦房结综合征患者病情的复发及各种心律失常的发生。我院于2008年5月26日收治了1例病态窦房结综合征患者，经安装单腔（心室）起博器后，对该患者实施了整体护理，达到了满意的效果，现报道如下。     

老年心脏病—病窦综合征

人类窦房结病变早在80年前即有报告,然而对此病的广泛认识只是近20年的事.病态窦房结综合征(sick sinus syndrome简称sss).多发生于老年人,是由于老年人窦房结发生特发性退化所致,其主要特征是:窦房结激动形成异常和/或窦房传导异     

窦房结电图在射频消融术中实验研究

目的　探索应用窦房结电图技术定位窦房结和记录低频、低振幅心电信息方法。方法　对 12只兔用常规镍合金电极导管和银 氯化银电极导管分别记录窦房结电图对比图形。以窦房结电图定位窦房结位置 ,取定位组织HE染色观察。在窦房结位置射频消融改良窦房结 ,观察心率变化。结果　非极化电极银 氯化银电极导管记录的心电活动的图形较极化电极镍合金电极导管记录的图形稳定 ,且干扰小。窦房结电图定位处组织中有 10 / 12可见窦房结组织的P细胞。 9/ 12只兔在射频消融改良窦房结中即刻达到窦性心率下降 30± 5 %的靶心率。射频消融改良窦房结前、后平均心率 (194± 41次 /min、16 2± 33次 /min) ,两组之间差异有显著意义 (P <0 0 1)。结论　非极化电极导管记录低频、低振幅心电信息图形稳定 ,且干扰小。在电生理检查窦房结电图可定位窦房结位置 ,射频消融改良窦房结达到减慢窦性心率的治疗目的     

心外膜窦房结电图指导窦房结细胞取材的价值

目的探索经心外膜窦房结电图指导窦房结细胞取材的准确性。方法长白山乳猪12只,行心外膜窦房结电图标测,A波前出现圆顶形或上斜形波形为窦房结电图,又称为"P前波",于"P前波"处取材行窦房结细胞培养及超极化激活环核苷酸门控阳离子通道(HCN4)免疫荧光定量测定。结果窦房结电图指导下窦房结细胞取材,培养的细胞有3种形态,即梭形、三角形与不规则形。培养梭形细胞较多,搏动频率较快;同时免疫荧光证实HCN4通道蛋白密度较高。结论窦房结电图提高窦房结细胞的取材的准确性。     

炙甘草汤加减治疗病态窦房结综合征18例报告

病态窦房结综合征（sick sinus syndrone，SSS）简称病窦综合征，是由于窦房结或其周围组织器质性病变导致窦房结冲动形成障碍，或窦房结至心房冲动传导障碍所致的多种心律失常和多种症状的综合征。     

动态心电图与食道电生理检查对病态窦房结的诊断价值

目的研究分析动态·心电图结合食道电生理检查对病态窦房结的诊断价值。方法回顾分析最近2年内湖北医药学院附属太和医院动态心电图检查的50例患者,选择R-R间期超过1500ms的患者,随后行食道电生理检查,其中确诊病态窦房结综合征38例。结果窦房结恢复时间大于或等于2000ms,窦房结传导时间大于或等于220ms,校正的窦房结恢复时间大于或等于750ms,患者动态心电图检测中可见长R—R间期大于1500ms,部分大于2000ms,明显窦性心动过缓及窦房传导阻滞。结论动态心电图检出长RR间期大于l500ms,应行食道电生理检查（窦房结功能测定）,二者结合是诊断病态窦房结综合征的较好方法。     

消旋去甲乌药碱对窦房结功能电生理的影响

目的:探讨消旋去甲乌药碱治疗病态窦房结综合征的作用机制.方法:40只杂种家兔随机分为窦房结功能正常组和窦房结功能受损(SND)组,每组随机分为用药组和对照组(n=10).采用甲醛溶液湿敷窦房结的方法制备SND模型.用药组5 min内经耳缘静脉注入消旋去甲乌药碱0.04 mg/kg,20 min后测定用药前、后窦房结功能电生理指标--窦房结恢复时间(SNRT)、纠正窦房结恢复时间(CSNRT)、总窦房传导时间(TSACT)和窦性心律周期(SCL)的变化;正常组用生理盐水10 ml作对照用药.结果:①窦房结功能正常组和SND组在给予消旋去甲乌药碱后,SNRT、CSNRT、TSACT和SCL均较对照组明显缩短(P<0.05或P<0.01).②消旋去甲乌药碱对SND组窦房结功能电生理影响明显大于窦房结功能正常组(P均<0.01);对窦房结功能受损引起的心律失常治疗作用有统计学意义(P<0.05).结论:窦房结自律性的提高及窦房、房室传导功能改善是消旋去甲乌药碱治疗病态窦房结综合征主要的电生理机制.     

