下食管括约肌运动和功能与胃食管反流病

目的　观察胃食管反流病 (GERD)患者与对照组餐前、餐后食管pH情况 ,下食管括约肌(LES )运动模式的变化以及酸反流事件与一过性下食管括约肌松弛 (TLESR )、低LES压力 (LESP)的关系。方法　两组受试者均接受连续性 4h食管压力测定 (分别为空腹和餐后 1、2、3h)和食管pH监测 (GERD组检测 4h ,对照组检测 2 4h)。结果　GERD组酸反流事件明显高于对照组 (P <0 0 5 )。两组间TLESR发生率差异无显著性 (P >0 0 5 ) ,但与空腹比较 ,两组餐后 1h和 2hTLESR发生率明显增多 ;GERD组伴有酸反流的TLESR明显高于对照组 (P <0 0 0 1)。 4 3% (2 9/ 6 8)的酸反流事件发生在TLESR期间。 31% (2 1/ 6 8)的酸反流事件出现于低LESP状态中。结论　GERD是多因素参与的病理过程。LES运动形式变化和功能不全是GERD的重要背景因素。     

健康青年志愿者一过性下食管括约肌松弛

目的　了解我国健康青年人一过性下食管括约肌松弛(TLESR)与酸反流的关系及脂肪含量不同的饮食对健康人TLESR和酸反流的影响。方法　采用下食管括约肌(LES)袖套式测压管、单晶锑pH 测定管,同步记录10 名志愿者空腹1 小时及餐后4 小时内的LES压力和食管pH 值。结果　酸反流均发生在LES压力低于2m m Hg 时,其中90.4% 发生在TLESR时。餐后酸反流显著增加( P< 0.01),TLESR及TLESR伴酸反流率也显著增加(P均< 0.01)。低脂餐与高脂餐对酸反流、TLESR及TLESR伴酸反流率的影响差异无显著性意义( P均> 0.05)。结论　TLESR是健康人酸反流发生的主要机制,健康人餐后酸反流增加主要是因为TLESR及TLESR伴酸反流增加。高脂餐并不增加健康人的TLESR及酸反流     

健康志愿者和胃食管反流病患者食管动力的性别差异

背景：食管动力受多种因素影响，性别因素对食管动力的影响尚不清楚。目的：探讨健康志愿者、非糜烂性反流病（NERD）和反流性食管炎（RE）患者食管动力的性别差异。方法：83例健康志愿者以及具有典型胃食管反流症状的NERD患者196例和RE患者104例纳入本研究。受试者行食管测压，测定下食管括约肌压力（LESP）和食管体部运动功能（包括食管体部各段蠕动收缩波幅、蠕动波传导速度和湿咽成功率）。结果：RE组男性患者比例显著高于NERD组（69．2％对43．4％，P〈0．05）。健康对照组和NERD组男性基础LESP较女性显著降低（P〈0．05），男性健康志愿者食管体部近端蠕动收缩波幅显著低于女性（P〈0．05），男性RE患者湿咽成功率显著低于女性患者（P〈0．05）。男性NERD患者LESP降低发生率显著高于女性患者（45．9％对29．7％，P〈0．05），男性RE患者食管体部运动功能障碍发生率显著高于女性患者（68．1％对46．9％，P〈0．05）。结论：无论是胃食管反流病（GERD）患者还是健康志愿者，男性的食管动力均较女性差，男性性别是GERD发病的危险因素之一。     

