葡萄糖与极化液对经皮冠状动脉介入治疗术后心肌损伤的随机对照研究

目的比较葡萄糖与极化液对减少经皮冠状动脉介入治疗（PCI）术后心肌损伤的不同作用。方法选择接受PCI治疗的冠心病患者100例,随机分为试验组和对照组,各50例。试验组在常规治疗的基础上于PCI术前2～4h给予10％葡萄糖溶液500ml,对照组则给予极化液（10％葡萄糖溶液500m1＋10％氯化钾溶液10ml＋胰岛素12U）。所有患者术前及术后次日检测磷酸激酶同工酶（CK—MB）和肌钙蛋白I（cTnI）浓度。结果试验组和对照组基线临床资料差异无统计学意义（P〉0．05）。试验组PCI术前快速血糖水平显著高于对照组[（11．9±3．6）w（5．3±3．7）mmol／L,P〈0．001];试验组PCI术后快速血糖水平亦显著高于对照组[（8．8±4．2）VS（5．1±3．9）mmol／L,P〈0．001]。试验组患者PCI术前快速血糖水平无1例≤5．0mmol／L,而对照组患者有7例（14．0％）出现快速血糖水平≤5．0mmol／L。两组患者PCI术后CK—MB和cTnI均显著升高,且对照组CK—MB和cTnI升高幅度更显著,对照组CK—MB和cTnI升高1～3倍者及〉3倍者的比例更高（均P〈0．05）。结论冠心病患者PCI术前应用葡萄糖较极化液可显著减少PCI术后心肌损伤。     

极化液治疗危重病患儿应激性高血糖的效果

目的探讨极化液治疗儿童应激性高血糖的疗效。方法应激性高血糖患儿30例随机分成极化液治疗组和对照组,每组各15例。在综合治疗基础上,治疗组予极化液降糖,对照组仅将葡萄糖输入量严格控制在4mg/（kg·min）以下。监测二组患儿治疗前、入院8～12h、第2、3天血糖。同时应用简化小儿危重病例评分法进行病情评估。结果入院时、入院8～12h、第2、3天血糖值,治疗组分别为（20.7±5.02）、（11.98±3.13）、（7.55±1.94）、（5.12±1.04）mmol/L,对照组分别为（19.16±4.49）、（14.89±3.42）、（10.7±2.63）、（5.95±1.33）mmol/L。与入院时血糖比较,治疗组血糖下降较快;8～12h及第2天二组血糖下降比较差异有显著性意义（Pa〈0.01）;第3天,二组血糖下降比较差异无显著性意义（P〉0.05）。二组入院时危重状态及极危重状态各分别为7和8例;第2天,治疗组3例仍为危重状态,其余转为非危重,转安率为80%;对照组尚有7例危重,2例极危重,转安率为40%,二组转安率比较差异有显著性意义（P〈0.05）。第3天,治疗组均转为非危重,对照组尚有2例危重状态、1例极危重状态。二组转安率分别为100%、80%,二组比较差异无显著性意义（P〉0.05）。结论应用极化液治疗儿童应激性高血糖安全有效,经济简便,利于疾病恢复。     

Low-Dose Glucose-Insulin-Potassium Is Ineffective in Acute Myocardial Infarction: Results of a Randomized Multicenter Pol-GIK Trial

Summary. We aimed to assess the clinical efficacy of glucose-insulin-potassium (GIK) in acute myocardial infarction. Experimental data provided evidence of the beneficial effects of GIK on ischemic myocardium. The clinical trials, mostly uncontroled and conducted mainly before the thrombolytic era, were inconclusive due to the small number of patients and discrepancies in protocols. In order to evaluate the efficacy of this intervention, we have performed a prospective multicenter randomized study. The study consisted of 954 patients with acute myocardial infarction (MI) randomized within 24 hours from the onset of symptoms to low-dose GIK (n = 494), which consisted of 1000 mL 10% dextrose, 32–20 U insulin, and 80 mEq K+, or to the control group (n = 460), which was given 1000 mL 0.09% sodium chloride, by intravenous 24-hour infusion at a rate of 42 mL/h. Cardiac mortality and the occurrence of cardiac events at 35 days did not differ between GIK and control-allocated patients (32 (6.5%) vs. 21 (4.6%), respectively; OR 1.45, 95% CI 0.79–2.68, P = 0.20; and 214 (43.3%) vs. 192 (41.7%), OR 1.07, 95% CI 0.82–1.38, P = 0.62). Total mortality at 35 days was significantly higher in the GIK than in the control group (44 (8.9%) vs. 22 (4.8%), respectively, OR 1.95, 95% CI 1.12–3.47, P = 0.01). The excess of noncardiac deaths in the GIK group may have occurred by chance. Low-dose GIK treatment does not improve the survival and clinical course in acute MI.     

