60例射频导管消融术后机体凝血系统活性的动态变化及低分子肝素的影响

目的探讨射频导管消融术(RFCA)后机体凝血系统活性的动态变化及低分子肝素的影响.方法选取60例行RFCA患者随机分为A组(n=29)和B组(n=31),另选22例行心内电生理检查患者为对照组.A组29例术后不予肝素,B组31例术后运用低分子肝素,A组以肝细胞生长因子(HGF)0.40 ng/ml为界分为高HGF者和正常HGF者.在不同时间测定凝血酶-抗凝血酶Ⅲ复合物(TAT)及HGF.结果①A组TAT呈现两次高峰术后即刻第一次高峰(42.8 4-15.7)ng/ml,术后3天第二次高峰(20.1±19.4)ng/ml,第二次高峰与对照组术后3天(2.7±1.5)ng/ml及B组术后3天(4.3±5.2)ng/ml比较差异有统计学意义(P＜0.05);②A组术后6 h HGF值与TAT两次高峰相关(r=0.553,P＜0.01);术后3天高HCF者TAT值明显高于正常HGF者(P＜0.05),差异有统计学意义.结论RFCA致凝血系统活性的动态变化可分两阶段术后即刻的急性阶段和术后3天的延迟阶段.术后肝素化可影响凝血系统,有阻止血栓形成的效果.     

射频消融术对凝血的影响及低分子肝素对其防治效果

目的旨在探讨预防射频消融术(RFCA)血栓栓塞并发症的方法。方法60例行RFCA患者随机分为两组,A组25例术后不应用肝素;B组35例术后6h开始予低分子肝素每日两次皮下注射,连用5天。两组患者再按左、右心导管操作各分成两个亚组。分别于术前、电生理检查(EPS)后即刻、RFCA后即刻及术后24h、3天及6天六个时段抽取静脉血,做血小板α颗粒膜糖蛋白140(GMP-140)、D-二聚体(DD)检测。结果①A组GMP-140EPS后开始升高,RFCA后即刻达到第一次峰值(20.95±2.02ng/ml),术后24h有所下降,术后3天达第二次峰值(22.24±1.94ng/ml)。B组RFCA后即刻GMP-140达到第一次峰值,术后3天未显示明显第二次峰值。术后3天、6天,B组明显低于A组。②两组DD自EPS后至术后3天逐渐升高,术后6天下降至术前水平。术后24h、3天、6天,B组明显低于A组。③两组亚组间GMP-140比较,各时刻均无差异。A组术后3天右心导管组DD明显高于左心导管组(1555±142ng/mlvs1352±193ng/ml),其余各时刻及B组各时段均无差异。结论RFCA术(无论左、右心导管操作)术后继续肝素化和联合抗血小板治疗十分必要。     

射频消融术后cTnT、cTnI、CK-MB测定及其影响因素

目的评价心肌肌钙蛋白T(cTnT)、心肌肌钙蛋白I(cTnI)、肌酸磷酸激酶同工酶(CK-MB)在诊断心肌损伤中的灵敏度和特异性;了解射频消融(RFCA)心肌损伤程度与消融因素的相关性.方法于术前、术后30 min、4 h、12 h、24h测量39例接受RFCA治疗者的血清cTnT和cTnI浓度及CK-MB活性.对照组(n=10)仅接受电生理检查(EPS).结果39例患者均无并发症出现.cTnT基础值为(0.01±0.004)ng/ml,术后30min为(0.27±0.13)ng/ml(P＜0.05),4 h达高峰水平[(0.29±0.12)ng/ml,P＜0.05].cTnI基础值(0.34±0.22)ng/ml,术后30min为(1.67±1.10)ng/ml(P＜0.05),4h达高峰水平[(1.72±1.50)ng/ml,P＜0.05].CK-MB术前、术后无显著差异.39例患者中29例(74%)cTnT≥0.1 ng/ml(P＜0.05),22例(56%)cTnI≥1.0 ng/ml(P＜0.05),两者无显著差异.cTnT峰值水平与消融靶点数、消融总时间、消融总次数、累积能量具有相关性;心室放电组cTnT水平明显高于心房放电组(P＜0.05).结论cTnT和cTnI诊断心肌损伤的灵敏度和特异性相似,且优于CK-MB;RFCA中应力求准确定位、减少试探性放电、缩短放电时间、降低放电功率,以最大限度地减少心肌损伤.     