胃食管反流病患者酸反流与食管运动功能障碍的关系

背景：异常酸反流和食管运动功能障碍与胃食管反流病（GERD）密切相关。目的：研究GERD患者的食管运动和酸反流与食管黏膜损害的关系，以及两者之间的相关性。方法：选取有反酸、烧心、胸痛等典型胃食管反流症状的患者72例行上消化道内镜检查、食管测压和24hpH监测。根据pH〈4总时间百分比〈4．5％且DeMeester计分〈14．7的标准。将食管炎患者分为生理性酸反流组（pH^-组）和病理性酸反流组（pH^＋组）。结果：内镜下食管炎组24hpH监测各项指标较无食管炎组显著增高（P〈0．05），病理性酸反流的发生率显著高于无食管炎组（P〈0．01）。两组食管测压各项指标无显著差异，食管炎组pH^＋者的食管下括约肌压力（LESP）较pH^-者显著降低，食管体部蠕动波传导速度减慢，湿咽成功率减少（P〈0．05）。结论：GERD患者食管炎的发生与酸反流密切相关，有病理性酸反流的GERD患者易见食管运动功能障碍。     

非糜烂性反流病患者食管动力特征分析

背景：食管动力障碍在胃食管反流病（GERD）的发生中起重要作用。目的：探讨不同类型非糜烂性反流病（NERD）的食管动力特征。方法：选取161例具有典型胃食管反流症状者和20名健康体检者,分别行上消化道内镜检查、24 h食管pH监测和食管测压。纳入内镜检查未见Barrett食管和食管黏膜破损、症状指数≥50%的NERD患者,根据其是否存在病理性酸反流分为异常酸反流组和食管酸高敏组,比较反流组（28例）、高敏组（13例）和对照组（15例）的食管测压结果。结果：反流组下食管括约肌（LES）长度较对照组显著缩短（P〈0.05）,LES压力显著降低（P〈0.05）,高敏组与对照组间则无明显差异。反流组和高敏组食管体部动力障碍均以食管远段为主,表现为收缩波幅降低、蠕动波传导速度减慢和非传导性收缩波比例增加,反流组改变更为明显。结论：不同类型NERD的食管动力特征存在差异。异常酸反流亚型NERD患者存在LES长度和压力异常,食管远段动力障碍更为明显。     

一过性下食管括约肌松弛的研究进展

近年来，一过性下食管括约肌松弛已被证实是胃食管反流发生的最主要机制，这一发现使得人们对胃食管反流病的发病机制有了新的认识，并为其治疗提供了新思路。此文就其定义、发生机制、影响因素及治疗方面的研究进展作一综述。     

无症状贲门松弛患者酸反流食管动力检测及意义

目的:探讨无反流症状贲门松弛对胃食管酸反流及食管动力的影响.方法:对25例内镜下贲门松弛且无明显反流症状患者及10例内镜检查正常的无症状健康志愿者均进行24 h食管pH监测及食管测压检查.结果:内镜下贲门松弛组24 h食管pH监测各项指标较正常对照组增高, 其中以pH<4总时间及DeMeester评分差异更明显(38.44±50.89min vs 10.60±7.75 min, 11.98±14.84 vs 5.06±3.19, 均P<0.05). 贲门松弛组病理性酸反流发生率较正常对照组差异有统计学意义(28%vs 0%, P<0.05). 两组食管测压各项指标包括LES静息压、LES长度、食管远近端蠕动波幅、食管体部传导速度、湿咽成功率等较对照组低, 但差异无统计学意义.结论:贲门松弛易于发生酸反流, 部分贲门松驰且酸反流患者无相关临床症状.     

老年人反流性食管炎食管外表现与酸反流的关系

目的 探讨老年人反流性食管炎(reflux esophagitis,RE)食管外表现与酸反流的关系.方法 选择经胃镜检查证实为RE老年患者69例,入选者均有胃灼热、反酸等胃食管反流症状及咳嗽、喉炎,哮喘等食管外症状.对所有患者行24 h食管pH值监测,根据监测结果将患者分为中重度病理性酸反流组(中重度组)40例和轻度病理性酸反流组(轻度组)29例.两组均给予口服埃索美拉唑治疗(20 mg,3次/d),疗程8周,观察治疗后症状改善情况. 结果酸反流中重组食管外症状总积分(14.4±2.71)分.明显高于酸反流轻度组(8.2±2.0)分,经埃索美拉唑治疗后,两组患者食管外症状比治疗前均有好转,治疗后中重度组食管外症状总积分为(12.2±1.9)分,较治疗前明显改善(P<0.01). 结论老年RE患者的食管外症状与酸反流显著相关.老年患者因慢性咳嗽、慢性喉炎及哮喘长期就诊而治疗效果不佳时,应详细询问病史,考虑到GERD的可能性,尽早行胃镜及24 h食管pH监测,以明确诊断,尽早治疗.     

