单纯性肥胖者进餐前后自主神经功能的变化特征

目的:观察单纯性肥胖者进餐前后自主神经活动特征,探讨其与肥胖者胃动力异常的关系.方法:采用十二导联动态心电记录仪,记录102例单纯性肥胖者和49例正常体重健康志愿者,餐前和餐后1 h心电信号,进行心率变异分析.结果:餐前肥胖组RR间期标准差的平均值(SDNNindex)和RR间期差值的均方根(RMSSD)、高频功率(HF)、超低频功率(ULF)显著高于对照组(87.31±15.64 ms,82.50±67.19 ms.31 168.60±6361.00 ms~2,22 814.17±4083.90 ms~2 vs 79.38±12.28 ms,56.04±10.15 ms.12 999.4±5995.00 ms~2,16 595.75±5615.09 ms~2,P<0.05,P<0.01),L/H显著低于对照组(0.65±0.43 vs 0.99±0.42,P<0.01);餐后肥胖组RMSSD,HF显著高于对照组(87.90±57.21 ms.36 158.56±6361.00 ms~2 vs 39.25±11.15 ms.6570.50±5995.80 ms~2.P<0.01),SDNNindex,ULF,LF/HF显著低于对照组(79.59±32.54 ms.14135.7±8083.90 ms~2,0.63±0.34 vs 141.67±10.28 ms.22 785.63±9615.20 ms~2,1.11±0.32,P<0.01);对照组餐后SDNNindex,ULF较餐前升高,RMSSD,HF较餐前降低,LF/HF餐后较餐前升高;肥胖组SDNNindeX,ULF较餐前降低,RMSSD,HF较餐前升高;LF/HF餐后和餐前无差异(P>0.05).结论:单纯性肥胖者餐前餐后均存在自主神经活动异常,自主神经活动异常可能是导致肥胖者胃动力亢进的主要原因之一.     

不同类型单纯性肥胖者近端胃功能特征分析67例

目的: 探讨不同类型单纯性肥胖者近端胃功能的变化特征.方法: 将67例单纯性肥胖志愿者根据饮食行为分为3组: 肥胖伴暴食组(A组)、肥胖饮食正常组(B组)、肥胖伴功能性消化不良组(C组);采用电子恒压器, 对3组肥胖者和D组(32例正常体质量健康志愿者)进行胃底机械性扩张,观察其可耐受容积和压力及顺应性的变化.结果: A组初始容积和最大耐受容积显著大于D组( t = -6.63, -5.20, 均P<0.01), 而C组显著低于D组( t = 3.48, 2.11, 均P<0.01). C组初始胃内压、最大耐受胃内压低于D组( t = 2.09, 2.08, 均P<0.05);A组初始及最大耐受顺应性显著大于D组( t = 2.44, -5.56, 均P<0.01), C组显著低于D组( t = 2.44, 2.32, 均P<0.05).结论: 暴食患者肥胖形成的主要原因是胃容积增加、顺应性增高、容受性增强及饱感延迟发生.     

静脉注射利多卡因对2型糖尿病患者气管插管期自主神经系统的影响

目的研究静脉注射利多卡因在全麻诱导气管插管期间对2型糖尿病患者自主神经系统功能的影响。方法 70例择期腹部手术2型糖尿病患者,随机分成利多卡因组(n=35,诱导前静脉注射1.5 mg/kg利多卡因)和对照组(n=35,诱导前静脉注射等容量氯化钠溶液),分别于麻醉诱导前(T0)、麻醉诱导后1 min(T1)、麻醉诱导后3 min(插管前,T2)及插管后1 min(T3)、6 min(T4)用心率变异功率谱分析技术观察患者的心率变异性(HRV)改变。结果与T0比较,T1^T2时,利多卡因组低频段(LF)和总功率频段(TP),对照组LF,高频段(HF),低频/高频比(LF/HF)及TP均显著降低(P<0.05),利多卡因组LF低于对照组,HF高于对照组(P<0.05);T3T2时,利多卡因组低频段(LF)和总功率频段(TP),对照组LF,高频段(HF),低频/高频比(LF/HF)及TP均显著降低(P<0.05),利多卡因组LF低于对照组,HF高于对照组(P<0.05);T3^T4,两组LF,HF及TP均较T0显著升高(P<0.05),而利多卡因组的LF/HF较T0差异无统计意义(P>0.05),对照组的LF/HF较T0显著升高(P<0.05);利多卡因组LF、TP升高程度显著低于对照组(P<0.05),HF组间差异无统计学意义(P>0.05)。与T0比较,T1T4,两组LF,HF及TP均较T0显著升高(P<0.05),而利多卡因组的LF/HF较T0差异无统计意义(P>0.05),对照组的LF/HF较T0显著升高(P<0.05);利多卡因组LF、TP升高程度显著低于对照组(P<0.05),HF组间差异无统计学意义(P>0.05)。与T0比较,T1^T2时,两组HR,SP,DP均显著降低(P<0.05);组间比较,利多卡因组SP,DP降低程度显著高于对照组(P<0.05),而两组间HR的改变差异无统计学意义。T3T2时,两组HR,SP,DP均显著降低(P<0.05);组间比较,利多卡因组SP,DP降低程度显著高于对照组(P<0.05),而两组间HR的改变差异无统计学意义。T3^T4,两组HR,SP,DP较麻醉诱导后均显著升高(P<0.01)。组间比较利多卡因组HR、SP及DP升高程度显著低于对照组(P<0.05)。结论全麻诱导气管插管对老年2型糖尿病患者自主神经功能一定干扰,静注利多卡因能明显抑制插管操作引起的对自主神经功能的干扰,有利于维护老年2型糖尿病患者围插管期心脏的自主神经调节功能。     

