高血压病患者脂餐后血管内皮功能受损

目的探讨高血压病患者高脂餐后血管内皮功能变化.方法 20例高血压病患者和20名正常对照者在禁食12 h后接受高脂餐负荷试验.分别测定餐前及餐后2、4、5、7 h血清血脂浓度.采用高分辨血管外超声法检测餐前及餐后4 h肱动脉血流介导的内皮依赖性血管舒张功能.结果两组受试者的空腹血脂水平无显著差异;餐后2、4、5 h血清甘油三酯(TG)浓度较空腹状态有显著升高.但高血压病组具有较高的餐后4、5、7 h血清TG浓度及其净增加值.两组受试者餐后内皮依赖性血管舒张功能均较空腹时显著受损.高血压病组,(5.38±1.95)% vs(2.21±1.06)%;对照组,(9.38±2.42)% vs(6.25±2.23)%;P<0.001.高血压病组的空腹以及餐后内皮依赖性血管舒张功能较对照组均显著受损(P<0.001),且餐后内皮依赖性血管舒张功能的受损程度显著高于对照组[(58±14)% vs (33±17)%,P<0.001].相关分析显示餐后4 h 血清TG浓度净增加值与餐后内皮依赖性血管舒张功能的变化率显著正相关(r=0.373,P<0.05).结论高血压病患者餐后显著而持久的高甘油三酯血症可导致餐后内皮依赖性血管舒张功能严重损害.     

银杏叶提取物对高脂饮食所致血管内皮功能损伤的保护及与对氧磷酶活性的关系

为探讨银杏叶提取物对高脂血症所致血管内皮功能损伤的保护作用及其机制 ,在大鼠高脂血症模型对比观察了银杏叶提取物和维生素E的作用。结果发现 ,大鼠高脂血症导致血管内皮依赖性舒张反应和非内皮依赖性舒张反应、血清一氧化氮浓度和对氧磷酶活性显著降低、血清丙二醛浓度显著升高。银杏叶提取物 [2 5mg (kg·d) ]或维生素E[10 0mg (kg·d) ]对高脂血症无明显抑制作用 (P >0 .0 5 ) ,但显著保护血管舒张功能和一氧化氮的血清浓度及对氧磷酶的活性 ,阻止了丙二醛的升高。在对照组、高脂组、银杏叶提取物和维生素E组 ,一氧化氮浓度(mmol L)分别为 5 .16± 1.3、3.35± 1.0 7、5 .0 5± 1.4 1和 4 .91± 1.6 5 (高脂组比对照组 ,P <0 .0 5 ;高脂组比银杏叶提取物和维生素E组 ,P <0 .0 5 ) ;内皮依赖性舒张反应分别为 95 .1%± 19.8%、4 7.1%± 15 .0 %、81.8%± 9.3%和 76 .2 %± 11.3% (高脂组比对照组 ,P <0 .0 1;高脂组比银杏叶提取物和维生素E组 ,P <0 .0 1) ;非内皮依赖性舒张反应分别为 98.2 %± 3.6 %、5 6 .7%± 7.9%、85 .8%± 7.2 %和 83.6 %± 4 .9% (高脂组比对照组 ,P <0 .0 1;高脂比银杏叶提取物和维生素E组 ,P <0 .0 1) ;对氧磷酶活性 (kU L)分别为 :18.0 %± 7.2 %、7.9%± 3.7%、16 .5 %     

维生素C对高脂餐后内皮依赖性血管舒张功能的保护作用

目的探讨维生素C对高脂餐后内皮依赖性血管舒张功能变化的影响。方法74例冠心病患者被随机分为两组,分别在禁食12h后进食高脂餐与维生素C2g（A组,n＝37）或单纯的高脂餐（B组,n＝37）。分别采集餐前及餐后2、4、5、7h静脉血标本,用以测定血清甘油三酯(TG)、总胆固醇、低密度脂蛋白-胆固醇（LDL-C）、高密度脂蛋白-胆固醇（HDL-C）浓度。采用高分辨血管外超声法检测餐前及餐后4h肱动脉血流介导的内皮依赖性血管舒张功能和硝酸甘油介导的内皮非依赖性血管舒张功能。结果冠心病患者空腹状态的内皮依赖性血管舒张功能显著受损。服用维生素C2g（A组）餐后4h内皮依赖性血管舒张功能较餐前无显著变化［（3.63±0.59）%∶（4.51±0.49）%,P=0.064］;未服用维生素C2g（B组）餐后4h内皮依赖性血管舒张功能较餐前相比严重受损［（3.58±0.63）%∶（0.58±0.40）%,P<0.001］。高脂餐后硝酸甘油介导的内皮非依赖性血管舒张功能的变化无统计学意义［A组（19.48±1.38）%∶（20.25±1.21）%,P=0.498;B组（18.71±1.53）%∶（16.36±1.53）%,P=0.135］。两组受试者餐后2～7h血清TG浓度均显著升高。经相关分析结果显示B组受试者的餐后2h血清TG浓度增高值与餐后4h内皮依赖性血管舒张功能下降值显著正相关（r=0.395,P<0.02）。结论高脂餐后内皮依赖性血管舒张功能显著受损,大剂量维生素C对其有保护作用。     