胃食管反流症24 h酸碱监测及食管下括约肌静息压变化

胃食管反流病(GERD)是由于食管下括约肌(LES)功能障碍引起胃内容物(包括十二指肠内容物)反流导致的一系列慢性症状和食管黏膜损害[1].该病发生率较高,病情易反复.笔者通过对236例具有GERD症状的患者进行了24 h食管酸碱监测及LES静息压(LESP)测定分析,探讨其发病规律,以期为临床治疗用药提供理论依据.现报告如下.     

体质量对反流性食管炎患者下食管括约肌压力和24h食管pH监测结果的影响

目的探讨反流性食管炎（RE）患者中,体质量对下食管括约肌压力（LESP）和24h食管pH监测结果的影响。方法对18例体质量正常RE患者和22例超重肥胖RE患者进行LESP和24h食管pH监测,对结果进行统计分析。结果超重肥胖组RE患者的LESP、pH〈4总反流时问百分比、反流时间〉5min的反流次数、总反流数、DeMeester分与体质量正常组RE患者比较,差异均有统计学意义（P均〈0．05）;而超重肥胖组RE患者与体质量正常组RE患者的下食管括约肌松弛率（LESRR）比较,差异无统计学意义（P〉0．05）。结论在RE患者中,超重肥胖可影响食管动力并增加食管的酸暴露,控制体质量对治疗RE可能有一定作用。     

Effect of l-NMMA on Postprandial Transient Lower Esophageal Sphincter Relaxations in Healthy Volunteers

In a previous study we showed that nitric oxide (NO) synthesis inhibition by N ^G-monomethyl-l-arginine (l-NMMA) reduced the number of transient lower esophageal sphincter relaxations (TLESRs) triggered by gastric balloon distention. The role of NO in postprandial TLESRs and gastroesophageal reflux, however, is unknown. Therefore, we studied the effect of l-NMMA on meal-induced TLESRs and reflux episodes with simultaneous recording of esophageal peristalsis, intraesophageal and intragastric pH, and gastric emptying in healthy volunteers. Ingestion of a solid meal resulted in an increase in TLESRs [8.5 (6.3–11.0) 60 min] which was significantly inhibited by l-NMMA [6.0 (4.0–8.8) 60 min, P < 0.05]. In addition, the total number of reflux episodes was reduced. l-NMMA had no effect on intragastric meal distribution and gastric emptying, but attenuated the postprandial increase in intragastric pH. These results confirm the involvement of NO in the neurocircuitry underlying the triggering of TLESRs. The reduction in reflux by l-NMMA has to be confirmed in patients with gastroesophageal reflux disease. NO may be involved in the regulation of gastric acid secretion.     

Different Effects of White and Red Wine on Lower Esophageal Sphincter Pressure and Gastroesophageal Reflux