经皮冠状动脉介入治疗患者应用普通肝素和低分子肝素对血浆肝细胞生长因子水平的影响

目的探讨不稳定型心绞痛患者经皮冠状动脉介入治疗(PCI)术中分别静脉应用普通肝素或低分子肝素对血浆肝细胞生长因子(HGF)的影响。方法74例不稳定型心绞痛患者根据PCI术时使用肝素类型分为普通肝素组(49例)和低分子肝素组(25例),分别在术前、术中、术后即刻以ELISA法测定外周血HGF的水平。结果两组术前HGF水平差异无统计学意义。普通肝素组和低分子肝素组术中及术后即刻HGF水平与术前相比均显著升高(术后中与术前比较:普通肝素组为12322.19±3723.31ng/L比1736.09±603.95ng/L,P<0.00001;低分子肝素组为9141.31±2521.91ng/L比1675.28±630.53ng/L,P<0.00001。术后即刻与术前HGF水平比较:普通肝素组为13565.60±3768.99ng/L比1736.09±603.95ng/L,P<0.00001;低分子肝素组为10092.35±2723.00ng/L比1675.28±630.53ng/L,P<0.00001)。低分子肝素组在PCI术中和术后即刻两个不同时段其外周血HGF水平均低于普通肝素组(P均<0.01)。结论不稳定型心绞痛患者在PCI术中无论是应用普通肝素还是低分子肝素,均可促进外周血HGF的释放,但在PCI术手术过程中,静脉注射普通肝素升高外周血HGF的作用比低分子肝素更强。     

射频消融术对凝血、抗凝系统的影响及阿斯匹林的作用

为探讨射频消融术 (RFCA)后外周血管栓塞的发生机制 ,将 6 0例室上性心动过速患者分为两组 (A组术前不用抗凝药 ,B组术前使用阿斯匹林 (ASA) ,在术前、插管完成心内电生理检测后、RFCA后即刻及术后两天 4个时段抽静脉血观察血小板α 颗粒膜糖蛋白 (Gmp 140 )、血栓烷B2 (TXB2 )、蛋白C(PC)、蛋白S(PS)的变化。结果 :A组病人 ,与术前比较 ,其他 3个时段血浆Gmp 140、TXB2 含量明显增加 (分别为 7.32± 0 .49,12 .87± 1.99,13.6 4± 1.47pg/mlvs 6 .2 6± 0 .75pg/ml,P <0 .0 5或 0 .0 1;80 .0 6± 2 .18,10 0 .42± 1.41,90 .0 8± 4.82pg/mlvs 70 .45± 2 .2 7pg/ml,P <0 .0 5或 0 .0 1) ,PC及PS血浆含量无变化 ,但左右心系统操作对Gmp 140、TXB2 变化无影响 ;B组与A组相比 ,术后相同时段的血浆Gmp 140、TXB2 含量减小 ,P <0 .0 5或 0 .0 1。提示RFCA可引起血小板的激活 ,对抗凝系统无明显影响 ,可致血栓形成 ;服用ASA可阻止血小板的激活 ,从而阻止血栓形成的作用     

血清肝细胞生长因子测定对急性冠脉综合征患者的临床意义

目的探讨急性冠脉综合征(ACS)患者血清肝细胞生长因子(HGF)水平变化的临床意义。方法入选59例ACS患者(急性心肌梗死组n=36,发病12h以内;不稳定型心绞痛组n=23)于入院时肝素注射前取静脉血,通过酶联免疫法测定血清HGF浓度。同时对与之性别及年龄相匹配的27例正常人测定相同指标。结果血清HGF浓度在AMI组[(1572.9±229.0)pg/ml]、UAP组[(899.2±63.9)pg/ml]较正常对照组[(619.5±31.1)pg/ml]明显增高;AMI发病3h内血清HGF水平也比正常对照组增高[(893.2±61.6)pg/mlvs(619.5±31.1)pg/ml];A-MI组血清HGF浓度与入院时cTnI、CK-MB及CK-MB峰值均无相关性;ACS患者血清HGF浓度与入院时CRP呈显著相关性。结论ACS患者血清HGF浓度增高,且与疾病的严重性呈正比;HGF的产生可能与ACS的炎症反应有关;血清HGF有可能成为临床上诊断早期AMI的一个新指标。     

