模拟缺血再灌注后心肌细胞胰岛素抵抗机制的初步研究

Objective Recent.studies have found a strong association of insulin resistance, which might occur during ischemia reperfusion in vitro in the experimental dogs, with disturbed function of cardiomyocytes. Obvious acute insulin resistance, along with glucose dysmetabolism in the reperfused cardiomyocytes, was furher observed in the study performed with ischemia-reperfused ventric- ular myocytes of rats. We tried to investigate preliminarily the molecular mechanisms of insulin resistance in the cardiomyocytes after ischemia reperfusion. Methods An experimental model of insulin-stimulated ischemia reperfusion (SI/R) was created by isolating cardiomyocytes from adult rats. Glucose uptake of the cardiomyoctyes was evaluated with isotope-labeling technique. Glucose trans- porter 4 (GLUT4) translocation induced by insulin was investigated with Western blot analysis, and the intracellular level of free Ca2+ ([Ca2+]I) was measured quantitatively with Ca2+ indicator Fura-2. Results Insulin can stimulated glucose uptake by cardiomyo- cytes, indicating that these cells were insulin-sensitive. Cardiomyocytes were demonstrated notable acute insulin resistmce during reperfusion. Insulin-stimulated GLUT4 translocation in the cardiomyocytes 15 minutes after reperfusion was 72.2% of that in the con- trol group(P<0.05), in which the GLUT4 content in plasma membrane remained unchanged. The finding suggested that a disturbed GLUT4 translocation might happen in the cardiomyocytes during insulin-stimulated ischemia-reperfusion. Calcium overload was identi- fied in the cardiomyocytes with ischemia reperfusion. At 15 minutes of reperfusion, [Ca2+]I was significantly higher in the reperfused cardiomyocytes than that in the control cardiomyocytes[(318.66±23.06)vs(130.70±0.82) nmol/L, P<0.05], and kept at a higher level [(177.79±17.46) nmol/L] at 60 minutes of reperfusion (P<0.05, vs control). Partial correlation analysis revealed a negative correlation of[Ca2+]I with insulin-induced ghcose uptake in the cardiomyoctyes (r = -0.557,P=0.006). Conclusion Disturbed GLUT4 translocation and decreased intrinsic activity may be important molecular mechanisms for the development of insulin resistance in the cardiomyocytes of rat during insulin-simulated ischemia reperfusion,. [Ca2+]I overload may account for the de- creased intrinsic activity d GLUT4.     

吡那地尔超极化心脏停搏液对再灌注后细胞因子及心脏功能的影响

目的观察犬体外循环(CPB)再灌注后吡那地尔超极化心脏停搏液与传统高钾心脏停搏液对肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)和心脏功能的影响. 方法 12只雄性杂种狼犬随机分为两组,对照组(n=6)主动脉阻断时用4℃ St.Thomas Ⅱ号心脏停搏液(K+ 20 mmol/L),每30分钟灌注1次;实验组(n=6)用4℃含吡那地尔50 μmol/L 的St.Thomas Ⅱ号心脏停搏液(K+ 5 mmol/L),每50分钟灌注1次.两组犬主动脉均阻断150分钟.在转流前和主动脉开放后180分钟时测定TNF-α和IL-6的含量,于转流前、主动脉开放后30、60、120和180分钟时监测血流动力学指标的变化. 结果主动脉开放后180分钟,两组TNF-α和IL-6与转流前比较均明显升高(P<0.01),但两组间比较差别无显著性意义.主动脉开放后120分钟和180分钟,两组平均动脉压(MAP)、心脏指数(CI)、每搏指数(SI)、左心室每搏作功指数(LVSWI)与转流前比较均明显降低(P<0.05),但两组间差别无显著性意义. 结论与传统高钾心脏停搏液比较,吡那地尔超极化心脏停搏液无明显的减轻炎性反应作用,其改善心功能的作用也并不优于传统的高钾心脏停搏液.     