乳兔窦房结定位、取材及纯化和培养

背景:分离和纯化培养的窦房结细胞是研究其超微结构及自律性的重要条件,然而,相应的培养方法尚未标准化.目的:建立乳兔窦房结进行定位、取材和纯化培养方法,观察并判断培养窦房结细胞中起搏细胞的形态特点.方法:新生24 h内乳兔心脏连续石蜡切片,苏木精-伊红染色,光镜下判断窦房结的位置并测定,计算其大小,光镜、电镜下观察纯化培养的窦房结细胞形态.结果与结论:乳兔窦房结位于上腔静脉根部前壁向下至界沟后外约0.32 mm处.培养的窦房结细胞主要有3种形态细胞:梭形、蜘蛛形、多边形,其中梭形细胞最多,占(59.6±7.3)%,搏动频率最快为(145±9)次/min,肌原纤维稀少,细胞器不发达.蜘蛛形和多边形细胞则和培养的心房肌细胞培养无差异.沿上腔静脉根部前壁向下至界沟后外侧可较精确地对窦房结进行取材.培养的乳兔窦房结细胞中,细胞体积小,搏动频率快,所占比率高的梭形细胞是窦房结的起搏细胞.     

高K+缓冲液对家兔心房钠尿肽分泌的影响

目的 探讨细胞外高K+对家兔心房钠尿肽(ANP)分泌的影响及其作用机制.方法 取大耳白家兔18只,利用乌拉坦麻醉后立即开胸取出心脏,剥离左心房固定在心房灌流装置上,并给予适宜的电刺激使其搏动.待心房搏动稳定后(约60 min),分3组按照如下3种实验步骤进行实验:①6只家免经过1个对照循环(每12分钟定为1个实验循环),然后处理高K+缓冲液(K+浓度为5.64 mmol/L;缓冲液的渗透压保持不变)3个循环,之后恢复正常缓冲液2个循环;②6只家兔经过1个对照循环,处理L-型Ca2+通道阻断剂硝苯地平(1.0 μmol/L)3个循环;③6只家兔经过1个对照循环,先处理L-型Ca2+通道阻断剂硝苯地平(1.0 μmol/L)3个循环,然后在硝苯地平存在下同时处理高K+缓冲液3个循环.观察心房ANP分泌和心房搏出量的变化.ANP浓度采用放射免疫法进行测定.结果 ①高K+缓冲液明显增加心房ANP的分泌(P均<0.01),而心房搏出量则呈现下降趋势,但与对照循环相比差异无统计学意义(P0.05),当恢复正常缓冲液时ANP分泌量和心房搏出量趋于回复正常水平,与对照循环相比差异无统计学意义(P0.05);②L-型Ca2+通道阻断剂硝苯地平(1.0 μmol/L)显著增加心房ANP分泌(P<0.01或P<0.05)的同时明显降低心房搏出量(P<0.01或P<0.05);③L-型Ca2+通道阻断剂硝苯地平(1.0 μmol/L)完全阻断高K+缓冲液促进ANP分泌的作用(P<0.01或P<0.05),并进一步抑制心房搏出量(P均<0.01).结论 细胞外高K+缓冲液促进家兔搏动的离体心房ANP的分泌,其作用与细胞外高K+竞争性抑制细胞外Ca2+内流有关.     

Nitric oxide, atrial natriuretic peptide, and cyclic GMP inhibit the growth-promoting effects of norepinephrine in cardiac myocytes and fibroblasts.

