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1.
In this study of the relationship between hypertensive left ventricular hypertrophy (LVH) and neurohumor factors and ventricular
arrhythmias, 180 cases were divided at random into 3 groups: 60 cases with primary hypertension and LVH (PH+LVH); 60 cases
with simple hypertension (PH), and with other diseases and LVH(NPH+LVH). The results showed that 1. The excitability of the
sympathetic nerve was not elevated while the activity of the vagus nerve was not significantly decreased in the patients with
PH+LVH. The increased sympathetic nervous tension was correlated with the ventricular premature beat which was statistically
correlated with the myocardial ischemia. 2. The patients’ condition in group PH+LVH was not correlated with the levels of
aldosterone and insulin and was not even positively correlated with the levels of renin and angiotensin-II. 3. The patients
in group PH+LVH had high incidence of ventricular premature beat and myocardial ischemia. 4. The patients’ condition in group
NPH+LVH was not even positively correlated with the neurohumor factors but their heart failure was positively correlated,
with the levels of aldosterone, sympathetic nervous tension, myocardial ischemia and ventricular premature beat. 相似文献
2.
目的 :探讨心律平和稳心颗粒联合治疗复杂性室性早搏的效果。方法 :对照组采用心律平 15 0mg ,每日 3次 ;观察组采用心律平 15 0mg ,每日 3次 ,稳心颗粒 1袋 ,一日 3次 ,两组均是 14d为一个疗程。结果 :观察组有效率为 91.4 3% ,1例出现Ⅱ°～Ⅰ型房室传导阻滞 ,对照组有效率为 6 5 .71% ,3例出现Ⅱ°或Ⅲ°房室传导阻滞。结论 :心律平和稳心颗粒联合应用治疗室性早搏明显优于单一应用心律平。 相似文献
3.
目的:探讨普罗帕酮对左心室流出道自律细胞的电生理效应.方法:应用常规的玻璃微电极细胞内记录技术,观察普罗帕酮对豚鼠左心室流出道(主动脉前庭)动作电位0相幅值(APA),最大除极速率(Vmax),动作电位时程(APD),50%复极化时间(APD50),90%复极化时间(APD90),自发电活动频率(HR)的影响.结果:1.用0.5μmol/L的普罗帕酮灌流后与正常对照组相比自发电活动频率(HR)显著下降(P<0.01);2.用1μmol/L的普罗帕酮灌流后与对正常照组相比动作电位0幅值(APA)下降(P<0.05),动作电位时程(APD)延长(P<0.05).结论:普罗帕酮能抑制左心室流出道(主动脉前庭)的动作电位0幅值,延长动作电位时程,使自发电活动频率下降. 相似文献
4.
目的:研究心得安对异丙肾上腺素所致左心室流出道自律性电活动改变的影响.方法:本实验采用标准玻璃微电极细胞内引导技术在记录离体豚鼠该部位自发慢反应电位的基础上,观测了心得安对异丙肾上腺素作用的影响.结果:100μmol/L异丙肾上腺素(Iso)可使自发放电频率(RPF)和4期自动去极速度(VDD)显著加快,动作电位幅度(APA)显著增大,0期最大去极速度(Vmax)明显加速,复极50%时间(APD50)缩短(P＜0.01或P＜0.001);5μmol/L心得安可拮抗100μmol/L Iso的电生理效应.结论:Iso可提高左心室流出道组织的自律性电活动,其效应可被心得安阻断. 相似文献
5.
右心室流出道电生理特性及临床意义 总被引：1，自引：0，他引：1
目的:研究右心室流出道的电生理特性,并探讨其与心室流出道心律失常的关系.方法:利用细胞内微电极记录技术,观察豚鼠右心室流出道组织的电活动特性.结果:在23例豚鼠右室流出道组织标本中4例(17.39%)可记录到自律性电活动.在紧靠瓣膜下及流出道光滑部的局部区域可记录到非自律性慢反应电位(MDP:62.28±8.14mv,APA:65.22±15.18mV,Vmax:22.27±8.13v/s,APD90:176.24±10.13ms,APD50:123.47±12.3 6ms)及形态不典型的自律性慢反应电位,其0相去极化速度、幅度及动作电位时程变异较大.大部分区域为非自律快反应动作电位(MDP:71.23±6.62mv,APA:79.33±5.48mV,Vmax:103.13±9.03v/s,APD90:166.23±20.33ms,APD50:126.33±16.26ms),其特征与普通心室肌细胞动作电位相似.结论:右心室流出道组织的电生理特性与普通心室肌不同,其自律性和电生理异质性可能是某些流出道心律失常的电生理学基础. 相似文献
6.