肝素对大鼠肝星状细胞中转化生长因子β1和Ⅰ型胶原的影响

目的: 研究肝素与大鼠肝星状细胞(hepatic stellate cells, HSC)作用后转化生长因子beta1(transforming growth factor beta1, TGF-beta1)和Ⅰ型胶原表达的变化及意义. 方法: 大鼠肝星状细胞以1×108/L浓度接种于96孔培养板, 每孔100 muL. 实验分组为肝素Ⅰ组、肝素Ⅱ组、肝素Ⅲ组, 加入肝素使各组培养液中肝素浓度分别是10, 100, 1000 mg/L, 加生理盐水为对照组(每组6孔重复3次)培养48 h. 培养终止后吸取上清液-20℃冰冻保存, ELISA法检测其上清液TGF-beta1和Ⅰ型胶原水平, MTT法观察细胞增殖情况. 结果: 肝素Ⅱ组和Ⅲ组HSC培养上清液TGF-beta1水平均显著低于对照组(4.59±1.27 ng/L, 3.34±1.13 ng/L vs 5.95±1.72 ng/L, P均<0.01), 肝素各组Ⅰ型胶原水平均低于对照组(87.20±9.30 ng/L, 73.17±12.04 ng/L vs 95.61±12.55 ng/L, 63.31±10.93 ng/L vs 95.61±12.55 ng/L, P均<0.05), 肝素Ⅲ组平均吸光度低于肝素Ⅰ组和对照组(0.29±0.07 vs 0.42±0.12, 0.46±0.17, P均<0.05). 结论: 大鼠肝星状细胞在肝素作用下TGF-beta1和Ⅰ型胶原分泌受抑制, 其增殖减少.     

转化生长因子-β1、血管性假性血友病因子的表达与急性心肌梗塞发病的相关性研究

AMI组24例入院即刻转化生长因子-β1(TGF-β1)达高峰(409.27±414.53)％,以后逐渐下降,至第3周为(230.8±189.96)％十分接近正常对照组10例(113.75±73.92)％(P=0.046)。AMI组入院即刻、1周血管性假性血友病因子(vWF)均显著高于对照组(P=0),在1周时达高峰(119.96±24.81)ng/ml,以后随病情恢复呈逐渐下降趋势。TGF-β1与vWF无相关性,二者在AMI时的关系有待进一步研究。表1参4     

布地奈德干预对卵白蛋白致敏小鼠抗原激发后气道炎症及气道重塑的影响

目的　观察早期及延迟应用布地奈德对支气管哮喘 (简称哮喘 )小鼠气道炎症和气道重塑的防治作用。方法　40只小鼠分为 5组,每组 8只。鸡卵白蛋白(OVA)致敏 /激发组 (A组 ),生理盐水对照组(B组),布地奈德 (BUD)早期治疗组 (C组 ),BUD延迟治疗组 (D组 ),OVA延迟对照组(E组)。小鼠于第 0、14天以OVA致敏,从第 1次致敏后第 24天开始雾化吸入 2.5%的OVA激发并持续 18d,建立气道重塑模型;分别在早期(抗原激发前 1d始)和延迟(第 1次抗原激发后第 18天始)雾化吸入BUD(0.5mg/ml),观察抗原激发及BUD应用后支气管肺泡灌洗液(BALF)中嗜酸粒细胞(EOS)数、上清液白细胞介素 5(IL-5)和γ干扰素 (IFN-γ)水平的变化,同时对肺组织切片行苏木精 伊红(HE)、过碘酸雪夫(PAS)、Masson三色染色,测定支气管壁周围EOS计数、定量杯状细胞百分比及黏液分泌评分并测定气道平滑肌增生高度及胶原面积。结果　经过反复抗原激发,A组BALF中EOS数为(57.460±11 060)×104 /ml,B组为[ (0.050±0.020)×104 /ml],两组比较差异有统计学意义(P<0.01);A组BALF中IL- 5水平及IFN -γ水平分别为(52.9±2.8)pg/ml、(39.5±3.2)pg/ml,B组分别为(16.8±1.5)pg/ml、(63.8±3.3)pg/ml,两组比较差异有统计学意义 (P<0.01 );A、B组支气管壁周围EOS数分别     