中心型肥胖患者内皮舒张功能与血清瘦素相关

目的探讨中心型肥胖患者内皮依赖性舒张功能异常与血清瘦素的关系。方法按配对方法分为中心型肥胖组和对照组,用放射免疫法检测血清瘦素水平,用高分辨超声技术检测肱动脉内皮舒张功能。结果中心型肥胖组肱动脉内皮依赖性舒张功能较对照组明显减退(6.71%±3.60%比13.81%±3.71%,P<0.01),非内皮依赖性舒张功能差异无显著性(19.71%±6.63%比18.60%±6.35%,P>0.05)。中心型肥胖组血清瘦素水平明显高于对照组,男性肥胖组与男性对照组比较(8.63±3.73μg/L比3.05±1.56μg/L,P<0.01)、女性肥胖组与女性对照组比较(16.73±6.93μg/L比7.93±3.66μg/L,P<0.01)差异均有显著性。Pearson相关分析显示肱动脉内皮依赖性舒张功能与血清瘦素水平呈显著负相关。结论中心型肥胖者存在内皮依赖性舒张功能异常,它与血清瘦素水平的增高有关。     

高血压病患者脂餐后甘油三酯代谢变化与血管内皮功能的关系

目的本研究旨在探讨高血压病(EH)患者脂餐后甘油三酯(TG)变化及其与血管内皮功能之间的关系.方法38例EH患者和20例健康人禁食10～12h后,采用高分辨率彩色血管超声、以肱动脉反应性充血前、后血管内径变化百分比反映血管内皮依赖性扩张功能.随后进行标准脂肪负荷试验,以TG8h曲线下面积(TG-AUC)和TG峰反应(TGPR)作为标准脂肪负荷后TG反应水平的指标.结果(1)EH组的肱动脉反应性充血前、后血管内径变化百分比显著小于对照组[(10.36±3.43)%比(15.48±4.36)%P<0.05];(2)EH组餐后TG水平的TGPR[(4.68±1.74)mmol/L比(1.84±0.67)mmol/L]及TG-AUC[(23.59±6.48)mmol/L比(9.49±3.47)mmol/L]均显著大于对照组(P<O.05);(3)EH合并餐后TG代谢障碍组(n=26)的肱动脉反应性充血前、后血管内径变化百分比较EH餐后TG代谢正常组(n=12)有明显降低[(10.98±1.32)%比(13.14±1.09)%,P<0.05].结论68.4%的EH患者伴有脂餐后TG代谢障碍和消除延迟,餐后TG代谢异常会加重EH患者血管内皮功能障碍.     

阿托伐他汀钙对高血压病患者餐后甘油三酯代谢异常及血管内皮功能的影响

目的阿托伐他汀钙(立普妥)对高血压病患者餐后甘油三酯代谢异常及血管内皮功能的影响。方法30例高血压病(Ⅰ级)患者并经标准脂肪负荷试验确定为餐后高甘油三酯症,采用高分辨率血管外彩超检测脂餐后4h肱动脉血流介导的内皮依赖性血管舒张功能(EDF),随后受试者随机分为立普妥治疗组和常规治疗组,常规治疗组服用双克25mgqd,而立普妥组在常规药物的基础上加服立普妥20mgqn。治疗4周后重复标准脂肪负荷试验和脂餐后4h肱动脉血流介导的内皮依赖性血管舒张功能。结果治疗前两组脂肪餐后EDF均较空腹明显下降(立普妥治疗组:13.89%±3.28%比9.88%±3.53%,P<0.05;常规治疗组:14.37%±3.51%比10.11%±3.62%,P<0.05),但两组间TGAUC,TGPR无显著性差别。治疗4周后两组血压均较治疗前有显著下降,立普妥组餐后TGAUC,TGPR较治疗前显著下降[TGAUC:(18.84±6.81比10.12±5.38)mmol/L,P<0.05;TGPR:(3.96±1.78比2.16±1.06)mmol/L,P<0.05],其餐前和餐后EDF较治疗前有明显改善(空腹:13.89%±3.28%比17.96%±3.87%,P<0.05,脂餐后4h:9.88%±3.53%比16.67%±3.35%,P<0.05),且空腹EDF和餐后EDF无显著差异。常规治疗组餐后TGAUC、TGPR、空腹EDF较治疗前无明显改善,餐后EDF虽有所改善,但仍较空腹受损(14.86%±2.75%比11.42%±2.65%,P<0.05)。相关分析显示餐后EDF下降值、SBP、DBP与餐后TGAUC,TGPR呈正相关(TGAUC:相关系数r分别为0.35,0.32,0.25,P<0.05;TGPR:相关系数r分别为0.34,0.31,0.21,P<0.05)。结论立普妥降脂治疗能显著改善高血压病患者餐后甘油三酯代谢及血管内皮功能。     