目的:为了研究高血压大鼠左室流出道电位的变化。方法:利用大鼠的离体心脏,采用常规玻璃微电极细胞内记录方法。观察静息电位(RP)、0相去极幅度(APA)、0相最大除极速度(Vmax)、复极时程(APD)以及复极50％(APD_(50))和复极90％(APD_(90))的时间。结果:高血压大鼠左室流出道诱发电位APD、APD_(50)、APD_(90)都明显高于正常同龄大鼠(P<0.01)。结论:高血压大鼠左室流出道动作电位复极时程延长。 相似文献
7.
山莨菪碱对静息状态下心肌细胞浆[Ca2+]i无显著影响,对高钾诱发心肌细胞浆[Ca2+]i升高,山莨菪碱10μmol·L-1虽有抑制作用,但与对照组相比天显著差异（P＞0.05）,山莨菪碱50μmol·L-1可显著抑制大鼠心肌细胞浆[Ca2+]i升高,与对照组相比,差异显著（P＜0．01） 相似文献
8.
杨晓东 《岳阳职业技术学院学报》2008,23(2):61-64
冠心病的病理学基础是动脉粥样硬化.目前认为动脉粥样硬化的形成和斑块的破裂与细胞外基质的破坏和重构有密切关系,而基质金属蛋白酶(MMPs)是降解细胞外基质的重要酶类.对近年来关于MMPs的结构、功能、基因表达以及在冠心病中的作用的研究取得的成果进行了综述. 相似文献
9.
应用实时三维超声心动图评价冠心病患者经皮冠状动脉介入术(PCI)后左室收缩功能的变化。研究对象分为两组,正常组14例为冠脉造影无异常发现者,冠心病组49例行冠脉内支架治疗。所有患者均于术前及术后14天行实时三维超声检查,测得左室收缩末容积(LVESV)、左室舒张末容积(LVEDV)及左室射血分数(LVEF)。结果,正常组术前与术后LVESV、LVEDV及LVEF差异无统计学意义;冠心病组术后LVESV、LVEDV显著小于术前(P<0.001),LVEF显著高于术前(P<0.001)。结果表明,实时三维超声心动图能准确评价左室收缩功能,冠心病患者PCI后左室收缩功能明显改善。 相似文献
10.
大鼠左心室流出道电生理特性的观察 总被引：1，自引：1，他引：1
目的为了观察大鼠左心室流出道组织是否具有自动节律性.方法利用细胞内微电极记录技术,观察了18例大鼠左心室流出道组织的电生理特征.结果16例(88.89%)出现了自律性电活动,并且可在局部组织记录到典型的慢反应动作电位.结论大鼠左心室流出道组织具有自律性.其生理功能有待进一步研究. 相似文献
11.
目的:为探讨氯化镍对心脏自律细胞的影响。方法:利用细胞内微电极记录技术,观察了18例家兔窦房结和左心室流出道自律细胞动作电位的特征。以分析Ni~(2 )对窦房结和流出道自律细胞作用的异同。结果:用180μmol/L NiCl_2灌流后两自律细胞自发慢反应电位的VDD、APA、Vmax、RPF均明显下降(P<0.01),而且窦房结细胞APD、APD_(90)也显著延长;二者的MDP、APD_(50)均无明显改变(P>0.05)。结论:NiCl_2对窦房结起搏细胞和主动脉前庭自律细胞动作电位0相和4相去极离子流有明显抑制作用。 相似文献
12.
目的探讨经胸超声心动图在膜部瘤型室间隔缺损介入封堵治疗中的应用价值。方法对19例介入封堵的膜部瘤型室间隔缺损患者进行术前超声分型、术中超声监测、术后超声随访。结果超声检查诊断结果分型：囊袋型9例、漏斗型5例、菜花型3例、管状型2例,共19例,除1例释放封堵器后超声心动图见少量残余分流外,余病例膜部瘤型室间隔缺损介入封堵均获得成功,成功率为95%。结论经胸超声心动图在膜部瘤型室间隔缺损的介入封堵治疗中具有重要的临床应用价值。 相似文献
13.
