胆汁反流、胃酸和幽门螺杆菌感染共同作用对胃黏膜损伤程度和分布的影响

背景:胆汁反流、胃酸和幽门螺杆菌（H.pylori）感染均是胃黏膜损伤的独立致病因素。然而,它们共同存在时有无协同致病作用尚不清楚。目的:探讨胆汁反流、胃酸和H.pylori感染共同作用对胃黏膜损伤程度和分布的影响。方法:37例胃镜检查疑有十二指肠胃反流者均经24h胃内胆汁监测证实,同时行胃内PH监测。胃体和胃窦黏膜有或无活动性炎症、萎缩、肠化和不典型增生分别记2分或1分。分别以胃体和胃窦黏膜的各项病理学改变为应变量,以胃内胆红素吸收值>0.14的时间百分比、pH<4的时间百分比和H.pylori感染状态指标为自变量进行多变量逐步Logistic回归分析。结果:37例患者胃内胆红素吸收值>0.14的时间百分比为34.49％±22.69％,pH<4的时问百分比为78.68％土 9.91％,H.pylori阳性率为29.73％。胆汁反流出现在以胃体和胃窦黏膜肠化以及胃体黏膜活动性炎症为应变量的Logistic回归模型中,H.pylori出现在以胃体黏膜活动性炎症为应变量的回归模型中。结论:胆汁反流是胃黏膜肠化的危险因素;胃内有胆汁反流存在时,H.pylori感染是导致胃体新膜炎症的重要病因。     

原发性病理性十二指肠胃反流致病的因素分析

目的 探讨原发性病理性十二指肠胃反流(DGR)胃黏膜病变、幽门螺杆菌(Hp)感染、胆汁反流之间的关系.方法 应用便携式胆汁监测仪监测86例原发性病理性DGR患者胃内24 h胆汁反流情况;另取胃黏膜组织活检,分别行快速尿素酶试验、改良Giemsa染色和HE染色,判断有无Hp感染,并观察胃黏膜慢性炎症、活动性、萎缩、肠化等组织学特征.结果 ①将患者根据有无Hp感染分为Hp阳性组和Hp阴性组,Hp阳性组胃窦部黏膜病理积分、胆红素吸收值≥0.25的时间百分比均显著低于Hp阴性组(P均＜0.05);两组胆红素吸收值≥0.25的时间百分比和胃窦、胃角部黏膜病理积分均呈显著正相关(P均＜0.05).②将患者根据胆汁反流程度分为高反流组和低反流组,高反流组Hp阳性率显著低于低反流组(P＜0.05),胃窦和胃角部黏膜肠上皮化生的检出率、胃窦部黏膜病理积分均显著高于低反流组(P均＜0.05).结论 原发性病理性DGR导致胃窦黏膜损伤的主要因素可能为胆汁反流,随胆汁反流程度加重,胃窦黏膜损伤程度加重;胆汁反流可能抑制Hp在胃窦部定植,Hp感染可能与胆汁反流协同作用导致胃体部黏膜损伤.     

胃黏膜胆色素染色对原发性病理性十二指肠胃反流的诊断价值

目的 探讨胃黏膜胆色素染色对原发性病理性十二指肠胃反流的诊断价值.方法 86例原发性病理性十二指肠胃反流病人和 42例正常志愿者对照胃黏膜胆色素染色后进行定量分析,应用便携式胆汁监测仪(Bilitec 2000)监测胃内24 h胆汁反流情况,以胆红素吸收值≥0.25的时间百分比作为评价胆汁反流程度的主要观察指标.结果 病例组中胃窦、胃角和胃体部黏膜胆色素沉积显著高于正常对照组(P＜0.01),胃窦和胃角部黏膜胆色素沉积显著高于胃体部(P＜0.01);病例组中胃窦和胃角部黏膜胆色素沉积与胃窦和胃角部黏膜新悉尼系统病理积分均呈正相关(r=0.521,P=0.000和r=0.468,P=0.002),胃体部黏膜胆色素沉积与胃体部黏膜新悉尼系统病理积分无相关性(r=0.185,P=0.236);病例组中胃窦和胃角部黏膜胆色素沉积与胆红素吸收值≥0.25的时间百分比均呈正相关(r=0.458,P=0.002和r=0.334,P=0.028),胃体部黏膜胆色素沉积与胆红素吸收值≥0.25的时间百分比无相关性(r=0.092,P=0.556).结论 胃窦部黏膜胆色素染色能够反映胆汁反流程度,并与黏膜损伤程度呈正相关,对原发性病理性十二指肠胃反流有诊断价值,可用于原发性病理性十二指肠胃反流的辅助诊断.     