阿托伐他汀钙对高血压病患者餐后甘油三酯代谢异常及血管内皮功能的影响

目的阿托伐他汀钙(立普妥)对高血压病患者餐后甘油三酯代谢异常及血管内皮功能的影响.方法30例高血压病(Ⅰ级)患者并经标准脂肪负荷试验确定为餐后高甘油三酯症,采用高分辨率血管外彩超检测脂餐后4 h肱动脉血流介导的内皮依赖性血管舒张功能(EDF),随后受试者随机分为立普妥治疗组和常规治疗组,常规治疗组服用双克25 mg qd,而立普妥组在常规药物的基础上加服立普妥20 mg qn.治疗4周后重复标准脂肪负荷试验和脂餐后4 h肱动脉血流介导的内皮依赖性血管舒张功能.结果治疗前两组脂肪餐后EDF均较空腹明显下降(立普妥治疗组13.89%±3.28%比9.88%±3.53%,P＜0.05;常规治疗组14.37%±3.51%比10.11%±3.62%,P＜0.05),但两组间TG-AUC,TGPR无显著性差别.治疗4周后两组血压均较治疗前有显著下降,立普妥组餐后TG-AUC,TGPR较治疗前显著下降[TG-AUC(18.84±6.81比10.12±5.38)mmol/L,P＜0.05;TGPR(3.96±1.78比2.16±1.06)mmol/L,P＜0.05],其餐前和餐后EDF较治疗前有明显改善(空腹13.89%±3.28%比17.96%±3.87%,P＜0.05,脂餐后4 h9.88%±3.53%比16.67%±3.35%,P＜0.05),且空腹EDF和餐后EDF无显著差异.常规治疗组餐后TG-AUC、TGPR、空腹EDF较治疗前无明显改善,餐后EDF虽有所改善,但仍较空腹受损(14.86%±2.75%比11.42%±2.65%,P＜0.05).相关分析显示餐后EDF下降值、SBP、DBP与餐后TG-AUC,TGPR呈正相关(TG-AUC相关系数r分别为0.35,0.32,0.25,P＜0.05;TGPR相关系数r分别为0.34,0.31,0.21,P＜0.05).结论立普妥降脂治疗能显著改善高血压病患者餐后甘油三酯代谢及血管内皮功能.     

波动性高血糖对血管内皮功能的影响

目的观察波动性高血糖对血管内皮功能的影响,探讨其致动脉粥样硬化的机制。方法选择新诊断的2型糖尿病患者72例,根据动态血糖监测结果分持续性高血糖组33例和波动性高血糖组39例,检测患者的肱动脉内皮依赖性舒张功能(EDD)及颈动脉内膜中层厚度(IMT)、血脂、空腹血糖、空腹胰岛素、餐后2 h血糖(2hPG)及餐后2 h胰岛素(2hINS)、高敏C反应蛋白(hs-CRP)、血管性假血友病因子(vWF)及尿微量白蛋白(MAU)。结果与持续性高血糖组比较,波动性高血糖组的2hPG、2hINS、hs-CRP、vWF、MAU及IMT明显升高(P<0.05,P<0.01),肱动脉EDD明显降低[(6.61±0.79)%vs(5.21±0.88)%,P<0.01]。结论波动性高血糖较持续性高血糖对血管内皮功能危害更大,可能与餐后高血糖、胰岛素抵抗和炎性因子增多有关。     

糖尿病不同时期血管内皮依赖性舒张功能变化

目的探讨糖尿病不同时期血管内皮依赖性舒张功能变化.方法 采用高分辨率血管外彩超,检测33例对照组和96例糖代谢异常者肱动脉内皮依赖性血流介导的血管舒张功能(EDF).其中糖代谢异常者包括糖耐量减低组30例、2型糖尿病无血管病变组30例和伴血管病变组36例.结果 与对照组(13.08%±4.90%)比较,糖耐量减低组已存在EDF降低(10.46%±4.54%), 糖尿病患者EDF则进一步降低(6.25%±2.95%),糖尿病血管病变组患者EDF最低[5.17%±2.11%;与无血管病变组(7.59%±3.29%)比较t=3.536, P<0.01].结论 在早期糖代谢紊乱即糖耐量减低和无血管病变临床证据的糖尿病患者,利用内皮依赖性血流介导的血管舒张功能检测,可早期发现血管内皮功能受损,这种受损随糖代谢紊乱加重而进一步恶化.     