目的 :探讨 4-AP对家鸽左心室流出道组织动作电位的影响。方法 :利用细胞内微电极记录技术 ,观察 1 2例家鸽左心室流出道组织的电生理特征 ,以分析 4 -AP对家鸽左心室流出道的作用。结果 :在局部组织记录到典型的慢反应动作电位 ;用 2mmol/L 4 -AP灌流后 ,慢反应电位RP、APA、Vmax均明显下降 (P <0 .0 5) ,而APD、APD90 也显著延长 ;APD50 无明显改变 (P >0 .0 5)。结论 :家鸽左心室流出道组织不同于普通心室肌组织 ;4-AP对家鸽左心室流出道组织慢反应动作电位去极和复极离子流有明显抑制作用 相似文献
14.
目的 :为进一步阐明Ca2 + 通道在心脏起搏中所起的作用 ,及左心室流出道 (主动脉前庭 )自律细胞的特性。方法 :利用常规的玻璃微电极细胞内记录技术 ,观察了 2 6例家兔窦房结和左心室流出道自律细胞动作电位的特征。以分析钙通道阻断剂 -维拉帕米 (VER)和氯化镍 (NiCl2 )对窦房结和流出道自律细胞的影响。结果 :(1)用 1μmol/LVER灌流后窦房结及主动脉前庭自律细胞的APA、Vmax、MDP绝对值、VDD、RPF均明显下降 ,APD90 延长 (P <0 .0 5 )。 (2 )用 180 μmol/LNiCl2 灌流后两自律细胞自发慢反应电位的VDD、APA、Vmax、RPF均明显下降 (P <0 .0 1) ,而且窦房结细胞APD90 也显著延长 ;二者的MDP、APD50 均无明显改变 (P >0 .0 5 )。结论 :钙通道阻断剂对窦房结起搏细胞和主动脉前庭自律细胞动作电位 0相和 4相去极离子流有明显抑制作用。 相似文献
15.
目的 :探讨高血压心肌肥厚过程中Na+ -K+ -ATPase活性的变化。方法 :用酶活性测定的方法 ,测定 12周、16周自发性高血压大鼠 (SHR)大鼠和Wistar大鼠的心肌Na+ -K+-ATPase酶的活性。结果 :(1)不同年龄SHR大鼠血压和左心室肥厚指数明显高于同龄Wis tar大鼠 ,但SHR大鼠间无显著差异。 (2 )SHR大鼠心肌Na+ -K+ -ATPase活性随年龄增加而明显降低 ,但两种大鼠 12周龄、16周龄间无显著差异。结论 :SHR大鼠血压和左心室肥厚指数明显增加 ,Na+ -K+ -ATPase活性发生下降 ,但是 12周与 16周间无明显差异。 相似文献
16.
XIA Qin-gui *L Oliver Chung Heidi Spitznagel Thomas Unger 《Journal of Zhejiang University. Science. B》2001,(4)
ＩＮＴＲＯＤＵＣＴＩＯＮＴｈｅＮａ /Ｈ ｅｘｃｈａｎｇｅｒ (ＮＨＥ)ｉｓａｐＨ ｒｅｇｕｌａｔｏｒｙｐｒｏｔｅｉｎｐｒｅｓｅｎｔｉｎｔｈｅｐｌａｓｍａｍｅｍ ｂｒａｎｃｅｏｆｃａｒｄｉｏｍｙｏｃｙｔｅｓａｎｄｏｔｈｅｒｃｅｌｌｔｙｐｅｓ.ＡｌｔｈｏｕｇｈｓｅｖｅｒａｌｉｓｏｆｏｒｍｓｏｆＮＨＥｈａｖｅｂｅｅｎｄｅ ｃｒｉｂｅｄ,ｔｈｅｐｒｅｄｏｍｉｎａｎｔｉｓｏｆｏｒｍｉｎｔｈｅｈｅａｒｔｉｓｔｈｅｕｂｉｑｕｉｔｏｕｓＮＨＥ 1 ,ｗｈｉｃｈｕｎｄｅｒｃｅｎｔａｉｎｐｈｙｓｉｏｌｏｇｉｃａｌｃｏｎｄｉｔｉ… 相似文献
17.