慢性胃炎患者胃内24小时胆汁监测

目的　胆汁反流是导致胃黏膜炎症的重要因素 ,该文研究不同类型慢性胃炎患者胃内胆汁反流情况。方法　分别对 45例慢性胃炎患者 (慢性浅表性胃炎 17例 ,慢性糜烂性胃炎 2 1例 ,慢性萎缩性胃炎 7例 )行胃内 2 4h胆汁监测 ,获得胆汁反流指标。分析胆汁反流总时间百分比、胆汁反流次数、胆汁反流 >5min次数和最长反流持续时间。结果　不同类型慢性胃炎组之间各项胆汁监测指标相差显著。胆汁反流总时间百分比在慢性萎缩性胃炎组 (16 .2± 18.0 )和慢性糜烂性胃炎组 (14.2± 12 .1)明显高于慢性浅表性胃炎组 (5 .3± 14.1,P <0 .0 1)。结论　胆汁反流与慢性糜烂性胃炎、慢性萎缩性胃炎的发生有关     

原发性十二指肠胃反流程度与胃黏膜炎性反应关系的研究

目的 分析原发性病理性十二指肠胃反流(DGR)患者胃黏膜病变、幽门螺杆菌(Hp)感染及胆汁反流变化以及相互间的关系.方法 对58例原发性病理性DGR患者进行24 h胃内胆汁监测,以反流时间百分23.60%为界,将患者分为高反流组(29例)和低反流组(29例).并行胃镜检查及胃黏膜活检.分析原发性病理性DGR患者胃黏膜炎性反应、Hp感染、胆汁反流间的关系.结果 高反流组及低反流组的Hp阳性率分别为20.7%(6/29)和48.3%(14/29),差异有统计学意义(P＜0.05).高反流组胃窦和胃角部黏膜肠上皮化生检出率高于低反流组(P＜0.05).胃窦、胃角部黏膜新悉尼系统病理积分Hp阳性组高于Hp阴性组(P＜0.05),高反流组高于低反流组(P＜0.05).Hp阳性组胆红素吸收值≥0.25的时间百分比低于Hp阴性组(P＜0.05),HP阳性组短时间反流频率、长时间反流频率、最长反流时间、吸收值最大值、平均值和中位值与Hp阴性组间差异无统计学意义(P＞0.05).Hp阳性组和阴性组胆红素吸收值≥0.25的时间百分比与胃窦、胃角部黏膜新悉尼系统病理积分均呈正相关(P＜0.05).结论 原发性病理性DGR导致胃窦黏膜损伤的主要因素可能为胆汁反流,胆汁反流可抑制HP在胃内定植,Hp感染可能与胆汁反流协同作用导致胃黏膜损伤.     

青年人生理性十二指肠胃反流的相关因素

目的:探讨生理性十二指肠胃反流的反流特点,反流与胃黏膜组织学改变的关系.方法:选取20名青年健康志愿者,分别接受常规胃镜检查,24 h动态胃内pH和胆汁反流监测,HE染色行常规组织病理学检查以及改良Giemsa染色行幽门螺杆菌检查.结果:胃镜与胃黏膜组织检查多为正常黏膜或轻度浅表性炎症,仅2名胃镜下有胆汁反流,6名H pylori阳性.未见溃疡、糜烂、萎缩及肠化生.胆红素监测均有不同程度的十二指肠胃反流,abs>0.14的时间百分比为12.5%±8.8%,短时间反流频率62.8±36.0次、长时间反流频率5.9±3.8次、最长反流时间53.5.0±50.3min,其中立位反流时间显著性长于卧位(P=0.017).胃内pH>4的时间百分比为13.91%±10.1%,与胃内abs>0.14的时间百分比比较无相关性.结论:正常生理条件下均存在生理性十二指肠胃反流,不同个体、不同体位其反流程度不一,但这种反流不引起胃黏膜的病理性改变,也不引起胃内pH的变化.     