老年原发性高血压微量白蛋白尿与血管内皮功能及颈总动脉粥样硬化

目的探讨老年原发性高血压(EH)患者微量白蛋白尿(MAU)与内皮依赖性舒张功能(EDF)及颈总动脉粥样硬化的关系。方法筛选老年高血压患者64例,根据24h尿白蛋白排泄率分成正常白蛋白尿组(NAU组)和微量白蛋白尿组(MAU组)。另设30例非EH老年人为对照组(NC组)。采用免疫比浊法测定24h尿白蛋白含量;采用彩色多普勒超声检测肱动脉内皮依赖性舒张功能,颈总动脉内中膜厚度(I MT)及其粥样斑块指数(PI)。结果(1)与对照组(9·1%±1·8%)比较,老年高血压患者NAU组已有内皮依赖性舒张功能降低(6·3%±1·1%,P<0·05),而MAU组内皮依赖性舒张功能则进一步降低(5·0%±1·4%,P<0·05)。(2)MAU组颈总动脉I MT较NAU组增高,且两组均较对照组增高[(1·0±0·2,0·9±0·1vs0·8±0·1)mm,P值均<0·05]。(3)MAU组的微量白蛋白尿与内皮依赖性舒张功能呈负相关(r=-0·597,P<0·001);微量白蛋白尿与颈总动脉I MT呈正相关(r=0·700,P<0·001)。结论老年EH患者均存在内皮依赖性血管舒张功能受损和颈总动脉粥样硬化,内皮依赖性舒张功能和I MT与微量白蛋白尿的发生密切相关。     

Randomized trial of insulin versus usual care in reducing restenosis after coronary intervention in patients with diabetes. the STent Restenosis And Metabolism (STREAM) study

BackgroundDiabetes status is an independent marker of restenosis after percutaneous coronary intervention (PCI). Previous studies suggest that metabolic abnormalities associated with diabetes increase stent restenosis by promoting intimal hyperplasia. Preclinical studies have indicated that insulin therapy reduces intimal hyperplasia. The objective of this study was to determine whether insulin-mediated glucose lowering reduces in-stent restenosis in patients with diabetes undergoing PCIs.MethodsWe conducted a prospective, randomized, multicenter, open-labeled study with blinded outcomes. Patients were randomized 1:1 to daily bedtime subcutaneous NPH insulin (Novo Nordisk) versus usual therapy with oral hypoglycemic agents. The main outcomes were change in volume of intimal hyperplasia within the stent measured by intravascular ultrasound and late lumen loss by quantitative coronary angiography at 6 months post-PCI.ResultsSeventy-eight patients (36 insulin, 42 usual care) were randomized. Eight patients in each group received drug-eluting stents. The insulin group achieved greater reductions in both glycosylated hemoglobin A1c (mean±S.D.) (insulin: 8.0%±1.2% to 6.7%±0.7% vs. control: 7.5%±1.2% to 7.1%±1.0 %, P=.0038) and fasting glucose (insulin: 9.3±3.8 to 5.8±1.7 vs. usual care: 8.4±2.4 to 7.7±2.0 mmol/l, P<.0001). There were no hypoglycemic events. At 6 months, there were no significant differences in either intravascular-ultrasound-determined neointimal volume (insulin: 41.2±38.9 vs. usual care: 48.4±40.2 mm³, P=.33) or late lumen loss by angiography (insulin: 1.29±0.74 mm vs. usual care: 1.02±0.71 mm, P=.17).ConclusionsAddition of a single bedtime dose of insulin in patients with diabetes does not influence in-stent restenosis.     