This study tested the hypothesis that nitric oxide (NO) and atrial natriuretic peptide (ANP) can attenuate the effects of adrenergic agonists on the growth of cardiac myocytes and fibroblasts. In ventricular cells cultured from neonatal rat heart, ANP and the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP) caused concentration-dependent decreases in the norepinephrine (NE)-stimulated incorporation of [3H]leucine in myocytes and [3H]thymidine in fibroblasts. In myocytes, the NO synthase inhibitor NG-monomethyl-L-arginine potentiated NE-stimulated [3H]leucine incorporation. In both cell types, ANP and SNAP increased intracellular cGMP levels, and their growth-suppressing effects were mimicked by the cGMP analogue 8-bromo-cGMP. Furthermore, in myocytes, 8-bromo-cGMP attenuated the alpha1-adrenergic receptor-stimulated increases in c-fos. Likewise, ANP and 8-bromo-cGMP attenuated the alpha1-adrenergic receptor- stimulated increase in prepro-ANP mRNA and the alpha1-adrenergic receptor-stimulated decrease in sarcoplasmic reticulum calcium ATPase mRNA. The L-type Ca2+ channel blockers verapamil and nifedipine inhibited NE-stimulated incorporation of [3H]leucine in myocytes and [3H]thymidine in fibroblasts, and these effects were not additive with those of ANP, SNAP, or 8-bromo-cGMP. In myocytes, the Ca2+ channel agonist BAY K8644 caused an increase in [3H]leucine incorporation which was inhibited by ANP. These findings indicate that NO and ANP can attenuate the effects of NE on the growth of cardiac myocytes and fibroblasts, most likely by a cGMP-mediated inhibition of NE-stimulated Ca2+ influx.     

The effect of atrial natriuretic peptide on cytosolic free calcium in cultured vascular smooth muscle cells

Effect of atrial natriuretic peptide (ANP) on cytosolic free calcium [( Ca2+]i) was studied in monolayers of cultured vascular smooth muscle (VSM) cells loaded with a fluorescent calcium indicator, fura-2. Vasoconstrictive hormones, angiotensin II (AII) and Arg8-vasopressin (AVP) induced initial rapid rises in [Ca2+]i, followed by sustained elevation of [Ca2+]i. ANP (Atriopeptin III 10(-8) M) decreased both the resting level and the sustained elevation of [Ca2+] i induced by AII and AVP. ANP also decreased the rise in [Ca2+]i induced by high potassium (K+) depolarization. AVP-induced initial rapid rise in [Ca2+]i was not inhibited by ANP in the presence or absence of the phosphodiesterase inhibitor, isobutylmethylxanthine 0.1 mM, which has been shown to fully enhance ANP-induced cyclic GMP accumulation. On the other hand, a calcium antagonist, nicardipine, inhibited the high K+-induced rise in [Ca2+]i, whereas it had no effect on not only initial but also sustained rises in [Ca2+]i induced by AVP or AII. These results suggest that ANP has an ability to decrease [Ca2+]i not through inhibition of voltage-sensitive calcium channels, and that neither ANP nor ANP-induced cyclic GMP may affect initial hormone-induced rise in [Ca2+]i. In conclusion, an ability to decrease [Ca2+]i is implicated in ANP-induced relaxation of VSM.     

Regulation of phosphorylase A formation and calcium content in aortic smooth muscle and smooth muscle cells: effects of atrial natriuretic peptide II

Atrial natriuretic peptide II (ANP II) raises cyclic GMP and relaxes vascular smooth muscle in vitro. The manner in which ANP II relaxes vascular smooth muscle is unknown but may involve alterations in the concentration of free intracellular Ca++. To examine this possibility, changes in intracellular Ca++ were monitored in rat aortic strips using the Ca++-dependent conversion of phosphorylase b to a, while Ca++ levels and phosphorylase were measured in cultured rat aortic smooth muscle cells. ANP II produced time- and concentration-dependent decreases in phosphorylase a and tension in norepinephrine-contracted aortic strips. The decrease in the formation of phosphorylase a was accompanied by an increase in cyclic GMP content. ANP II also decreased phosphorylase a formation in K+-depolarized tissues but to a lesser extent. Agonists such as angiotensin II and arginine vasopressin, and depolarizing concentrations of K+ elevated Ca++ levels in cultured aortic cells. ANP II inhibited Ca++ accumulation to either agonists or K+, but was more effective against agonists. Phosphorylase a formation which was increased by agonists and K+ in cultured cells was also inhibited by ANP II. We conclude that phosphorylase a formation can be a useful indicator of intracellular Ca++ concentrations in smooth muscle preparations and that ANP II regulates Ca++ levels in agonist and depolarized smooth muscle, suggesting that ANP II affects mainly Ca++ removal from the cytoplasm.     

