功能性消化不良病人胃动力检测初步探讨

目的：研究功能性消化不良病人胃动力系统的复杂电过程和运动机理，包括它的节律、传导、胃排空过程以及影响它们的因素，提取胃动力系统生物电和运动机理方面的信息。方法：按照临床判断标准筛选15例功能性消化不良患者。从体表提取的胃阻抗信号和胃电运用小波多分辨分析处理，利用小波变换将胃阻抗信号从呼吸和血流信号中分离出来。通过能谱和频谱分析方法，以及主能量和支配频率将信号分类。胃电信号和胃阻抗信号的频率，信号的功率谱、动态谱、节律大小、正常胃电和胃阻抗节律的功率等参数由系统提供。结果：初步的功能性消化不良病人的胃动力测量和评估的实验表明用药一周后，患者主观认为症状还没有缓解，或者消除，但患者胃电参数大都有显著性改变，来源于阻抗信号的胃动力参数没有显著性变化。结论：基于胃阻抗和同步胃电信号测量的综合应用可能提供一种无创的技术来研究和估计与胃肠生理学和病理学情况一致的胃动力状况。     

生物电阻抗法检测胃动力功能

在胃排空、胃收缩或胃蠕动时,由于胃的形态、容积及其内容物组成情况的改变较大,电特性变化非常明显,变化规律与胃动力学状况相对应,相关性强。采用生物阻抗方法可以实现无创、高灵敏、准确地提取与胃动力学状况相对应的电特性及其变化信息。在介绍了胃动力功能及其检测方法的基础上,着重阐述了检测胃动力的电阻抗方法的发展动态、关键技术及其存在的问题。     

65例胃大部切除术后碱性反流性胃炎临床分析

胃大部切除术是治疗胃和十二指肠疾病的常用方法，由于术后胆汁、胰液、十二指肠液反流或改道流经残胃，引起碱性反流性胃炎，有文献报道毕氏Ⅱ胃空肠吻合术后64％病例有明显的反流，其中97％有明显的吻合口炎、80％有残胃炎，严重地影响了术后病人的身体健康。经多年临床观察，胃大部切除术后虽疗效较为满意，但常出现各种各样的术后并发症，术后数月至数年发生的碱性反流性胃炎亦较为常见。本文总结了我院10年内65例碱性反流性胃炎患者病例，报告如下。     

阻抗胃动力检测方法与功能性消化不良评价

采用无创生物阻抗技术和同步胃电检测相结合的胃动力检测与评价新方法,对功能性消化不良病人进行初步的临床应用研究。同时提取体表胃电活动和机械运动信息,研究从胃电活动到机械收缩、蠕动的复杂胃动力过程,对采集信号提取时域、频域和变异系数等参数并进一步统计分析。功能性消化不良病人的胃运动正常节律百分比（PNF）和正常功率百分比（PNP）明显小于健康组,节律变异系数（FIC）和功率变异系数（PIC）大于健康组。功能性消化不良病人经一周用药后其EGG节律有较好的恢复,但反映胃机械运动的阻抗信号变化不大,提示经一周治疗的功能性消化不良病人,其胃动力的电学机制还没有耦合到机械收缩过程中,其胃动力功能还没有得到有效的改善。     

基于阻抗法的胃动力信息检测系统设计

临床将胃电信号作为胃动力紊乱诊断依据．但胃电信号并不完全对应于胃的活动．特别是胃的蠕动、胃的排空等机械活动。如果将与胃机械活动对应的胃阻抗信息也作为诊断依据之一，那就为建立新的、更准确的胃动力评价方法提供可能。本文基于阻抗法设计了一个新的获取胃动力信息的方法，不仅获得常规检测参数胃电，也通过小波变换技术分离出与胃电同步的胃阻抗信息，为临床胃动力学研究提供新途径。     

胃动力信息检测系统的设计与实现

将胃电与胃机械活动相关的胃阻抗信息作为诊断依据,建立新的、更准确的胃动力评价方法.基于阻抗法设计了获取胃动力信息的系统,通过小波变换技术分离与胃电同步的胃蠕动信息.结果表明系统通过了调试,实现设计功能,采集到了阻抗和同步胃电信号.小波变换提取的信号排除了干扰,获得了胃蠕动信息.基于阻抗技术的方法可检测胃蠕动状态,联合同步胃电分析技术为临床检测提供了新方法.     