何首乌总甙抑制动脉粥样硬化病变形成

的　研究何首乌总甙对载脂蛋白E基因缺陷小鼠实验性动脉粥样硬化病变形成的保护作用。方法　将载脂蛋白E基因缺陷小鼠随机分为4组:何首乌总甙高剂量组[15 0mg/ (kg·d) ]、低剂量组[2 5mg/ (kg·d) ]、阿托伐他汀阳性药物组[5mg/ (kg·d) ]及空白对照组,给药第10周后全部处死,酶法检测四组血清脂质含量,图象分析法测定主动脉粥样硬化斑块面积和管腔面积,计算斑块面积与管腔面积的比值。结果　(1)何首乌总甙高、低剂量组及阳性药物组总胆固醇分别为6 4 9.3±72 .2mg/dL、6 32 .6±5 5 .1mg/dL和4 97.4±14 0 .8mg/dL ,均显著低于空白对照组(80 9.4±4 2 .6mg/dL ,P <0 .0 1) ;甘油三酯分别为12 6 .6±4 8.1mg/dL、14 5 .6±37.9mg/dL和172 .1±15 .7mg/dL ,均显著降低于空白对照组(2 5 3.3±4 2 .6mg/dL ,P <0 .0 1) ;而高密度脂蛋白胆固醇分别为117.1±14 .9mg/dL、113.5±2 3.3mg/dL和12 6 .7±12 .8mg/dL ,均显著高于空白对照组(6 7.3±10 .6mg/dL ,P <0 .0 1) ;治疗组间无显著性差异(P >0 .0 5 )。(2 )何首乌总甙高剂量组、低剂量组及阳性药物组载脂蛋白E基因缺陷小鼠主动脉粥样硬化病变减轻且动脉粥样硬化斑块面积/管腔面积比值分别为3.97%±0 .6 2 %、3.11%±0 .0 1%和0 .86 %±0 .0 7% ,均小于空     

Salsalate improves glycemic control in patients with newly diagnosed type 2 diabetes

Chronic inflammation contributes to insulin resistance and type 2 diabetes mellitus (T2DM). We investigated whether treatment with salsalate, an anti-inflammatory medication, improves glycemia in a group of newly diagnosed drug-naïve patients with T2DM. The study was a randomized, double-blind, placebo-controlled trial. Diagnosis of T2DM was made within 2 months of enrollment, and participants had not received any anti-glycemic agent. Sixty adults were randomized to receive salsalate (3 g/day) or placebo for 12 weeks. Fasting plasma glucose and insulin, glucose 2 h after 75 g oral glucose, HbA1C, lipid profile, HOMA-IR, and HOMA-B were determined before and after treatment. Salsalate reduced fasting glucose from 6.3 ± 0.2 mmol/l to 5.4 ± 0.2 mmol/l (P < 0.01) and TG from 1.9 ± 0.2 mmol/l to 1.5 ± 0.2 mmol/l (P < 0.03). Fasting insulin levels were increased in the salsalate group from 18.8 ± 1.6 to 21.6 ± 3.9, while they decreased in the placebo group. HbA1c rose in the placebo group from 6.2% ± 0.2 to 7.9% ± 1.1 mmol/mol, but decreased in the intervention group from 6.1% ± 0.5 to 5.6% ± 0.2 mmol/mol (P < 0.04 for between-group comparison). HOMA-IR did not change but HOMA-B increased ~1.7-fold (P = 0.06) in the salsalate group. The results show that salsalate is effective in improving glycemic control in newly diagnosed naïve patients with T2DM. The optimal duration of treatment with salsalate and sustainability of its effect requires further study (IRCT138709011465N1).     

慢性情绪应激对高脂饮食大鼠炎症反应和主动脉Toll样受体4表达的影响

目的通过观察慢性情绪应激对高脂饮食大鼠脂代谢、炎症反应和主动脉内皮细胞TLR4表达的影响,探讨慢性情绪应激在动脉粥样硬化病变形成中的作用、机制。方法雄性Wistar大鼠40只,随机分为正常对照组(NC)、无应激组(NS)、生理应激组(PS)和情绪应激组(ES),每组各10只,并制作慢性情绪应激模型。于末次应激结束后采集血标本,全自动生化分析仪检测血清TC、TG、HDL-C、LDL-C和hs-CRP,ELISA法测定血清ox-LDL、放免法检测TNF-α水平;HE染色观察大鼠主动脉形态学变化;免疫组化法(S-P)测定主动脉内皮细胞TLR4表达。结果 (1)ES组大鼠较其他3组出现了明显的脂代谢紊乱和炎症反应。与PS组、NS组、NC组比较,ES组TC、LDL-C、ox-LDL水平明显升高[TC:(5.30±0.69)mmol/L比(3.94±0.42)mmol/L、(3.82±0.48)mmol/L、(2.07±0.26)mmol/L;LDL-C:(1.57±0.22)mmol/L比(1.18±0.13)mmol/L、(1.11±0.11)mmol/L、(0.75±0.11)mmol/L;ox-LDL:(65.18±6.51)μg/dl比(45.65±2.70)μg/dl、(38.35±2.27)μg/dl、(14.99±1.46)μg/dl,均为P<0.01];ES组HDL-C[(0.94±0.14)mmol/L]低于NS组[(1.09±0.14)mmol/L,P<0.05],低于NC组[(1.16±0.18)mmol/L,P<0.01];与PS组、NS组、NC组比较,ES组hs-CRP、TNF-α水平升高[hs-CRP:(1.748±0.082)mg/L比(1.485±0.067)mg/L、(1.381±0.067)mg/L、(0.757±0.069)mg/L;TNF-α:(2.447±0.083)μg/L比(2.189±0.099)μg/L、(2.181±0.085)μg/L、(1.772±0.075)μg/L,均为P<0.01];(2)ES组大鼠主动脉出现早期动脉粥样硬化性改变;(3)ES组大鼠主动脉内皮细胞TLR4表达明显上调,其阳性细胞单位面积平均吸光度值(A)高于PS组、NS组和NC组[(0.334±0.010)比(0.250±0.012)、(0.238±0.015)、(0.082±0.008),均为P<0.01]。结论慢性情绪应激可能在动脉粥样硬化形成的早期,部分通过激活TLR4释放炎性细胞因子引起机体的炎症反应,进而导致动脉粥样硬化病变形成。     