主动脉右心室隧道1例及文献复习

主动脉右心室隧道(Aorto—Right Ventricular Tunnel ARVT)是非常罕见的一种先天性心脏畸形。经检索CBMDISC和MEDLINE光盘及网上检索MEDLNE数据库,从1966年到1998年的32年献中,共有7例报道。     

模拟缺血再灌注后心肌细胞胰岛素抵抗机制的初步研究

Objective Recent.studies have found a strong association of insulin resistance, which might occur during ischemia reperfusion in vitro in the experimental dogs, with disturbed function of cardiomyocytes. Obvious acute insulin resistance, along with glucose dysmetabolism in the reperfused cardiomyocytes, was furher observed in the study performed with ischemia-reperfused ventric- ular myocytes of rats. We tried to investigate preliminarily the molecular mechanisms of insulin resistance in the cardiomyocytes after ischemia reperfusion. Methods An experimental model of insulin-stimulated ischemia reperfusion (SI/R) was created by isolating cardiomyocytes from adult rats. Glucose uptake of the cardiomyoctyes was evaluated with isotope-labeling technique. Glucose trans- porter 4 (GLUT4) translocation induced by insulin was investigated with Western blot analysis, and the intracellular level of free Ca2+ ([Ca2+]I) was measured quantitatively with Ca2+ indicator Fura-2. Results Insulin can stimulated glucose uptake by cardiomyo- cytes, indicating that these cells were insulin-sensitive. Cardiomyocytes were demonstrated notable acute insulin resistmce during reperfusion. Insulin-stimulated GLUT4 translocation in the cardiomyocytes 15 minutes after reperfusion was 72.2% of that in the con- trol group(P<0.05), in which the GLUT4 content in plasma membrane remained unchanged. The finding suggested that a disturbed GLUT4 translocation might happen in the cardiomyocytes during insulin-stimulated ischemia-reperfusion. Calcium overload was identi- fied in the cardiomyocytes with ischemia reperfusion. At 15 minutes of reperfusion, [Ca2+]I was significantly higher in the reperfused cardiomyocytes than that in the control cardiomyocytes[(318.66±23.06)vs(130.70±0.82) nmol/L, P<0.05], and kept at a higher level [(177.79±17.46) nmol/L] at 60 minutes of reperfusion (P<0.05, vs control). Partial correlation analysis revealed a negative correlation of[Ca2+]I with insulin-induced ghcose uptake in the cardiomyoctyes (r = -0.557,P=0.006). Conclusion Disturbed GLUT4 translocation and decreased intrinsic activity may be important molecular mechanisms for the development of insulin resistance in the cardiomyocytes of rat during insulin-simulated ischemia reperfusion,. [Ca2+]I overload may account for the de- creased intrinsic activity d GLUT4.     

缺血心肌及其功能转归

缺血心肌及其功能转归西安医科大学第一临床医学院隋东虎综述刘治全杨鼎颐审校近年来，随着冠状动脉腔内成形术及急性心肌梗塞溶栓治疗等的临床应用，以及正电子发射计算机断层显像（ＰＥＴ）、核磁共振（ＭＲ）等检查技术的开展，人们发现再灌注后缺血受损的心肌并非只有...     

体外循环时间及主动脉阻断时间不同时再灌注后细胞因子的变化及其与心功能的关系

目的：探讨在体外循环时间和主动脉阻断时间不同时再灌注后细胞因子的变化及其与心功能的关系，方法：12条雄性杂种狼犬，按体外循环升主动脉阻断时间不同分为两组，组I（n=6):主动脉阻断25min，组Ⅱ（n=6)：主动脉阻断150min。分别于转流前和再灌注后180min抽取动脉血检测肿瘤坏死因子α（TNF－α）和白细胞介素6（IL－6）的水平，监测血流动力学，结果：再灌注后血浆TNF－α和IL－6与转流前比较组I无明显升高（P＞0．05），组II与转流前比较显著升高，转流后两组之间比较组II明显高于组I（P均＜0．05），终止体外循环后组I心功能无明显变化（P＞0．05），组II平均动脉压，心脏指数，每搏指数，左心室每搏作功指数均显著降低并低于组I（P＜0．01），TNF－α和IL－6与上述心功能指标呈明显的负相关，结论：长时间体外循环和主动脉阻断是造成再灌注后细胞因子升高的主要原因；而细胞因子升高与心功能障碍的发生明显相关。     