进餐对老年人心脏自主神经功能的影响

目的 探讨进餐对老年人心脏自主神经功能的影响。方法 应用短时心率变异时域，频域分析方法对50名正常老年人进餐前，后心脏自主神经功能状态进行定量分析研究。结果 正常老年人进餐后HRVI显低于进餐前（P＜0．05）；LF／HF显高于进餐前（P＜0．05）；进餐后MRR，DNN，SDSD，PNN50，VLF，LF，HF，TP与进餐前无显性差异（P＞0．05）。结论 进餐使正常老年人心脏自主神经平衡状态发生改变，交感神经活动增强，迷走神经活动相对降低。     

特发性室性早搏与自主神经张力的关系

目的 探讨特发性室性早搏(室早)的发生与自主神经机制之间的关系.方法 采用单中心回顾性研究方法,选择24 h动态心电图记录到频发室早(≥10000次/d或室早负荷≥10％)的156例特发性室早患者(室早组)和同期健康体检者84例(对照组)为研究对象.根据24 h动态心电图检查结果,计算心率变异性指标rMSSD、pNN50、高频功率(HF)、标准化的高频功率(HFnorm)、低频功率(LF)与HF的比值(LF/HF).比较两组自主神经张力间的差异,并分析室早负荷与自主神经张力变化的关系.结果 与对照组相比,室早组患者rMSSD、pNN50、HF和HFnorm均明显增加(P<0.01),LF/HF显著降低(P<0.01).室早组患者24 h室早负荷与rMSSD、pNN50和HF呈正相关(相关系数分别为0.492、0.425、0.372,P<0.01),而与LF/HF呈负相关(相关系数为-0.206,P<0.05);其中28.8％(45/156)的患者每小时室早负荷与每小时HFnorm呈正相关,16.0％(25/156)的患者与每小时LF/HF呈正相关,53.8％(84/156)的患者与每小时HFnorm和每小时LF/HF均无相关性.结论 部分特发性室早的发生与交感和(或)迷走神经张力变化相关.     

老年糖尿病手术患者自主神经功能与无症状性心肌缺血的关系

目的探讨老年糖尿病(DM)患者手术前后心脏自主神经功能变化与无症状性心肌缺血(SMI)的关系。方法选择择期非心脏手术老年患者54例,其中非DM患者18例(NDM组),DM患者16例(DM组),DM合并SMI患者20例(SMI组)。监测3组患者心率变异性的变化,包括总功率(TP)、高频功率(HF)、低频功率(LF)、极低频功率(VLF)及LF/HF。结果与NDM组比较,DM组及SMI组术前TP、HF显著降低(P<0.05)。3组术后TP、HF、LF及VLF总的趋势是降低,其中SMI组下降最为明显。术后1天,SMI组TP、HF及VLF与术前比较明显降低,TP、HF、LF及VLF与NDM组差异明显(P<0.01,P<0.05),HF和VLF与DM组差异明显(P<0.05)。术后2天,除DM组LF外,3组TP、HF、LF及VLF分别与术前形成明显差异(P<0.05,P<0.01)。结论DM患者合并有心脏自主神经病变,手术应激引起机体自主神经调节心脏功能的进一步紊乱,是造成DM患者围手术期SMI高发的重要原因。     

阵发性心房颤动发作前后心率变异性的变化

目的探索自主神经活动在阵发性心房颤动中的作用.方法在动态心电图上测量分析了25例阵发性房颤患者53阵次心房颤动发作前后及白天(6:00～22:00)和夜间(22:00～6:00)的心率变异指标(SDNN、LF、HF、LF/HF)的变化.结果房颤发作前1h SDNN、HF较终止后1h显著升高(p＜0.01),LF/HF显著降低(p＜0.01),LF无变化;LF、HF白天均高于夜间(分别为p＜0.05和p＜0.01),夜晚LF高于HF(p＜0.05),白天与夜间SDNN、LF/HF无差异,白天LF与HF无差异.结论阵发性心房颤动患者存在着明显的自主神经功能失常,特别是白天迷走神经张力增强;迷走神经张力增强是阵发性房颤的重要原因.     