极化液对围术期老年患者室性心律失常和心率变异性的影响

目的观察极化液(GIK)对非心脏手术老年患者围术期室性心律失常和心率变异性的影响。方法选取80例非心脏手术老年患者,并将其随机分为观察组和对照组,每组40例。2组患者均于术前给予常规准备,观察组术中根据血糖情况持续大剂量输注GIK。麻醉前及术后12、24、36、48 h应用标准视觉模拟评分法(VAS)对2组患者进行疼痛评分。术前12 h及术后12、24、36、48 h对2组患者发生各类室性心律失常的情况进行比较。对2组患者术前,术后第1、2天的各项心率变异性指标进行比较。结果手术开始时和结束时,观察组患者的血糖水平均显著低于对照组(P0.05);观察组在术后12~24 h、24~36 h和36~48 h的室性早搏次数增加的患者比例显著少于对照组(P0.05);观察组术后第2天的总功率(TP)、极低频功率(VLF)、正常R-R间期的标准差(SDNN)等指标均显著高于对照组(P0.05)。结论在非心脏手术老年患者术中持续大剂量输注GIK能够缓解患者的应激性高血糖症状,降低室性心律失常的发病概率和心率的变异性。     

胺碘酮与胺碘酮联合用药治疗心房纤颤疗效的比较

目的:观察单纯用药与联合用药对心房纤颤（房颤）治疗效果。方法: 选择119例房颤患者随机分为2组:单纯用药组54例,给予静脉胺碘酮150~300 mg后,继之以口服胺碘酮维持;联合用药组65例,使用极化液、硝酸甘油和小剂量利尿剂、胺碘酮,胺碘酮使用的剂量与方法同单纯用药组。观察两组房颤转复率和窦性维持率。结果: 联合用药组的房颤转复率较单纯组明显提高（80% vs. 94%,P＜0.05）,复律时间减少［（55±19） vs.(39±15） s,P＜0.05］,追踪复律半年后的维持率,联合用药组明显高于单纯用药组（81% vs. 95%,P＜0.05）。复查B超显示:联合用药后,左心房内经明显缩小,从［(46±6) mm减少到(42±6) mm,P＜0.05］,左心室舒张末期内径缩小,从(52±7) mm减少到(45±6) mm(P<0.05);而单纯用药组这两项指标均无明显改变。结论: 联合用药组较单纯用药组能明显提高对房颤患者的转复率和窦性维持率。     

Patient Self-Management of Oral Anticoagulant Therapy: An International Update

While glucose-insulin-potassium (GIK) has been suggested to be cardioprotective, few studies have assessed its effect on anatomic myocardial infarct size in an ischemia-reperfusion protocol. Anesthetized rabbits were subjected to a 30-minute coronary artery occlusion followed by 4 hours of reperfusion. Rabbits were pretreated with a GIK infusion lasting 90 minutes or placebo. GIK infusion markedly increased serum glucose levels by over twofold, but the area of necrosis expressed as the area at risk was not reduced by GIK infusion (25%) versus control (20%). In a rabbit infarct model of ischemia/reperfusion, GIK failed to reduce myocardial infarct size.     

Glucose-insulin-potassium solution improves left ventricular mechanics in diabetes

BACKGROUND: The mechanism by which glucose-insulin-potassium solutions enhance recovery of left ventricular function after myocardial ischemia in diabetic patients is not well understood. We evaluated the effect of glucose-insulin-potassium on ventriculoarterial coupling and left ventricular mechanics in a chronic ovine model of diabetes. METHODS: Diabetes was induced in 6 sheep with streptozotocin. After 6 months of diabetes, the response of the left ventricular pressure-volume relationship to 60 minutes of intravenous glucose-insulin-potassium solution (1,000 mL of 5% dextrose in water, 100 IU of regular insulin, 90 mmol of KCl at 1.5 mL x kg(-1) x h(-1)) was determined. RESULTS: Glucose-insulin-potassium solution increased end-systolic elastance 68% (p = 0.01) and improved ventriculoarterial coupling (1.7+/-0.3 to 1.0+/-0.1; p < 0.01). Potential energy decreased 35% (p = 0.01), and pressure-volume area decreased 20% (p = 0.01). However, stroke work did not change; therefore stroke work efficiency increased from 50.1%+/-3.5% to 60.2%+/-5.1% (p = 0.01). CONCLUSIONS: Glucose-insulin-potassium solution improves left ventricular contractility and ventriculoarterial coupling in diabetes. Left ventricular mechanics is improved by decreasing total mechanical work without significantly affecting stroke work, resulting in improved stroke work efficiency. Improved efficiency facilitates understanding of the enhanced tolerance to myocardial ischemia afforded by glucose-insulin-potassium solution.     