784例胃内胆汁返流现象相关因素分析

目的 分析胃内胆汁返流现象的相关因素，提供有助于胆汁返流性胃炎诊断的临床依据。方法 对784例近2年胃镜检查时见黏液湖黄染和黏膜有胆汁斑块附着、且无胃手术史的患者进行临床表现、内镜诊断和病理组织学改变及快速尿素酶试验结果进行总结，分析其相关因素及临床表现特点。结果 黏液湖黄染和黏膜黄染者多见于30～60岁的慢性胃炎患者，其它多见球部溃疡，快速尿素酶试验阳性者占51％，病理组织学改变见胃小凹增生者极少。临床表现以上腹饱胀、进食胀痛多见，但无特异性表现。结论 胆汁返流是慢性胃炎时内镜下多见的一种表现，也是慢性胃炎和消化性溃疡发病机制中重要的损害因素。Hp感染和胆汁返流对慢性胃炎和消化性溃疡是互相独立的致病因素。胆汁返流现象多数不够条件诊断胆汁返流性胃炎。内镜见黏液湖黄染和胃窦、胃体均广泛充血，散在糜烂可临床诊断胆汁返流性胃炎。胆汁返流性胃炎时病理组织学改变并不以胃小凹增生具特异性，其并不多见。     

原发性胆汁反流性胃炎诊断的探讨

目的　探讨原发性胆汁反流性胃炎的诊断方法及十二指肠胃反流 (DGR)的临床意义。方法　用便携式胆红素监测仪 (Bilitec2 0 0 0 )对 2 0例健康人及 42例有腹痛、腹胀、恶心及呕吐胆汁等症状的非溃疡性消化不良患者进行 2 4h胃内胆红素监测、临床症状评分、胃镜检查及组织活检。分析DGR的严重度与症状、内镜所见和组织学改变之间的关系。结果　 2 4h胆汁反流总时间百分率在健康组和有症状组中分别为 (2 92± 2 39) %及 (1 7 68± 1 7 89) % (P <0 0 1 ) ,病理性DGR的检出率为55 %。内镜下黏液湖胆染、胃窦黏膜糜烂、胆染伴胃窦黏膜糜烂、胆染伴中度以上的充血者中病理性DGR的检出率分别为 86 %、88%、8/8、85 %。内镜检查发现黏液湖胆染和胃窦黏膜糜烂和 (或 )中度以上充血并被Bilitec2 0 0 0证实存在病理性DGR的胆汁反流性胃炎 (BRG)者共有 1 1例。幽门螺杆菌(Hp)阴性的BRG者 ,组织学上活动性炎症比生理性DGR组Hp阴性者严重 (P <0 0 5)。各项临床症状的发生率在各组间差异无显著性 (P值均 >0 0 5) ,但BRG组腹胀、恶心及呕吐胆汁等症状的严重程度显著重于生理性DGR组 (P值均 <0 0 5)。结论　完整胃内镜检查发现黏液湖胆染同时伴胃窦黏膜糜烂和 (或 )中度以上充血并被Bilitec2 0 0 0证实存在病理性DG     

胆汁在胃食管反流病中的作用

随着24 h食管pH监测和胆汁监测技术的开展,胃、十二指肠液混合反流在胃食管反流病(GERD)的发生、发展中的作用已被逐步认识.胆汁反流在GERD发病过程中所扮演的角色,成为近年来人们研究的焦点之一.基础研究证明胆汁在不同酸碱环境、不同浓度对食管黏膜的损伤作用是不同的.不少临床试验对GERD进行研究发现,胆汁反流与症状和食管损伤严重度存在一定关系,但研究结果不尽一致,胆汁在GERD中的作用仍有争议.明确胆汁在GERD中的作用,有助于为预防此类疾病开辟新的道路.本文就有关胆汁反流在胃食管反流病中的作用的研究进展作一综述.     