苯那普利对肾性高血压大鼠心率变异的影响

目的:探讨苯那普利对肾性高血压大鼠降压同时对心率变异的影响。方法:制备肾性高血压大鼠模型,给予苯那普利治疗,分析其心率变异(HRV)的变化,并测定大鼠血浆血管紧张素Ⅱ(AngⅡ)的浓度。结果:高血压鼠血浆AngⅡ水平明显升高,心率变异时域指标中SDNN(全程记录期间所有窦性心搏R-R间期的标准差).rMSSD(相邻R-R间期差值的均方根)明显降低,频域指标中TP(总功率谱),VLF(极低频功率谱),LF(低频功率谱),HF(高频功率谱)明显降低,LF／HF(低高频比值)升高,P均<0.01;治疗后SDNN.rMSSD,TP,HF明显提高,LF／HF明显降低,P均<0.01。结论:苯那普利降压同时可改善自主神经调节功能。     

放松训练对不稳定性心绞痛患者心率变异性的影响

目的研究放松训练对不稳定性心绞痛患者自主神经活性的影响。方法选取不稳定性心绞痛患者191例,按照随机数字表法随机分为实验组(97例)和对照组(94例),实验组给予放松训练(约30 min),对照组给予静息平卧30 min,无专业人员进行放松训练,分析实验前及实验后的心率变异性(HRV)指标,包括时域指标〔心率平均值(MHRT)、NN间期标准差(SDNN)、相邻NN间期差值均方根(RMSSD)、相邻NN间期差值超过50 ms所占NN间期百分比(PNN50)〕,频域指标〔HRV信号频域上小于0. 40 Hz的能量总和(TP)、0. 04～0. 15 Hz的能量总和(LF)、0. 16～0. 40 Hz的能量总和(HF)、LF/HF〕。结果实验组放松训练后SDNN、PNN50、TP及HF均较放松训练前显著升高(P0. 05),MHRT、LF/HF较放松训练前显著降低(P0. 05),而RMSSD及LF较放松训练前升高,但差异无统计学意义(P0. 05)。结论放松训练可以提高不稳定性心绞痛患者的HRV,增强副交感神经活性,降低交感神经张力,改善交感神经及副交感神经之间的平衡。     

晕船病的心率变异性分析

目的研究晕船病者的心率变异性（HRV）,分析两者间的关系。方法 88名健康学员根据航海中是否出现晕船反应分为晕船病组（A组）46例和不晕船组（B组）42例,分别采集其陆上安静状态下和海上航行中的短程HRV,分析其时域、频域指标,判断自主神经功能状态。结果①在陆上安静状态下,SDNN、PNN50、HRVI、VLF、LF、HF、TP指标A组高于B组,MRR、rMSSD在二组间无差异,而LF/HF A组低于B组。②海上航行中,A组MRR、SDNN、rMSSD、PNN50、HRVI、LF、HF、TP高于B组。VLF二组间无差异。结论晕船病者固有的自主神经张力较高,在发生晕船病时自主神经张力明显增高,特别是以迷走神经张力为主。HRV检测可以作为预测晕船病的一个敏感指标。     

From gastric inflammation to gastric cancer

The majority of gastric adenocarcinomas are related to chronic inflammation induced by Helicobacter pylori infection. For intestinal-type gastric cancer, a multistep process of mucosal alterations leading from gastritis via glandular atrophy, intestinal metaplasia and dysplasia to invasive carcinoma is well recognized. Ongoing clinical studies focus on a 'point of no return'. It is defined as a situation when certain alterations are no longer reversible by H. pylori eradication and progression to gastric cancer may continue. H. pylori affects the mucosal as well as the systemic immune response by secretion of cytokines and the recruitment of distinct inflammatory cells. The immune response is characterized by a balance between a Th1-dominated response and the recruitment of antigen-specific regulatory T cells that allow the bacteria to persist in human gastric mucosa. Besides immune-mediated effects, H. pylori induces cellular alterations as well as genetic alterations in genes that are essential for the epigenetic integrity and mucosal homeostasis. These genetic alterations during gastric cancer development are in focus of intensive research and should ultimately allow the identification of risk factors involved in gastric carcinogenesis. The detection of individuals at high risk for gastric cancer would help to design appropriate strategies for prevention and surveillance.     

