钠钙交换器抑制药在心律失常治疗中的应用

心肌钠钙交换在调节心肌细胞内外钠、钙平衡中发挥重要作用。钠钙交换分为前向型和逆向型2种。在心力衰竭、心肌缺血、心肌再灌注等病理情况下,通过钠钙交换器的离子交换可产生致心律失常性的一过性内向电子流,引起延迟后除极和非折返激动型的室性心动过速。钠钙交换器抑制药在预防这些病理情况下的心律失常具有潜在的作用。     

病毒性心肌炎及扩张型心肌病患者心内膜心肌活检标本中免疫球蛋白的检测

对病理学确诊的25例病毒性心肌炎（VMC）和10例扩张型心肌病（DCM）患者心内膜心肌活检标本，运用ABC技术，进行了免疫球蛋白IgG、IgM、IgA和补体C3的检测。结果：20例VMC和9例DCM的标本中，发现了IgG和IgM的沉积，主要分布于心肌肌膜和毛细血管内皮，IgG的肌膜沉积与同步做的病理切片中观察到的心肌细胞坏死和炎性细胞浸润有病理形态学联系。两组患者中均未发现IgA和C3沉积。结果显示，IgG是参与VMC和DCM心肌损伤的主要免疫球蛋白，心肌病变与抗体诱导的免疫反应有关。     

老年心功能不全血浆心钠素浓度的变化

采用放射免疫法测定31例老年心功能不全患者血浆心钠素(ANP)浓度,发现老年心功能不全组ANP明显低于对照组(P<0.01)。血浆ANP含量随心功能不全的严重程度而明显减少(P<0.05)。病程与ANP浓度呈负相关 (r=-0.441,P<0.05)。不同病种、不同受累部位及有或无房颤之间ANP差异无显著性(P<0.05)。     

CRRT治疗老年顽固性心力衰竭的疗效观察

顽固性心力衰竭(CHF)是临床常见而又难治的心脏疾病,其病死率一直居高不下,虽然国内外许多学者采用了多种综合性措施,如主动脉内气囊反搏、植入心脏起搏器等,然而其预后仍较差。近几年来国外学者采用血滤或血透的方法矫治顽固性CHF取得了一些进展。由于研究结果差异较大,已成为     

重度充血性心力衰竭患者心率和每搏输出量的凌晨分离现象研究

目的 研究重度充血性心力衰竭患者血流动力学的昼夜节律改变.方法 选择2005年12月至2006年6月在南京中医药大学无锡附属医院心内科住院的重度充血性心力衰竭患者120例为心衰组,同期门诊体检的无心血管疾病者20名为对照组,采用生物阻抗法每小时1次动态监测心率(HR)和每搏输出量(SV).结果 心衰组与对照组HR、SV均存在昼夜节律,但分布规律存在差异,心衰组HR明显快于对照组(P＜0.5),而SV明显低于对照组(P＜0.05);对照组HR与SV呈正相关(P＜0.01),而心衰组HR与SV总体上也呈正相关(P＜0.01),但在凌晨100～400之间,两组HR与SV分布曲线明显不同,心衰组HR与SV分布曲线出现分离现象,HR下降而SV上升,呈负相关(P＜0.01),而同时段的对照组HR与SV则仍呈正相关(P＜0.01).结论 重度充血性心力衰竭患者HR和SV分布的昼夜节律受损,在凌晨100～400之间,HR与SV分布趋势存在分离现象.     

加味生脉饮治疗心衰合并低钠血症临床观察

目的 :评价加味生脉饮对心衰合并低钠血症的疗效。方法 :84例心衰合并低钠血症患者随机分为治疗组和对照组。治疗组 4 2例以加味生脉饮为主治疗 ,对照组 4 2例单纯西药治疗。结果 :治疗组心衰控制率、低钠血症改善率及预后均优于对照组 (P <0 0 5 )。结论 :中药对心衰合并低钠血症的治疗具有一定的价值。     

Altered neuropeptide Y Y1 responses in mesenteric arteries in rats with congestive heart failure

The aim of the present study was to elucidate if the potentiating effect of neuropeptide Y on various vasoactive agents in vitro is (1) altered in mesenteric arteries from rats with congestive heart failure and (2) mediated by the neuropeptide Y Y₁ receptor. The direct vascular effects of neuropeptide Y and its modulating effects on the contractions induced by endothelin-1-, noradrenaline-, 5-hydroxytryptamine (5-HT)-, U46619-(9, 11-dideoxy-11, 9-epoxymethano-prostaglandin F₂) and ATP, and acetylcholine-induced dilatations were studied in the presence and absence of the neuropeptide Y Y₁ antagonist, BIBP3226 (BIBP3226{(R)-N2-(diphenylacetyl)-N-[(4-hydroxyphenyl)methyl]- -arginine-amide}). Neuropeptide Y, per se, had no vasoactive effect in the arteries. The potency of endothelin-1 was significantly decreased in congestive heart failure rats. Neuropeptide Y and neuropeptide Y-(13–36) potentiated the endothelin-1-induced contraction in congestive heart failure mesenteric arteries. In 20% of the congestive heart failure rats, sarafotoxin 6c induced a contraction of 31±4%. Neuropeptide Y also potentiated U46619- and noradrenaline-induced contractions but not 5-HT-induced contractions in congestive heart failure arteries. In sham-operated animals neuropeptide Y potentiated noradrenaline- and 5-HT-induced contractions. These potentiations were inhibited by BIBP3226. Acetylcholine induced an equipotent relaxation in both groups which was unaffected by neuropeptide Y. In conclusion, neuropeptide Y responses are altered in congestive heart failure rats. The potentiating effect differs between vasoactive substances. Neuropeptide Y Y₁ and non-neuropeptide Y₁ receptors are involved.