A comparison of intensive mixture therapy with basal insulin therapy in insulin-naïve patients with type 2 diabetes receiving oral antidiabetes agents

Aim: In patients with type 2 diabetes, insulin therapy is commonly initiated with either a single dose of basal insulin or twice‐daily premixed (basal plus prandial) insulin despite no widely accepted recommendation. We compared the glycaemic control, as measured by a change in HbA1c, of intensive mixture therapy (IMT), a basal plus prandial regimen using insulin lispro mixture 50/50 (50% lispro and 50% NPL) before breakfast and lunch and insulin lispro mixture 25/75 (25% lispro and 75% NPL) before dinner, vs. once‐daily insulin glargine therapy, while continuing patients on oral antidiabetes medications. Methods: Following inadequate glycaemic control (HbA1c 1.2–2.0 times the upper limit of normal) and at least 2 months of two or more oral antidiabetes agent therapy, 60 insulin‐naïve patients with type 2 diabetes were randomized to one of the insulin regimens for 4 months with crossover to the alternative regimen for an additional 4 months. Glycaemic goals were preprandial blood glucose <120 mg/dl (6.7 mmol/l) and 2‐h postprandial blood glucose <180 mg/dl (10.0 mmol/l). The insulin dose was optimized by investigators without forced titration. Results: Mean prestudy (baseline) HbA1c for all patients was 9.21 ± 1.33% (±s.d.). IMT compared to glargine resulted in both a lower endpoint in HbA1c (7.08 ± 0.11% vs. 7.34 ± 0.11%; p = 0.003) and a greater change in HbA1c from pretherapy (?1.01 ± 0.10% vs. ?0.75 ± 0.10%; p = 0.0068). Forty‐four per cent of patients receiving IMT and 31% of patients receiving insulin glargine achieved HbA1c ≤ 7%. Two‐hour postprandial glucose values (for all three meals) and predinner glucose values were significantly less with IMT than with insulin glargine (p = 0.0034, 0.0001, 0.0066 and 0.0205). Overall hypoglycaemia throughout the complete treatment period was infrequent (IMT vs. Glargine: 3.98 ± 4.74 vs. 2.57 ± 3.22 episodes/patient/30 days, p = 0.0013), and no severe hypoglycaemia was observed during the study with either therapy. There was no difference in nocturnal hypoglycaemia between the two therapies. The mean insulin dose at the end of therapy was greater for IMT than for once‐daily insulin glargine (0.353 ± 0.256 vs. 0.276 ± 0.207 IU/kg, p = 0.0107). Conclusions: In combination with oral antidiabetes agents, multiple daily injections of a basal plus prandial insulin IMT regimen (using premixed insulin lispro formulations) resulted in greater improvements and a lower endpoint in HbA1c compared with a basal‐only insulin regimen. IMT also resulted in improved postprandial blood glucose control at each meal and enabled administration of a greater daily dose of insulin, which most likely contributed to these lower HbA1c measures. This greater reduction in HbA1c with IMT is accompanied by a small increased occurrence of mild hypoglycaemia but without any severe hypoglycaemia. Greater consideration should be given to initiating insulin as a basal plus prandial regimen rather than a basal‐only regimen.     