Control of gastric emptying by gastric tone

During ingestion of food, the stomach relaxes to accommodate the meal and, subsequently, a progressive gastric contraction parallels gastric emptying. Intestinal nutrients trigger feedback relaxatory mechanisms that regulate gastric tone and, hence, the nutrient load delivered into the small intestine. This regulation of gastric tone is mediated, at least in part, via the vagus. Defective gastric tone is associated with impaired gastric emptying, as seen in patients with postsurgical gastroparesis. However, increased intragastric pressure, corresponding with defective gastric accommodation, induces abdominal symptoms, but does not alter the gastric emptying pattern. These data indicate that gastric emptying is controlled by complementary mechanisms: gastric tone exerts an emptying force, but gastric outlet resistance is also an important regulator.     

胃起搏对胃动力紊乱犬胃排空及胃肌电活动的影响

目的　研究胃起搏对胃动力紊乱犬胃排空及胃电参数的影响。方法　采用双侧迷走神经干切断术联合应用胰高血糖素建立胃动力紊乱犬模型 ;采用 4导联胃肠电系统微机分析仪记录胃肠浆膜肌电活动 ;99mTc 植酸钠标记的半固体试餐 ,单光子计算机断层显像技术 (SPECT)检测胃半排空时间(GEt1/ 2 ) ;采用适宜起搏参数从胃体、胃窦在腹部投影部位输入起搏信号驱动胃电节律。结果　迷走神经干切断术后犬的GEt1/ 2 为 (79.4 2± 1.91)min ,较术前 (5 6 .35± 2 .99)min明显延迟 (P <0 .0 0 1) ,但行胃起搏治疗后GEt1/ 2 为 (6 4 .94± 1.75 )min ,较治疗前明显加快 (P <0 .0 0 1) ;胃起搏治疗前迷走神经干切断犬餐后的胃电频率为 (0 .0 81± 0 .0 0 7)Hz、胃电幅度为 (2 .32± 0 .35 )mV、慢波的传播速度为 (4 .0 6± 0 .4 0 )cm/s ,均较正常对照犬显著降低 [(0 .0 90± 0 .0 0 6 )Hz ,(4 .2 5± 0 .12 )mV ,(6 .92± 0 .2 4 )cm/s,(P <0 .0 5 ) ],治疗后其餐后胃电频率 (0 .0 92± 0 .0 0 5 )Hz、胃电幅度 (3.97± 0 .19)mV和慢波的传播速度 (5 .5 7± 0 .4 8)cm/s均明显高于治疗前 (P <0 .0 5 )。结论　采用适宜起搏参数输入起搏信号可完全触发胃电慢波 ,改善胃电参数 ,纠正药物导致的异常胃电节律 ,加速胃排空 ,恢     

Pedunculated gastric carcinoma demonstrating a gastric foveolar phenotype

We report a case of gastric cancer complicated with very well differentiated adenocarcinoma containing signet ring cells. An endoscopic examination revealed a pedunculated polyp in the fornix of the stomach. A surgical operation was performed and the pathological findings showed very well differentiated adenocarcinoma mimicking gastric foveolae with a poorly differentiated component containing signet ring cells. This is the first case of pedunculated gastric cancer complicated with very well differentiated adenocarcinoma containing signet ring cells and also demonstrating a gastric foveolar phenotype.     

Relationship between gastric mucosal hemodynamics and gastric motility

Continuous measurement of gastric mucosal hemodynamics (the index of mucosal hemoglobin concentration, the index of oxygen saturation and blood flow) in rats showed oscillatory changes. The mechanism of the oscillations was investigated using a probe specially designed for simultaneous measurement of hemodynamics and intragastric pressure. A hemodynamics-measuring probe for either reflectance spectrophotometry or laser-Doppler flowmetry was tied to a pressure microtransducer, inserted through an incision in the forestomach, and brought into gentle contact with the corpus mucosa. Synchronous oscillatory changes (4-6 cycles/min) in hemodynamics and motility were observed in the resting state (mean blood pressure: 120 mmHg). During moderate hemorrhagic hypotension (mean: 81 mmHg), oscillations in the hemodynamics increased in both amplitude and frequency, while motility remained constant. Oscillations in the hemodynamics were also affected by fluctuations in blood pressure and by topical application of norepinephrine to the corpus serosa. In water-immersion restraint rats, changes in the oscillations in the hemodynamics and motility were virtually synchronous; frequency decreased and amplitude increased. These findings suggest that oscillatory changes in gastric mucosal hemodynamics are regulated not only by gastric motility but also by arteriolar vasomotion of the gastric wall.