Background: White wine and beer induce gastroesophageal reflux (GER). We investigated the effects of white and red wine on lower esophageal sphincter pressure (LESP) and GER. Methods: Twenty healthy volunteers received 300 ml white wine, red wine, or water together with a standardized meal. The LESP was continuously monitored with a Dent sleeve the 1st h postprandially, and the esophageal pH measured with a glass pH electrode. Results: The LESP was decreased after intake of white wine (median, 14.9 mmHg; range, 5.6-19.5 mmHg) compared with red wine (20.4 mmHg; 13.1-22.3 mmHg; P &lt; 0.05) and tap water (19.5 mmHg; 16.2-29.1 mmHg; P &lt; 0.01). The fraction time esophageal pH &lt;4 was increased after both alcoholic beverages compared with tap water (0.9%; 0.2-5.8%; P &lt; 0.01 versus white wine, P &lt; 0.05 versus red wine) with a greater fraction time after white wine (13.2; 0.3-58.1) than after red wine (2.3; 0.7-24.4; P &lt; 0.05). The decreased sphincter pressure after white wine was accompanied by a change in the reflux pattern with increased `stress reflux' and the occurrence of `free reflux'. Conclusion: White wine and red wine exert different effects on LESP and GER.     

Transient Lower Esophageal Sphincter Relaxations and Gastroesophageal Reflux Episodes in Healthy Subjects and GERD Patients During 24 Hours

Still little is known about the 24-hr pattern of transient lower esophageal sphincter relaxations (TLESRs), particularly in patients with GERD. The aim of our study was to evaluate the 24-hr esophageal and LES motor pattern and esophageal pH and to identify the relationship between TLESRs and gastroesophageal reflux in healthy subjects and in GERD patients. Ten healthy subjects and nine patients with esophagitis (grade I–II) underwent a 24-hr pH manometric recording by means of a portable electronic device. The recording aimed at identifying the temporal relationships between reflux episodes and LES motor events. The GERD patients showed a greater number of either reflux episodes or TLESRs during the 24 hr as compared to controls. While most refluxes occurred during TLESRs in both groups, a small percentage of TLESRs was followed by reflux episodes in healthy people, with only a slight increase in GERD patients. In conclusion, although representing an important motor pattern during gastroesophageal reflux both in healthy subjects and in patients with GERD, TLESR could probably be considered one of the pathophysiologic mechanisms of gastroesophageal reflux more than the primary cause of reflux episodes.     

Transient Lower Esophageal Sphincter Relaxations and Esophageal Body Muscular Contractile Response in Reflux Esophagitis

In patients with gastroesophageal reflux disease (GERD), transient lower esophageal sphincter relaxations (TLESRs) are more frequently accompanied by acid reflux than in normals. The role of esophageal tone during gastroesophageal reflux events is unknown. We studied the tonic motor activity in the body of the esophagus during TLESRs with and without acid reflux in 11 patients with erosive esophagitis and compared the results with those previously obtained in healthy subjects. Esophageal peristaltic contractions were recorded 13, 8, and 3 cm above a sleeve that measured LES pressure. An intraluminal balloon was inflated 8 cm above the sleeve to induce an esophageal tonic contraction [artificial high pressure zone (HPZ)]. The percentage of TLESRs with acid reflux was significantly higher in patients with esophagitis than in healthy controls (58.3% vs 37.3%, P < 0.05). TLESRs per se were not associated with an inhibition or increase in esophageal body contractility, which, however, changed substantially immediately after reflux. In patients with esophagitis the esophageal body tonic contractility was inhibited in 59.5% of TLESRs vs 36% in controls (P < 0.05). Esophageal contractions during TLESRs traveled down the esophagus in 77% of the instances in patients vs 96.5% in controls (P < 0.05). In conclusion, gastroesophageal reflux during TLESRs was more frequently associated with inhibition of esophageal body tonic contractility in patients with esophagitis than in normals. The different response of the esophageal body to reflux observed in GERD patients may partially contribute to the higher prevalence of reflux during TLESRs in these patients.     