清胆和胃汤治疗胆汁反流性胃炎110例临床观察

目的观察清胆和胃汤治疗胆汁反流性胃炎的监床效果.方法采用自拟方清胆和胃汤治疗胆汁反流性胃炎110例,并与同期用西药治疗的60例进行对照观察.结果治疗组总有效率93.64%.对照组总有效率75.00%,两组总有效率比较有显著差异(P＜0.05).结论清胆和胃汤治疗胆汁反流性胃炎效果肯定.     

一种新型胃动力检测系统的设计与实现

目的 以生物阻抗技术为基础设计胃动力检测系统.方法 检测系统由采集平台和分析平台2部分构成.前者实现胃电和胃动力阻抗信号的同步采集和数据传输,后者对提取的胃动力阻抗信号和胃电运用小波多分辨分析进行处理,并提取信号的时域、频域和支配频率等参数完成统计分析.结果 实验结果表明功能性消化不良患者（病理组）的胃运动正常节律百分比（PNF）和正常功率百分比（PNP）明显小于健康大学生志愿者（对照组）,病理组的节律变异系数（FIC）和功率变异系数（PIC）大于对照组.结论 胃动力检测系统的实现不仅使胃电和胃阻抗信息得到同步获取,同时为胃动力研究和临床检测提供一种电-机复合过程的检测方法.     

基于HHT的生物电阻抗胃动力信号分析方法

目的 采用HHT时间序列分析方法处理从人体采集到的胃动力信号.方法 通过经验模态分解(EMD)技术将一非线性、非稳态过程的原始胃动力序列分解为一组内在模态函数(IMFs),对每一个IMF进行Hilbert 变换,得到信号的瞬时频率,然后选择与胃动力相关的频率成分,即0.03-0.06 Hz之间的IMF进行重构提取胃动力...     

便携式长时间胃电记录系统的研制

体表胃电图(electrogastrogram,ECG)具有幅值小,频率低和窄带宽的特点,并且极易受到心电、呼吸以及运动等干扰.我们研究了一种基于单片机的胃电检测方法,可以有效地从体表记录到胃电信号,采用低功耗设计,可长时间进行胃电测量.将MMC卡作为胃电的存储器,通过在MMC卡上创建FAT文件系统,可使记录的胃电数据以标准文件的格式存储在MMC卡上,保证了后续的Windows环境下数据的处理.     

Perception of Gastric Contractions and Self-Control of Gastric Motility

The hypothesis was that self-control of a visceral response is dependent on ability to perceive occurrence of the response. Subjects were asked to judge whether or not a signal light coincided with a stomach contraction on each of approximately 200 trials. In a different session heart beat perception was tested by asking subjects to judge whether or not signal light flashes coincided with heart beats. Subjects then were tested for ability to increase and to decrease gastric motility prior to biofeedback training, after which half received 4 hrs of visual feedback while the others practiced without feedback. Control of motility without feedback was subsequently retested. Initially, subjects were unable to control gastric motility, but with feedback they could increase motility on command. Ability to perceive gastric contractions was unrelated to control of gastric motility before, during, or following biofeedback training, indicating that self-control of a visceral response is not dependent on perceptual sensitivity. Perception of stomach contractions correlated significantly (r= .51) with perception of heart beats, suggesting that there may be a generalized tendency to be aware of or to attend to visceral events.     

多通道电阻抗方法胃动力测量机制研究

建立多通道电阻抗信号与胃收缩传导过程的关系,明确生物电阻抗方法检测胃动力的测量机制。应用COMSOL软件建立圆柱容积导体模型,模拟胃环行肌收缩传导过程,进行电磁场正问题仿真计算,获取边界测量电压波形。设计专用实验装置,制作了不同电导率的三层琼脂模型,模拟胃部和胃收缩扰动,完成盐水槽动态模拟实验。仿真研究结果表明,轴向和径向激励模式下,边界测量电压波形清晰显示了胃收缩发生的部位及传导过程,相邻通道间存在明显的相位差。模拟实验结果中,对于电导率为1.35 S/m的被测琼脂模型,轴向激励模式各测量通道出现双波谷的时间差约为9 s;径向激励模式各测量通道出现双波谷的时间差约为6 s,与各测量通道的电极安放位置和间距正好相对应。胃内容物为高电导率和低电导率情况下,边界电压波形的变化趋势相同,方向相反。参数δ,〖AKU-〗和U_max/U_min定量评价结果表明,靠近激励电极的测量通道,电压敏感性和均值较高。多个通道测量的电阻抗信号,能够有效地反映胃内容物电导率的变化、胃不同部位的收缩、以及胃运动传导的时相关系。     