经皮冠状动脉介入治疗中静脉注射那屈肝素的抗血栓疗效及安全性评价

目的比较经皮冠状动脉介入治疗(PCI)中静脉注射那屈肝素或普通肝素的抗血栓疗效及安全性.方法采用前瞻性、随机、单盲、多中心研究的设计,共入选98例因患冠心病需行PCI的患者,随机分为那屈肝素组(0.075 ml/10 kg,手术时间超过1 h补充半量)及普通肝素组(100 U/kg,手术时间超过1 h补充2000 U).PCI前静脉注射那屈肝素或普通肝素.那屈肝素组前22例患者分别在注射前、注射后8 min、1 h、2 h和4 h,用发色底物法测定血浆抗Ⅹa因子活性.出血程度的判断根据TIMI研究的标准进行.结果 (1) 性别、年龄、体重、血压、血红蛋白含量、红细胞压积、合并糖尿病的例数、冠心病类型、进行冠状动脉介入治疗的部位、介入治疗的手术方式及术前血浆cTNI>2 ng/ ml的例数在二组之间分布均衡,差异均无统计学意义;(2) 那屈肝素组前22例患者血浆抗Ⅹa因子活性测定显示,用药前、用药后8 min、1 h、2 h及4 h血浆抗Ⅹa因子活性分别为(0.10±0.00) IU/ ml、(1.89±0.24)IU/ ml、(0.96±0.24) IU/ ml、(0.47±0.13)IU/ ml和(0.30±0.12) IU/ ml.注射那屈肝素后8 min及1 h,所有患者血浆抗Ⅹa因子活性均在治疗水平(>0.5 IU/ ml),注射后2 h及4 h分别仅有45%及9%的患者血浆抗Ⅹa因子活性维持在治疗水平.(3)那屈肝素组术后血红蛋白数量、红细胞压积及出血指数分别为(129.5±13.6) g/L、(39.0±3.9)%和(1.16±5.80) g/L,与普通肝素组相似[分别为(125.5±14.9) g/L、(37.9±4.6)%和(0.90±6.5) g/L,P值分别为0.175,0.205和0.858);(4) 二组均无显微镜下血尿、无黑便或大便隐血阳性的患者;均无按TIMI试验标准所诊断的大出血或轻度出血的患者,无需要输血的患者;无穿刺部位的血肿;(5) PCI术后30 天内二组均无死亡、心绞痛复发及需行血管再通术等临床事件发生,那屈肝素组有1例患者PCI术后发生急性心肌梗死,普通肝素组无发生心肌梗死的病例,二组之间差异无统计学意义.结论 PCI术前注射那屈肝素能达到理想的抗血栓疗效; 与普通肝素相比,那屈肝素不增加出血事件和心血管病事件的发生率.     

Delayed thrombogenesis following radiofrequency catheter ablation.

The cause and duration of the thrombogenesis provoked by radiofrequency catheter ablation (RF-CA) was investigated by measuring the thrombin-antithrombin III complex (TAT) in 43 patients who underwent RF-CA and in 20 control subjects who underwent an electrophysiologic study. Blood samples were collected at 7 different times: before introducing the sheaths, during the ablation procedure and at 30 min, 6 and 24h, and 3 and 6 days after the procedure. Hepatocyte growth factor (HGF) was simultaneously measured in the ablation group. Plasma TAT concentration exhibited a double peaked pattern in the ablation group: the first peak occurred during the ablation procedure (42.8+/-15.5 ng/ml), and the second peak 3 days later. Plasma TAT at 3 days after the procedure was significantly higher than that of the control group (21.3+/-19.0 vs 2.5+/-1.4, p=0.0003). The first peak significantly correlated with the procedure time prior to the administration of heparin (r=0.669), but the second peak did not (r=0.132). A subgroup with a serum HGF >0.40 ng/ml at 6 h after the procedure exhibited a significantly high second peak. The thrombogenesis caused by RF-CA has 2 phases; in the acute phase, there is hemostasis during placement of the catheters, and in the delayed phase thrombogenesis is the result of endothelial damage from the RF current.     

Hepatocyte growth factor production may be related to the inflammatory response in patients with acute myocardial infarction.