Endoscopic Ultrasonography of the Lower Esophageal Sphincter in Reflux Esophagitis and Achalasia

Abstract: The endoscopic ultrasonography findings at the lower esophageal sphincter (LES) were compared in patients with reflux esophagitis and esophageal achalasia to clarify the differences in wall structure between these diseases. In reflux esophagitis, the esophageal wall was hypertrophied at the LES and featured both irregularity and interruption of the submucosa, muscularis propria, and adventitia. In achalasia, there was generalized hypertrophy of the esophageal wall at the LES including the mucosa, submucosa, muscularis propria and adventitia but for each layer the normal 5-layer structure was visualized well. Thus achalasia and reflux esophagitis both featured hypertrophy at the LES, but the detailed findings were quite different. This difference was thought to arise from the presence of inflammation in reflux esophagitis and no inflammation in achalasia.     

Effects of Endoscopic Injection Sclerotherapy for Esophageal Varices on the Reflux Prevention Mechanisms of the Lower Esophageal Sphincter

Abstract: Lower esophageal sphincter pressure (LESP) was measured before and after endoscopic injection sclerotherapy (EIS) in 41 patients with esophageal varices in order to evaluate the effects of the therapy on the reflux prevention mechanisms. LESP was measured by the infusion method before, upon completion of EIS and 6 months after EIS. The magnitude of the decreases in LESP were significantly greater in patients who had ulcers following EIS than in those who did not. A close correlation was noted between the incidence of clinical symptoms of reflux esophagitis (such as heartburn and retrosternal pain), ulcer formation and decreases in LESP. This finding suggests that ulcer formation by EIS affects the reflux prevention mechanisms of the lower esophageal sphincter. However, disorders of the lower esophageal sphincter seem, transient and also reversible because decreases in LESP recovered and the patients' clinical symptoms improved within 6 months of the EIS.     

Effect of Amino Acids on Lower Esophageal Sphincter Characteristics and Gastroesophageal Reflux in Humans

The effect of a commercially available mixedamino acids solution, when given either intravenously orintragastrically, on lower esophageal sphincter (LES)pressure, frequency of transient LES relaxations (TLESRs) and gastroesophageal reflux (GER) wasinvestigated in six healthy volunteers. LES pressure andesophageal pH were simultaneously recorded on threeseparate occasions 1 hr before (basal) and 3 hr during intravenous or intragastric infusion ofamino acids (250 mg protein/kg/hr) or saline (control).No significant changes in LES pressure were seen in thecontrol experiment. Intravenous amino acids caused a rapid and sustained (P < 0.01)decrease in LES pressure whereas intragastric aminoacids decreased LES pressure only gradually andtemporarily (P < 0.01). In the three experiments nosignificant differences were observed in TLESR frequency,the number of GER episodes, the mechanism of reflux, orduration of acid exposure. In healthy subjects bothintragastric and, especially, intravenous infusion of amino acids significantly decrease LESpressure but do not affect the frequency of TLESRs orGER episodes during a continuous liquid gastricload.     

Absence of an Upper Esophageal Sphincter Response to Acid Reflux

Manometric studies of the upper esophageal sphincter (UES) were done on 17 volunteer subjects and 16 patients with endoscopically evident esophagitis. Subjects entered one or both of two protocols designed to assess the effect of esophageal acid exposure on UES pressure. In protocol 1, continuous 3-h postprandial recordings were obtained; a modified sleeve sensor was used to measure UES pressure, and an intraluminal pH electrode was used to detect occurrences of spontaneous gastroesophageal acid reflux. In protocol 2, UES pressure was continuously monitored during a 10-min control period, followed by a 25-min period of esophageal perfusion with 0.1 N HCl. Our findings were that: 1) basal UES pressure measured during the 3-h recording was similar in the normal volunteers and in the group of patients with esophagitis, 2) episodes of spontaneous gastroesophageal acid reflux were not associated with a change in UES pressure in either the normal volunteers or in the patients with esophagitis, and 3) esophageal perfusion with HCl did not affect the UES pressure in either group, although severe heartburn occurred in most of the esophagitis patients. We conclude that the upper esophageal sphincter exhibits normal basal pressure in patients with esophagitis and that esophageal acid exposure, either spontaneous or experimental, does not affect UES pressure in normal volunteers or in patients with esophagitis.