胃酸在十二指肠液反流诱发食管腺癌中的作用

目的　探讨胃酸在十二指肠液反流诱发食管腺癌 (EAC)过程中的作用。方法　采用SD大鼠 ,通过手术产生三个实验组 :胃食管反流 (GER)组、十二指肠食管反流 (DER)组以及十二指肠胃食管反流 (DGER)组 ,并设无反流的假手术 (SO)对照组。术后 2 0周观察各组动物食管黏膜病变。结果　SO组未见明显病理学改变。各反流组均引发不同程度的食管炎。DER和DGER组基底细胞增生、鳞状上皮不典型增生和溃疡发生率显著高于GER组 (P <0 .0 1)。GER组没有出现Barrett’s食管 (BE)和食管腺癌 (EAC)。DER和DGER组BE发生率分别为 91.4 %和 84 .4 % ,EAC发生率分别为 2 5 .7%和5 3.1% ,均显著高于GER组 (P <0 .0 1)。DGER组EAC发生率显著高于DER组 (P <0 .0 5 )。结论　胃、十二指肠液反流均造成食管黏膜损伤 ,后者更为严重 ;十二指肠液反流在BE、EAC发展中发挥着尤为关键性的作用 ;胃酸在十二指肠液反流诱发EAC过程中起促进作用 ,显著增加十二指肠液反流诱发EAC的危险性     

Effects of bile reflux on gastric mucosal lesions in patients with dyspepsia or chronic gastritis

AIM: To investigate the influences of bile reflux on profiles of gastric mucosal lesions in patients with dyspepsia or chronic gastritis. METHODS: A total of 49 patients diagnosed with dyspepsia and chronic gastritis underwent 24-h ambulatory and simultaneous monitoring of intragastric bilirubin absorbance and pH values, and then they were divided into bile reflux positive group and bile reflux negative group. Severity of pathological changes in gastric mucosa including active inflammation, chronic inflammation, intestinal metaplasia, atrophy and dysplasia as well as Helicobacter pylori (H pylori) infection at the corpus, incisura and antrum were determined respectively according to update Sydney system criteria. The profiles of gastric mucosal lesions in the two groups were compared, and correlations between time-percentage of gastric bilirubin absorbance >0.14 and severity of gastric mucosal lesions as well as time-percentage of gastric pH >4 were analyzed respectively. RESULTS: Thirty-eight patients (21 men and 17 women, mean age 44.2 years, range 25-61 years) were found existing with bile reflux (gastric bilirubin absorbance >0.14) and 11 patients (7 men and 4 women, mean age 46.2 years, range 29-54 years) were bile reflux negative. In dyspepsia patients with bile reflux, the mucosal lesions such as active inflammation, chronic inflammation, intestinal metaplasia, atrophy or H pylori infection in the whole stomach, especially in the corpus and incisura, were significantly more severe than those in dyspepsia patients without bile reflux. Moreover, the bile reflux time was well correlated with the severity of pathological changes of gastric mucosa as well as H pylori colonization in the near-end stomach, especially in the corpus region. No relevance was found between the time of bile reflux and pH >4 in gastric cavity. CONCLUSION: Bile reflux contributes a lot to mucosal lesions in the whole stomach, may facilitate H pylori colonization in the corpus region, and has no influence on acid-exposing status of gastric mucosa in patients with dyspepsia or chronic gastritis.     