目的：探讨持续不卧床腹膜透析（CAPD）患者不同腹膜转运功能下微炎症的发生情况、心脏结构、营养状况及存活率情况。方法：腹膜透析患者腹膜透析治疗3个月～1年并除外炎症、肿瘤、急性冠脉综合症等伴随疾病的患者人选本研究,通过腹膜平衡试验（PET）判断腹膜通透性,根据试验结果将患者分为2组：高转运、高平均转运的患者为高通透性组（H／A;D／Pcreat≥0．65,D为透析液肌酐浓度,P为血浆肌酐浓度）;低转运和低平均转运患者为低通透性组（L／A;D／P〈0．65）。对入选患者随访26个月或腹膜治疗终点（死亡或转为血液透析或行肾移植）,观察结束检测患者血CRP,了解患者微炎症的发生情况。同时检测患者的血白蛋白、血红蛋白、主观综合营养评估（SGA）、KT／Vurea,心脏B超检查记录各心腔的大小,计算左心室心肌重量指数,并对两组间生存率分析。结果：高通透性组CRP升高（CRP〉5mg／L）的比例大于低通透组（P〈0．05）;营养状况较低通透组差并普遍存在左心室肥大（P〈0．05）,但小分子清除率方面差异无统计学意义（P〉0．05）;高通透组2年生存率79．24％,低通透性组两年生存率89．39％。结论：腹膜高通透性患者微炎症的发生率高于低通透性患者,且营养情况差,左心室肥大发生增加,存活率降低,提示我们对腹膜高通透性患者应早期给予干预措施以提高患者存活率、改善预后。 相似文献
18.
通过化学方法提取槭叶总碱，作用于氯仿--肾上腺素诱发家兔室性心率失常，说明槭木草对于心动过速有减缓心跳作用。 相似文献
19.
Zhao LL Chen HJ Chen JZ Yu M Ni YL Zhang WF 《Journal of Zhejiang University. Science. B》2008,9(6):448-454
Objective: To assess the effect of angiotensin Ⅱ type 1 (AT1) receptor antagonist losartan on myocardium connexin43 (Cx43) gap junction (GJ) expression in spontaneously hypertensive rats (SHRs) and investigate possible mechanisms. Methods: Sixteen 9-week-old male SHRs and 8 age-matched male Wistar-Kyoto (WKY) rats were included in this study. SHRs were randomly divided into two groups to receive losartan at 30mg/(kg·d) by oral gavage once daily for 8 weeks (SHR-L) or vehicle (0.9% saline) to act as controls (SHR-V); WKY rats receiving vehicle for 8 weeks served as normotensive controls. At the end of the experiment, rats were sacrificed and the hearts were removed. Expressions of Cx43 and nuclear factor-kappaB p65 (NF-κB p65) proteins in all three groups were observed and further investigations on the effect of angiotensin Ⅱ type 1 receptor antagonist losartan (30mg/(kg·d), 8 weeks) on Cx43 expression were conducted with Western blot and immunohistochemistry. NF-κB p65 protein in nuclear extracts was determined by Western blot. Results: Left ventricular (LV) hypertrophy was prominent in SHRs, Cx43 and NF-κB p65 protein expressions were obviously upregulated and Cx43 distribution was dispersed over the cell surface. Treatment with losarton reduced the over-expressions of Cx43 and NF-κB p65 in LV myocardium. The distribution of Cx43 gap junction also became much regular and confined to intercalated disk after losartan treatment. Conclusion: Cx43 level was upregulated in LV myocardium of SHR during early stage of hypertrophy. Angiotensin Ⅱ type l receptor antagonist losartan prevented Cx43 gap junction remodeling in hypertrophied left ventricles, possibly through the NF-κB pathway. 相似文献
20.
Objective: In addition to pH regulation, Na+/H+ exchange (NHE) has been shown to facilitate cell growth and proliferation. However, the effects of long-term inhibition of
Na+/H+ exchange on cardiac structural and functional remodeling post myocardial infarction (MI) are still controversial. The present
study was therefore carried out to further investigate the effects of long-term treatment with cariporide, a specific inhibitor
of NHE-1, on cardiac remodeling after MI in rats; Methods: Male Wistar rats that underwent coronary ligation were randomly
selected for cariporide treatment starting 6 h after induction of MI or no treatment. Treatment was continued up to 6 weeks
post MI, after which, the arterial, venous and left ventricular catheters were chronically implanted. Twenty-four h later,
after hemodynamic signals were recorded in conscious rats, they were sacrificed and hearts were taken out for morphological
examinations; Results: Cariporide treatment decreased the heart weight and heart weight to body weight ratio (bothP<0.05), decreased left ventricular end-diastolic pressure (P<0.001), improved myocardial contractility (dP/dt
max) (P<0.05) and tended to increase the survival of treated rats compared to that of untreated infarct rats; Conclusion: The results
of the present study indicate that the long-term inhibition of NHE with cariporide can attenuate cardiac structural remodeling
and improve left ventricular dysfunction in infarcted rats, and suggest that Na+/H+ exchange inhibition could be an effective therapeutic strategy for myocardial infarction-induced heart failure. 相似文献