A Case of Gastritis Associated with Gastric Capillariasis

This report is about the case of gastritis associated with capillariasis. The patient was a 52-yr-old Korean woman who occasionally ate raw fish and chicken. She complained of mild abdominal pain and nausea, but not diarrhea. An endoscopic examination revealed an exudative flat erosive change on the gastric mucosa of the antrum. She was microscopically diagnosed as chronic gastritis with numerous eosinophil infiltrations. The sectioned worms and eggs in mucosa were morphologically regarded as belonging to the genus Capillaria. This is the first case of gastric capillariasis reported in the Republic of Korea.     

基于超声定位的胃动力检测系统的设计

目的:由于胃的形状、大小、位置、方向存在个体差异,及胃在蠕动、排空过程中容积的变化较大对胃动力信息检测造成了比较上的困难.因此本系统的设计引入超声作辅助定位.方法:设计全数字超声定位模块,通过USB接口把采集的数据传输到PC机,并开发相应的超声图像采集程序.结果:系统设计通过调试,成功的采集到胃的超声横断面图,获得的胃部结构图能够满足本系统辅助定位要求.结论:超声辅助定位的引入,可以有效解决胃动力信息的横向比较困难问题.     

Effects on Gastric Motility from the Cerebellar Fastigial Nucleus

In acute experiments on chloralosed cats gastric motility, blood pressure and heart rate were investigated for influences exerted by the fastigial nucleus. Besides pressor responses, fastigial stimulation could produce either gastric excitation or relaxation and the background of these responses was analysed by selective nerve sectioning and administration of suitable autonomic blocking agents. Suppression of prevailing gastric motility was found to be mediated mainly by increased discharge in adrenergic nerve fibres but also by adrenal catecholamine release.–Gastric excitation could be induced in three different ways, first via increased activity in vagal cholinergic fibres, second, by fastigial suppression of the vago-vagal non-adrenergic relaxatory reflex. In addition, when laparotomy or other noxious abdominal stimuli had induced inhibitory gastric reflexes, the consequent sympathetic discharge could be suppressed by fastigial stimulation resulting in enhanced gastric motility.–The importance of background activity in the various nervous pathways for the fastigially induced gastric responses is discussed.     

Mechanisms of Gastric Mucosal Cell Loss In Autoimmune Gastritis

The causes of target cell death in organ-specific autoimmune diseases are not precisely known. In the case of EAG, parietal cell death depends on Th1 CD4 T cells and Fas/Fas-ligand, either through interaction between infiltrating CD4 T cells with gastric parietal cells that have upregulated Fas expression or through homotypic interactions between the parietal cells. TNF-α does not appear to have a role in this process. The accompanying loss of zymogenic cells is likely a consequence of the interruption of the normal developmental pathway in the gastric mucosa that follows the destruction of parietal cells in the gastric mucosa.     

On Adrenergic Influence on Gastric Motility in Chronically Vagotomized Gats

Experiments were performed on chloralosed cats, which had been vagotomized 9–102 days previously. In contrast to the situation in acutely vagotomized cats, recordings of gastric motility revealed pronounced and regular contractions, which persisted after exclusion of spinal pathways but could be completely blocked by small doses of atropine. These contractions therefore appeared to be the result of enhanced activity of the intramural cholinergic ganglionic cells, presumably due to sensitization to local excitatory influences after decentralization.–This type of motility could be markedly inhibited by even weak activation of the gastric adrenergic supply. Intestinal distension, or afferent stimulation of me:enteric nerve fibres as well as efferent low frequency stimulation of the splanchnic supply to the stomach, promptly inhibited the stomach contractions. After administration of atropine the above types of adrenergic activation elicited at most only very weak inhibitory response of the stomach, and then only after a long latency.–The data presented are compatible with the view that the adrenergic fibres to the stomach exert their primary action on stomach motility by inhibiting the intramural cholinergic ganglion cells rather than the smooth muscle cells, responsible for gastric myogenic tone, or by any “presynaptic inhibitory action” on the preganglionic vagal nerve endings.