高剂量葡萄糖-胰岛素-氯化钾极化液治疗病毒性心肌炎的临床研究

目的探讨高剂量葡萄糖-胰岛素-氯化钾极化液（HGIK）对病毒性心肌炎的临床治疗作用。方法60例病毒性心肌炎患者随机分为非极化液对照组（n=30）和高剂量葡萄糖-胰岛素-氯化钾极化液组（n=30）,两组均给予常规基础治疗：大剂量能量合剂（VitC6.0g）＋辅酶Q10胶囊,在此基础上再分别给予HGIK组高剂量葡萄糖-胰岛素-氯化钾极化液（25%葡萄糖＋60U/L胰岛素＋80mmol/L氯化钾）治疗,非极化液对照组病毒唑治疗。观察各组病例在症状、体征、心肌酶学、心电图等方面的疗效变化。结果譹HGIK治疗病毒性心肌炎具有显著临床疗效,临床症状改善总有效率明显高于非极化液对照组（P〈0.05）;譺HGIK对病毒性心肌炎早搏具有明显的治疗作用,总有效率明显高于非极化液对照组（P〈0.05）;譻HGIK能显著降低CK-MB和cTnI水平（P〈0.01）;与非极化液对照组差异具有显著性（P〈0.05）。结论HGIK对病毒性心肌炎具有显著临床疗效。     

Different effects of interventions suppressing free fatty acid metabolism on myocardial ischemia

We studied the effects of different metabolic interventions, which stimulate oxidative myocardial carbohydrate metabolism, on ischemic stress during repeated coronary occlusions of three minutes in open-chest dog hearts. Increase of glucose concentration in plasma and decrease of peripheral lipolysis by glucose-insulin-potassium (n = 6) had no substantial beneficial effects on myocardial damage indicated by hemodynamic, electrocardiographic, and metabolic parameters. Infusion of lactate and pyruvate (10 mM, n = 6) was detrimental. Only activation of pyruvate dehydrogenase by dichloroacetate (n = 6) without influence on plasma osmolality reduced epicardial ST-segment elevations (-42%) and myocardial release of potassium (-36%), phosphate (-58%), and lactate (-39%). Elevations of plasma osmolalities by 10 and 20 mOsm with the metabolically inert mannitol increased ECG changes, functional loss and release of potassium, phosphate, and lactate during ischemia in our model. It is suggested, that the oxygen-saving potency of metabolic interventions can exert univocal beneficial effects in experimental and in clinical conditions only when systemic hyperosmolality and hypervolemia are avoided.     

GIK对缺血/再灌注犬心肌超微结构的影响

目的:观察葡萄糖-胰岛素-钾液（GIK）、葡萄糖-钾液（GK）对急性心肌缺血/再灌注（MI/R）犬心肌缺血区内心肌细胞改变的影响,分析GIK中的胰岛素对MI/R心肌细胞的保护作用。 方法: 将犬心肌定量缺血(左前降支血流量降低80%) 50 min,再灌注4 h,建立犬MI/R模型。24只杂种犬随机分为GIK组、GK组和盐水对照组(n=8),于再灌注前5 min,分别输注GIK、GK和生理盐水。再灌注4 h后,计算梗死区占缺血区重量的百分比,并制作电镜切片于透射电镜下观察。 结果: GIK可显著减少心肌梗死(MI)的范围［GIK组（5.2±0.8）% vs. 盐水对照组（9.4±0.8）%,P<0.05］;而GK组MI的范围（8.5±0.9）%则与盐水对照组无明显差异。与盐水对照组相比,GIK组对非缺血心肌的超微结构无影响,对缺血心肌有一定的保护作用。GK对缺血心肌无保护作用。结论: 再灌注时,静脉输注GIK可减轻心肌超微结构的损伤,其中的胰岛素是GIK上述作用的关键成分。