胃肠原发性淋巴瘤的CT诊断

[目的]探讨胃肠道原发性淋巴瘤的CT检查方法和表现.[方法]回顾分析了26例经手术病理或内镜活检证实胃肠道原发性恶性淋巴瘤的CT检查资料,检查方法包括传统法口服阳性对比剂CT扫描(10例)及口服甘露醇胃肠造影后CT检查(16例).[结果]胃淋巴瘤CT表现可分为3类:①弥漫浸润或多发型10例,②节段型4例,③息肉型2例;肠道淋巴瘤的CT表现分为4类:①壁内浸润型5例,②多发结节型3例,③肠系膜受累伴腔外肿块型1例,④肿块型1例.[结论]弥漫浸润型和多发结节型是胃肠原发性淋巴瘤的两种主要CT表现类型."动脉瘤样肠腔扩张征"、"夹心面包征"、受累肠段较长及呈多发节段性分布是小肠性淋巴瘤的主要特征性CT表现,具有较可靠的定性诊断价值.     

Sulfonylurea drug--a new sulfonylurea drug for type 2 diabetes

The incidence of diabetes mellitus has been increased year by year and now 5-6 millions are diabetic patients in Japan. Studies of DCCT and UKPDS concluded that tight control of diabetes was benefit for prevention of diabetic complications in type 1 and type 2 diabetes, respectively. New type of sulfonylurea (glimepiride) has been developed by Hoechst Marion Roussel company which continues clinical trials in Japan. Grimepiride is an insulin sparing sulfonylurea drug for the treatment of type 2 diabetes patients whose high blood glucose cannot be controlled by diet and exercise alone. In Europe and United State glimepiride has been used as a monotherapy or in combination with insulin. Glucose control was effectively observed in type 2 diabetics including obese and hypertensive patients by the drug. Mechanism of sulfonylurea which stimulates insulin release is supposed by binding to a regulatory subunit of plasma membrane ATP-sensitive K+ (KATP) channel. The consequent closure of KATP channel leads to depolarization, opening of voltage-dependent Ca2+ channels, Ca2+ influx, and a rise in intracellular [Ca2+], resulting in insulin secretion. However, it has been suggested that sulfonylurea may have an additional action on secretion, independent of changes in intracellular [Ca2+] but dependent on the activity of protein kinase C (PKC). It is controversial whether or not sulfonylurea is a risky drug to the process of diabetic macroangiopathy, by suppressing KATP channels in the heart.     

海马脑片锥体神经元钙离子通道动力学特性的盲法膜片钳研究

目的观察大鼠海马脑片盲法全细胞记录技术研究CA1区锥体神经元电压门控性Ca2+通道的动力学特征,为在海马脑片上进行神经科新药开发提供依据。方法选用出生20～30d的Wistar雄性大鼠20只,断头取脑,将海马切为厚400μm的薄片,解剖镜下选CA1区锥体神经元细胞线行盲法全细胞记录。结果大鼠海马脑片CA1区锥体神经元电压门控性Ca2+通道电流具有如下特点:①激活的阈电位偏低,为(-49±9)mV,范围为-65～-30mV(n=23)。②衰减时间常数τ值较大,且变化范围大(100～700ms)(n=12),并且衰减具有Ca2+电流幅值的依赖性。③稳态失活呈现电压依赖性,半失活电压为(-55±10)mV,斜率因子为(5.3±0.9)(n=10)。④当细胞外Ca2+浓度为2.5mmol/L时,Ca2+通道的反转电位为(55±13)mV(n=10)。⑤尾电流成分较为单一,不表现电压依赖性。另外,Ca2+电流对戊脉胺及双氢吡啶类化合物硝苯地平均不敏感。结论海马脑片CA1区锥体神经元上的Ca2+通道主要以N型为主。     

Interactions of atrial natriuretic peptide with the sympathetic and endocrine systems in the pithed rat