不同程度老年阻塞性睡眠呼吸暂停低通气综合征患者髓过氧化物酶和胰淀素水平分析

目的研究不同程度老年阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血清髓过氧化物酶(MPO)和胰淀素水平变化及意义。方法回顾性分析2012年2月至2016年10月成都市第六人民医院耳鼻咽喉科收治的老年OSAHS患者134例,根据呼吸暂停低通气指数(AHI)分为重度组55例、中度组41例和轻度组38例。比较3组患者多导睡眠监测(PSG)指标及MPO和胰淀素水平,Spearman相关法分析胰淀素及MPO的影响因素。应用SPSS 13.0统计软件对数据进行分析。依据数据类型采用方差分析或χ~2检验进行组间比较。结果相比重度组患者,轻度组和中度组患者AHI、氧减指数(ODI)、呼吸暂停和低通气次数显著降低,夜间最低血氧饱和度(LSaO_2)和平均动脉血氧饱和度(MSaO_2)水平显著升高,差异均具有统计学意义(P0.05)。重度组持续气道正压通气治疗前相比轻度组和中度组患者血清胰淀素[(47.85±6.41)和(20.29±3.06)ng/ml;(47.85±6.41)和(31.57±5.27)ng/ml]和MPO[(37.92±9.88)和(7.61±2.04)ng/mg;(37.92±9.88)和(23.33±4.56)ng/mg]水平高,差异均具有统计学意义(P0.05)。重度组患者持续气道正压通气治疗6个月及1年后相比治疗前血清胰淀素[(34.17±4.96)和(47.85±6.41)ng/ml;(27.14±3.86)和(47.85±6.41)ng/ml]和MPO[(21.06±8.39)和(37.92±9.88)ng/mg;(12.17±7.53)和(37.92±9.88)ng/mg]水平显著降低,差异均具有统计学意义(P0.05)。Spearman相关分析结果表明MPO和胰淀素水平与LSaO_2、MSaO_2负相关,与AHI、呼吸暂停次数正相关。结论血胰淀素和MPO水平测定对老年OSAHS患者并发胰岛素抵抗危险及持续气道正压通气治疗效果评估具有参考价值。     

Many patients with Type 1 diabetes estimate their prandial insulin need inappropriately

Background: Many factors contribute to the need for prandial insulin in Type 1 diabetes. However, patients’ success in achieving normal postprandial glucose concentration is understudied. The aim of the present study was to determine how often patients with Type 1 diabetes achieve normal postprandial glucose concentrations and to evaluate factors associated with postprandial hypo‐ and hyperglycemia. Methods: Data on food intake, physical activity, insulin administration, and blood glucose concentration were collected using a self‐administered questionnaire from 331 patients with Type 1 diabetes (43% men; mean age 49 ± 12 years; mean diabetes duration 32 ± 13 years). Of these, 179 provided data on blood glucose concentrations measured 110–150 min postprandially. One such meal per patient was randomized for analyses. Results: Hypoglycemia (<4.0 mmol/L), normoglycemia (4.0–7.9 mmol/L), and hyperglycemia (≥8.0 mmol/L) were observed after 23%, 36%, and 41% of meals, respectively. The three postprandial glycemia groups did not differ with respect to the meal composition or the timing of the postprandial blood glucose measurement. In women, postprandial hyperglycemia was associated with shorter diabetes duration and higher preprandial blood glucose concentration, whereas postprandial hypoglycemia was associated with higher physical activity. No single factor explained the postprandial glycemic state in men. Conclusions: A total of 64% of patients estimated their prandial insulin need inappropriately, suggesting that estimation of the optimal prandial insulin dose is not easy, even after a long duration of diabetes.     

双心室绝对不应期电刺激对心力衰竭兔心功能的影响

目的观察双心室绝对不应期电刺激对慢性心力衰竭兔心功能和心室重构的影响,探讨绝对不应期电刺激,即心脏收缩调节(CCM)信号治疗慢性心力衰竭的最佳模式和安全性。方法 30只新西兰大白兔分为假手术组、左心室刺激组和双心室刺激组各10只,通过升主动脉根部套扎法建立慢性心力衰竭模型,之后对左心室刺激组和双心室刺激组发放CCM信号,每天刺激6 h,连续刺激7 d,于电刺激前后观察心室结构、心脏功能及CCM信号刺激的心电学方面变化。结果与假手术组相比,左心室刺激组和双心室刺激组心脏质量、心脏质量指数、左心室收缩末内径、左心室舒张末内径和血浆脑利钠肽水平均下降[(5.23±0.56)g和(4.41±0.36)g比(6.72±0.82)g;(1.41±0.27)g/kg和(1.18±0.17)g/kg比(1.82±0.25)g/kg;(10.26±0.49)mm和(8.95±0.41)mm比(11.76±0.49)mm;(13.54±0.53)mm和(12.50±0.71)mm比(14.32±0.71)mm;(52.9±13.7)ng/ml和(41.3±13.4)ng/ml比(66.3±12.5)ng/ml,均为P<0.05],以双心室刺激组下降更明显;而左心室射血分数和左心室短轴缩短率明显升高(46.50%±4.31%和55.75%±4.53%比37.00%±3.10%;24.21%±2.94%和28.20%±2.67%比17.90%±1.69%,均为P<0.05),以双心室刺激组升高更明显。各组刺激前后室间隔厚度、左心室后壁厚度、E峰、A峰和E/A比值未见明显变化;24 h动态心电图显示,左心室刺激组和双心室刺激组发放CCM信号时与关闭信号时相比未见心率变化,而与假手术组相比,未见室性心律失常增加。结论双心室绝对不应期电刺激可增加慢性心力衰竭者的心肌收缩力,改善心功能,逆转心室重构,且不增加室性心律失常的发生,较单心室电刺激有更大优势。     