Hepatocyte growth factor (HGF) is a well-known powerful proliferative factor of vascular endothelial cells and it has been reported that plasma HGF concentrations are increased in acute myocardial infarction (AMI), although the mechanisms are not yet well delineated. Serum HGF levels and C-reactive protein (CRP) were measured in 22 patients with unstable angina pectoris (UAP) (15 males, 7 females; class IIb or IIIb of the Braunwald classification), 60 patients with AMI (37 males, 23 females; average time from the onset of symptoms to admission 4.6+/-0.7h, range, 0.5-12h), and 20 normal subjects. Immediate angioplasties were performed in 51 patients with AMI, and the time course of the HGF levels were measured in 31 patients among them. Heparin dramatically increased the HGF level and it declined to the normal range 18h after heparin injection. Blood samples were taken before heparin treatment, or at least 24h after. Serum HGF levels on admission was significantly increased in UAP (mean+/-SE: 0.30+/-0.03ng/ml, p<0.01), and AMI (0.27+/-0.02ng/ml, p<0.01) compared with the normal subjects (0.19+/-0.01 ng/ml). Even in the early stage (within 3 h of onset of symptoms to admission, average time was 1.8+/-0.1 h), serum HGF levels were already elevated (0.25+/-0.02 ng/ml, p<0.05). There was no significant difference between the HGF levels in UAP and AMI. Fifty-one of the 60 patients with AMI underwent immediate percutaneous transluminal coronary angioplasty and blood samples were obtained from 31 of them on days 7, 14, and 21 after MI. Serum HGF levels peaked on day 7 (0.34+/-0.04ng/ml, p<0.01) and there was a weak relationship between peak creatine kinase and serum HGF levels at that time. A statistically significant correlation was found between peak CRP and serum HGF levels on day 7 (r=0.62: p<0.001). Serum HGF levels decreased to nearly normal by day 21 (0.22+/-0.01 ng/ml). The study shows that serum HGF levels during the early stage of AMI increased significantly and peaked by day 7 after the onset, at which time there was a strong correlation with peak CRP levels. These data suggest that HGF production may be related to the inflammatory response in AMI.     

Dopaminergic modulation of arginine mediated growth hormone and prolactin release in man

The mechanism of arginine (ARG) induced growth hormone (GH) and prolactin (PRL) release is poorly understood. Though dopamine (DA) is known to inhibit a number of GH and PRL secretagogues, it has been reported not to affect arginine mediated GH release. Our study was undertaken to study the interaction of DA and ARG further. Six healthy male volunteers received DA (4μg/kg/min) or saline from 0–240 min on two separate days. ARG (30 gms) was given 150–180 min on both days (Protocol I). In Protocol II 5 subjects received ARG on different days 30–60 min into a DA or saline infusion. On a third day only DA was given. Arginine alone was given in 2 separate infusions spaced 135 minutes apart to 5 volunteers (Protocol III). In Protocol I when ARG was given at 150 min, the maximal GH peak of 11.1 ± 1.3 ng/ml, which occurred 45 min later, was blunted by DA treatment (5.3 ± 1.1 ng/ml, p < 0.005). On the DA day prior to ARG, there was also a GH peak at 75 min of 8.1 ± 1.9 ng/ml. In Protocol II, when the ARG and DA responses coincided, the mean maximal GH response to both stimuli was 20.5 ± 3.3 ng/ml which was greater than to either DA (7.7 ± 2.2 ng/ml, p < 0.01) or ARG alone (14.6 ± 3.0 ng/ml, N.S.). Moreover, the area under the curve for DA and ARG together (1196 ± 186 ng/ml/150 min) was greater than for DA (484 ± 160 ng/ml/150 min, p < 0.001) or ARG separately (544 + 70 ng/ml/150 min, p < 0.05). During the double arginine, which mirrored temporally the pattern of GH release observed in Protocol I, the peak GH responses after each infusion were similar (9.0 ± 2.1 and 8.8 ± 2.1 ng/ml). The maximal PRL responses to ARG were 11.1 ± 3.8 ng/ml and 15.7 ± 4.8 ng/ml in Protocol I and II respectively, but these responses were abolished by the DA infusion in both studies. Our data, therefore, provide further evidence to support a dual role of DA in GH release. DA stimulates basal GH secretion and this effect is additive to that of ARG. However, when ARG administration is delayed, the GH response is now blunted. The inhibitory action of DA is not mediated by its prior release of GH, since the GH responses are similar after sequential ARG infusions. Consequently, the role of DA is directly related to the degree of secretion. This duality is not seen with PRL secretion, where DA is always inhibitory.     