模拟缺血再灌注后心肌细胞胰岛素抵抗机制的初步研究

Objective Recent.studies have found a strong association of insulin resistance, which might occur during ischemia reperfusion in vitro in the experimental dogs, with disturbed function of cardiomyocytes. Obvious acute insulin resistance, along with glucose dysmetabolism in the reperfused cardiomyocytes, was furher observed in the study performed with ischemia-reperfused ventric- ular myocytes of rats. We tried to investigate preliminarily the molecular mechanisms of insulin resistance in the cardiomyocytes after ischemia reperfusion. Methods An experimental model of insulin-stimulated ischemia reperfusion (SI/R) was created by isolating cardiomyocytes from adult rats. Glucose uptake of the cardiomyoctyes was evaluated with isotope-labeling technique. Glucose trans- porter 4 (GLUT4) translocation induced by insulin was investigated with Western blot analysis, and the intracellular level of free Ca2+ ([Ca2+]I) was measured quantitatively with Ca2+ indicator Fura-2. Results Insulin can stimulated glucose uptake by cardiomyo- cytes, indicating that these cells were insulin-sensitive. Cardiomyocytes were demonstrated notable acute insulin resistmce during reperfusion. Insulin-stimulated GLUT4 translocation in the cardiomyocytes 15 minutes after reperfusion was 72.2% of that in the con- trol group(P<0.05), in which the GLUT4 content in plasma membrane remained unchanged. The finding suggested that a disturbed GLUT4 translocation might happen in the cardiomyocytes during insulin-stimulated ischemia-reperfusion. Calcium overload was identi- fied in the cardiomyocytes with ischemia reperfusion. At 15 minutes of reperfusion, [Ca2+]I was significantly higher in the reperfused cardiomyocytes than that in the control cardiomyocytes[(318.66±23.06)vs(130.70±0.82) nmol/L, P<0.05], and kept at a higher level [(177.79±17.46) nmol/L] at 60 minutes of reperfusion (P<0.05, vs control). Partial correlation analysis revealed a negative correlation of[Ca2+]I with insulin-induced ghcose uptake in the cardiomyoctyes (r = -0.557,P=0.006). Conclusion Disturbed GLUT4 translocation and decreased intrinsic activity may be important molecular mechanisms for the development of insulin resistance in the cardiomyocytes of rat during insulin-simulated ischemia reperfusion,. [Ca2+]I overload may account for the de- creased intrinsic activity d GLUT4.     

体外循环术后并发急性胰腺炎一例

患者　男 ,18岁。术前诊断为先天性心脏病 ,法洛三联症合并动脉导管未闭 ,于 1999年 12月 2 1日在我院行法洛三联症根治术、动脉导管内口缝合术。术中体外循环时间 6 1分钟 ,主动脉阻断时间 2 6分钟 ,手术顺利 ,术后第 8天出院。出院后第 5天 ,患者出现发热 ,伴持续性腹胀、腹痛 ,以剑突下及上腹部明显 ,不向其它部位放射 ,无恶心、呕吐和腹泻。查体 :体温37.5℃ ,脉搏 114次 /分 ,血压 90 /5 1mm Hg (1k Pa =7.5 mm Hg) ,急性痛苦病容 ,皮肤巩膜无黄染 ,心肺 (- ) ,腹稍膨隆 ,脐周、右上腹压痛及反跳痛 ( ) ,墨菲征 (- ) ,移动性浊音 ( …     

体外循环围术期血清SIL—2R变化及临床意义

应用双抗体平似ＥＬＩＳＡ法动态观察了２６例体外循环围术期患者血清ＳＩＬ－２Ｒ变化，结果显示：ＣＰＢ后ＳＩＬ－２Ｒ水平显著增高，第７天渐恢复，１４天仍未恢复术前水平；术后并发感染组较无感染组ＳＩＬ－２Ｒ增高更显著，且持继高水平。     

先天性左房房壁瘤手术矫治1例

先天性左房房壁瘤手术矫治１例黄庆恒，杨鼎颐，隋东虎，梁立德，李兆志病人女，３１岁。发作性心慌、气短２年余，加重２月入院。查体：心界明显向左侧扩大。快速心律失常，且与体位有关，但无病理性杂音。肝－颈回流征阳性。心电图示房颤，房扑伴３：２房室传导阻滞交替...