Nateglinide combination therapy with basal insulin and metformin in patients with Type 2 diabetes

Aims To compare the effect of adding nateglinide or placebo on postprandial glucose excursions (PPGEs), glycated haemoglobin (HbA_1c), diurnal glucose profiles and hypoglycaemia in patients with Type 2 diabetes treated with the combination of basal insulin and metformin. Research design and methods This was an investigator‐initiated, double‐blind, randomized, parallel‐group, study in five centres. Patients with Type 2 diabetes (n = 88, age 56.0 ± 0.9 years, duration of diabetes 9.4 ± 0.5 years, HbA_1c 7.8 ± 0.1%, body mass index 32.4 ± 0.5 kg/m²) treated with basal insulin and metformin entered a 24‐week period, during which basal insulin was titrated to optimize glucose control. Thereafter, the patients were randomized to receive either nateglinide (120 mg three times daily) or placebo before their main meals for 24 weeks. Results During the optimization period, HbA_1c decreased by ?0.3 ± 0.1 and ?0.4 ± 0.2% (NS) and insulin doses increased by 10.0 IU (2.0–32.0) [0.09 IU/kg (0.02–0.34)] and 10.0 IU (0.0–19.0) [0.11 IU/kg (0.0–0.25)] (NS) in the nateglinide and placebo groups. Mean postprandial glucose during weeks 20–24 averaged 9.0 ± 0.3 and 10.0 ± 0.3 mmol/l in the nateglinide and placebo groups (P = 0.025) and mean PPGE averaged 2.4 ± 0.2 and 3.1 ± 0.2 mmol/l, respectively (P = 0.019). At 24 weeks as compared with 0 weeks, mean HbA_1c had decreased by 0.41 ± 0.12% in the nateglinide group and by 0.04 ± 0.12% in the placebo group (P = 0.023). The frequency of confirmed, symptomatic hypoglycaemia was 7.7 episodes/patient‐year vs. 4.7 episodes/patient‐year in the nateglinide and placebo groups (P = 0.031). Conclusions Addition of a short‐acting insulin secretagogue at main meals improves postprandial hyperglycaemia during combination therapy with basal insulin and metformin, but increases the frequency of hypolycaemia.     

氨氯地平阿托伐他汀钙对高血压合并血脂异常患者血管功能的影响

目的研究复方氨氯地平阿托伐他汀钙对高血压合并高脂血症患者血管功能的影响。方法入选180例高血压合并血脂异常患者,按随机双盲法分为对照组90例(氨氯地平5 mg/d)和试验组90例(复方氨氯地平阿托伐他汀钙1片/d),治疗12个月。测定治疗前后患者的血压、血糖、血脂、颈动脉内中膜厚度(IMT)、肱动脉内径及血浆内皮素1(ET-1)及一氧化氮(NO)水平。结果与氨氯地平相比,复方氨氯地平阿托伐他汀钙可延缓颈动脉IMT的进展[(-0.17±0.07)mm比(-0.11±0.05)mm,P<0.05],并提高患者NO水平[(35.0±6.5)μmol/L比(19.5±6.4)μmol/L,P<0.05]和肱动脉扩张能力(10.1%±3.1%比8.8%±3.2%,P<0.05),降低ET-1水平[(-31.8±6.5)ng/L比(-21.8±7.1)ng/L,P<0.05];但二者的降压作用差异无统计学意义[(-29±7.5/-16.5±7.5)mm Hg比(-26±9.0/-13.5±9.0)mm Hg,P>0.05]。结论复方氨氯地平阿托伐他汀钙较氨氯地平血管保护功能更强。