Plasma level changes of fibrinopeptide a after uncomplicated coronary angioplasty

Fibrinopeptide A (FPA) is a small polypeptide cleaved from fibrinogen by thrombin, has a short half-life, and is considered a sensitive biochemical marker of thrombin activity, fibrin generation, and ongoing thrombosis. Increased plasma levels of FPA have been reported in various procoagulable and thrombotic medical and cardiovascular disorders, including acute myocardial infarction, unstable angina, and sudden cardiac death. However, activation of thrombosis by the arterial injury incurred during coronary angioplasty has not been systematically examined with use of plasma FPA measurements. To detect and monitor activation of thrombosis by coronary angioplasty, plasma levels of FPA were obtained by venipuncture and measured by radioimmunoassay before, immediately after, 24 to 48 h later, and 1 and 3 months after uncomplicated coronary angioplasty. From December 1990 through June 1991, FPA was measured in 30 patients (28 men and 2 women, aged 54 ± 9 years) with coronary artery disease who were undergoing coronary angioplasty. The mean left ventricular ejection fraction was 55 ± 7%. The dilated vessel was the left anterior descending coronary artery in 20 patients (together with a second vessel in 2), the right coronary artery in 9, and the left circumflex in 1. The procedure was successful and free of major complications in all patients. Before angioplasty the FPA levels averaged 6.50 ± 1.18 ng/ml. Shortly after angioplasty they rose to 20.20 ± 7.91 ng/ml (p = 0.08) despite intravenous heparin. At 24 to 48 h and after heparin had been discontinued for at least 4 h, the mean FPA levels were significantly higher (32.33 ± 10.86 ng/ml) compared with baseline values (p = 0.025 ). At 1 month after the procedure, the FPA levels measured in 22 patients were lower but still elevated (20.25 ± 9.29 ng/ml), albeit nonsignificantly, compared with baseline values, and at 3 months they had fallen to baseline values (4.84 ± 2.20 ng/ml, n = 11). No patient developed restenosis during the study period of 1 to 3 months, during which all patients were receiving aspirin. We conclude that, as reflected by increased FPA levels, angioplasty, most likely due to arterial injury incurred, activates thrombin and generates ongoing coronary thrombosis, which is not suppressed by heparin or aspirin and appears to extend at least through the first month after the procedure.     

Changes of serum hepatocyte growth factor in coronary artery disease

Hepatocyte growth factor (HGF) is an endothelial cell specific growth factor involved in the repair of endothelial cells and collateral formation, however, the role for coronary artery disease is still unknown. We measured serum HGF level in various coronary artery diseases to examine the clinical significance. Serum HGF level was measured using the enzyme-linked immunosorbent assay method in patients with stable effort angina pectoris (n = 26), old myocardial infarction (n = 18), unstable angina pectoris (UAP; n = 10) and acute myocardial infarction (AMI; n = 21). As a control group, we selected 11 patients with neurocirculatory asthenia. Blood samples from peripheral veins were collected at cardiac catheterization before heparin administration. In the AMI group, blood samples were also collected at 48, 72 hr, 1, 2, 3 and 4 weeks from the peripheral veins and 48 and 72 hr after reperfusion from the coronary sinus. Serum HGF level was significantly higher in the UAP (0.41 +/- 0.12 ng/ml, p < 0.001) and AMI groups (0.38 +/- 0.26 ng/ml, p < 0.05) compared to the control group (0.19 +/- 0.09 ng/ml). Serum HGF level peaked 48 hr after reperfusion in both the peripheral veins (0.42 +/- 0.16 ng/ml) and coronary sinus (0.58 +/- 0.23 ng/ml) in the AMI group, with a significantly higher level in the coronary sinus than the peripheral veins (p < 0.05). No significant correlation between peak HGF level in the peripheral veins and peak creatine kinase (CK), CK-MB, ejection fraction and cardiac index was observed. Serum HGF was elevated in acute coronary syndrome, indicating advanced endothelial cell damage. HGF is produced, at least partially, in the heart in patients with AMI. Serum HGF level may be useful to detect endothelial cell damage rather than myocardial cell damage.     