We have found previously that atrial natriuretic peptides (ANPs) attenuate pressor response to alpha-2 adrenoceptor agonists but not to alpha-1 agonists in the pithed rat. We have now investigated the effects of ANP on other pressor agonists and on sympathetically mediated responses in rats. Bolus-injected ANP (0.1-10.0 nmol/kg) attenuated pressor responses to angiotensin II, vasopressin and alpha-2 adrenoceptor-mediated component of norepinephrine (NE)-induced responses (up to 17, 27 and 15%, respectively) in pithed rats. The threshold antipressor dose of ANP was the lowest for angiotensin II (comparable to normal levels of circulating ANP-immunoreactivity in rats) whereas it was higher for vasopressin and NE (comparable to plasma ANP-immunoreactivity stimulated by volume expansion). A 30-min infusion of ANP (0.15 nmol/kg/min) shifted the NE dose-pressor response curve 1.7-fold to the right. Conversely, neither that rate of ANP infusion nor the highest dose of bolus injected ANP altered pressor and plasma NE responses to sympathetic stimulation in demedullated pithed rats. However, at higher infusion rates, ANP reduced sympathetic stimulation-induced pressor responses (2.6-fold) and elevations of plasma NE levels (1.6-fold), without altering NE clearance. Similarly in conscious rats, ANP infusion prevented a reflex increase in plasma NE concentrations associated with hypotension. Thus, although the intrajunctional alpha-1 and presynaptic alpha-2 adrenoceptors are inaccessible to the short term bolus-induced elevation of circulating ANP during longer term increases in plasma ANP, it does reach the junction, reduces NE release and limits effects of receptor activation, possibly by diminishing Ca++ entry.(ABSTRACT TRUNCATED AT 250 WORDS)     

Abnormal ryanodine receptor function in heart failure

The abnormally regulated release of Ca2+ from an intracellular Ca2+ store, the sarcoplasmic reticulum (SR), is the mechanism underlying contractile and relaxation dysfunctions in heart failure (HF). According to recent reports, protein kinase A (PKA)-mediated hyperphosphorylation of ryanodine receptor (RyR) in the SR has been shown to cause the dissociation of FK506 binding protein (FKBP) 12.6 from the RyR in heart failure. This causes an abnormal Ca2+ leak through the Ca2+ channel located in the RyR, leading to an increase in the cytosolic Ca2+ during diastole, prolongation of the Ca2+ transient, and delayed/slowed diastolic Ca2+ re-uptake. More recently, a considerable number of disease-linked mutations in the RyR have been reported in patients with catecholaminergic polymorphic ventricular tachycardia (CPVT) or arrhythmogenic right ventricular dysplasia type 2. An analysis of the disposition of these mutation sites within well-defined domains of the RyR polypeptide chain has led to the new concept that interdomain interactions among these domains play a critical role in channel regulation, and an altered domain interaction causes channel dysfunction in the failing heart. The knowledge gained from the recent literature concerning the critical proteins and the changes in their properties under pathological conditions has brought us to a better position to develop new pharmacological or genetic strategies for the treatment of heart failure or cardiac arrhythmia. A considerable body of evidence reviewed here indicates that abnormal RyR function plays an important role in the pathogenesis of heart failure. This review also covers some controversial issues in the literature concerning the involvement of phosphorylation and FKBP12.6.     

Atrial natriuretic peptide in human essential hypertension

We measured the circulating levels of atrial natriuretic peptide (ANP) in 62 patients with untreated uncomplicated essential hypertension and in 30 normotensive subjects. In the hypertensive patients, mean systolic and diastolic blood pressures were 148 and 101 mm Hg, respectively, and the mean heart rate was 73 beats/min. ANP concentrations were not elevated in the hypertensive group but were actually decreased slightly over those of the control group (27.4 +/- 1.8 pg/ml versus 35.3 +/- 2.4 pg/ml [P less than 0.02]). No relationship was found between ANP levels and diastolic blood pressure, plasma renin activity, urinary sodium excretion, or serum creatinine level. In 8 of the 62 patients with essential hypertension, 6 weeks of treatment with a dihydropyridine calcium channel blocker, nitrendipine, significantly reduced plasma ANP levels from 28.6 +/- 4.3 pg/ml to 18.7 +/- 1.8 pg/ml (P less than 0.05). In 17 additional patients treated with the hypotensive agent ketanserin, ANP levels were not significantly reduced after treatment. Thus, this study demonstrates that circulating plasma ANP levels are not increased but are slightly decreased in patients with uncomplicated essential hypertension in comparison with normotensive subjects. Furthermore, antihypertensive treatment with a calcium channel antagonist reduced plasma levels of ANP.