经心内膜右房线形消融治疗心房颤动的安全性评价

为探讨经心内膜右房线形消融治疗心房颤动（简称房颤）的安全性，１２只犬以乙酰胆碱静脉滴注和（或）电刺激建立房颤模型，观察射频导管消融前、后实验犬的病理生理变化。结果显示：①与消融前相比，消融后窦性心率（１５０．８２±３６．７１ｂｐｍｖｓ１６３．６７±３０．９９ｂｐｍ）、窦性Ｐ波时限（７３．６４±１６．８０ｍｓｖｓ６９．５８±１２．１４ｍｓ）、ＰＲ间期（１２０．７３±２６．２９ｍｓｖｓ１１４．０２±１９．２１ｍｓ）、校正窦房结恢复时间（７６．２５±１８．８７ｍｓｖｓ７２．５０±１１．９０ｍｓ）、右房压力（０．４９±０．０６ｋＰａｖｓ０．４６±０．０８ｋＰａ）以及血浆心钠素（０．４８±０．１１ｎｇ／ｍｌｖｓ０．５０±０．０７ｎｇ／ｍｌ）变化均无显著性差异（Ｐ均＞０．０５）。血清磷酸肌酸激酶于消融后即刻明显升高（５２５．９５±４２６．４９Ｕ／Ｌｖｓ１１５．２７±２８．７０Ｕ／Ｌ，Ｐ＜０．０１），但术后１４日与消融前相比已无显著性差异（１１４．０２±２３．３５Ｕ／Ｌｖｓ１１５．２７±２８．７０Ｕ／Ｌ，Ｐ＞０．０５）。②４只犬发生并发症，其中１只损伤窦房结，２只发现心脏巨大附壁血栓，另１只术后出现一过性房性早搏、短阵房?     

Acute Changes in Plasma Levels of Hepatocyte Growth Factor During Low‐Density Lipoprotein Apheresis

Abstract: Hepatocyte growth factor (HGF) is a mesenchyme‐derived pleiotropic factor, and angiogenesis is included in a variety of its functional effects. HGF levels were measured in 5 sessions of low‐density lipoprotein (LDL) apheresis in 3 patients with severe hypercholesterolemia. Blood was collected at the start (T0) and at 1,000 ml (T1), 2,000 ml (T2), and 3,000 ml (T3) plasma treatments. During LDL apheresis, HGF levels increased from 1.59 ± 0.78 (mean ± SE, n = 5) ng/ml at T0 to 6.64 ± 0.97 at T1, 6.28 ± 0.97 at T2, and 5.20 ± 0.94 at T3. In one apheresis session, HGF increased immediately at the 100 ml plasma treatment stage. HGF was adsorbed completely by a dextran‐sulfate (DS) column. Despite the adsorption by the DS column, HGF in the patient blood increased to the levels with functional effects. The improvement of ischemic symptoms due to LDL apheresis may be related to the angiogenic activities of HGF.     

Hepatocyte growth factor effects on motility of stone-diseased and stone-free human gallbladders

Hepatocyte growth factor (HGF) has unique morphogenic activity for several cell types. Besides its major effect upon liver regeneration, its motogenic activity to enhance motility has not been verified for smooth muscles. Therefore we evaluated the impact of HGF in an in-vitro model of human gallbladder motility. Twelve stone-diseased and eight stone-free muscle strips were preincubated with HGF (100 ng/ml, 200 ng/ml). For the analysis of motility, cholecystokinin (CCK) was added (0.1 nM, 0.5 nM, 2 nM, 10 nM, and 100 nM). Twelve stone-diseased and eight stone-free strips without HGF incubation served as the control group. The tone of healthy (tone/100 nM CCK: control group, 12.4 ± 3.6 mN; HGF group, 19.5 ± 4.5 mN) and stone-diseased (tone/100 nM CCK: control group, 10.8 ± 3.8 mN; HGF group, 17.3 ± 4.8 mN) muscle strips, preincubated with HGF, was increased, with a higher sensitivity to CCK. Our results suggest that there is a clear motogenic response of stone-diseased human gallbladders to HGF. Received: October 26, 1998 / Accepted: April 16, 1999