Duodenogastric reflux causes growth stimulation of foregut mucosa potentiated by gastric acid blockade

We investigated whether duodenogastric reflux (DGR) together with gastroesophageal reflux causes growth stimulation of the foregut mucosa and if additional gastric acid suppression enhances the effect of DGR. DGR was induced in rats using a split gastroenterostomy. A cardiomyotomy was performed across the gastroeophageal junction in order to enhance reflux into the esophagus. DGR rats were divided into six subgroups: DGR, DGR + truncal vagotomy, DGR + omeprazole, DGR + gastrin receptor blockade, DGR + omeprazole + gastrin receptor blockade, and DGR + gastrin. Two sham groups, one with and one without omeprazole treatment, served as controls. DGR significantly increased the weight and DNA content of the esophageal and gastric mucosa, which was further enhanced by vagotomy or omeprazole. Histology revealed foveolar hyperplasia in the stomach and esophageal mucosal hyperplasia in these groups. In addition, severe esophagitis was found in the DGR group receiving omeprazole. Omeprazole without DGR had no growth-stimulating effect on the foregut mucosa. DGR-induced growth stimulation was accompanied by hypergastrinemia. Increased growth in the stomach but not the esophagus was inhibited by gastrin receptor blockade. Gastrin administration did not result in enhancement of DGR-induced growth stimulation of the foregut mucosa. It is concluded that DGR, often present in severe reflux esophagitis, causes mucosal growth of the foregut of rats. This trophic response may explain why severe reflux esophagitis is associated with an increased risk of esophageal adenocarcinoma. DGR-induced growth stimulation of the foregut is potentiated by gastric acid suppression, suggesting that chronic antisecretory medication in gastroesophageal reflux may not always be advisable. Omeprazole + DGR caused severe esophageal damage, which may explain why antisecretory medication may fail to heal severe reflux esophagitis.     

Trypsin Activity and Bile Acid Concentrations in the Esophagus After Distal Gastrectomy

The pathogenesis of reflux esophagitis is not well understood and remains controversial. Distal gastrectomy serves as a model to assess the role of duodenal reflux with low gastric acidity in the development of reflux esophagitis. We investigated the relationship between the severity of esophagitis and gastroduodenal juice reflux, with particular focus on trypsin and bile acids after distal gastrectomy reconstructed with Billroth I anastomosis. Twenty-eight patients with gastroesophageal reflux disease after distal gastrectomy were enrolled. Esophageal and duodenal contents were aspirated under endoscopical examination, and their trypsin activity and bile acid concentrations were measured. The grade of reflux esophagitis was assessed by endoscopy and the symptoms were scored. Moreover, the grade of infiltration of inflammatory cells and the expression of COX-2 mRNA in the esophageal epithelium were evaluated. Patients with severe esophagitis had a higher amount of trypsin activity and bile acid concentrations in the esophagus, but not in the duodenum, compared to patients with mild esophagitis (P < 0.05). There was a strong positive correlation between the trypsin activity and the bile acid concentrations in the esophagus (r = 0.743, P = 0.0001). Moreover, the COX-2 mRNA expression and the grade of infiltrating inflammatory cells in the esophageal mucosa significantly correlated with the trypsin activity and bile acid concentrations in the esophagus. Thus, duodenogastroesophageal reflux with low gastric acidity is one of the pathogeneses in the development of reflux esophagitis from the present clinical study with patients after distal gastrectomy reconstructed with Billroth I anastomosis.     

胃及十二指肠液对食管粘膜损伤的实验研究

目的：通过动物实验,研究胃及十二指肠液反流对食管粘膜的损伤情况及其分别在胃食管反流病（ｇａｓｔｒｏｅｓｏｐｈａｇｅａｌ ｒｅｆｌｕｘ ｄｉｓｅａｓｅ,ＧＥＲＤ）发病中所占的地位。方法通过不同手术方式制作三种食管反流动物模型,分别为单纯胃液反流（Ｇ组）、单纯十二指肠内容物反流（Ｄ组）及十二指肠胃内容物混合反流（ＤＧ组）。于不同病程分批取得食管标本进行大体及光镜下形态学。结果各实验组出现程度不等的反流     

以胃黏膜胆汁酸浓度评估胆汁反流对胃黏膜组织的作用

背景:胃黏膜胆汁酸水平可直接反映胃黏膜细胞胆汁酸暴露的程度,并体现胆汁酸对胃黏膜的损伤程度。目的:探讨以胃黏膜组织胆汁酸浓度评估胆汁反流对胃黏膜病理改变的影响。方法:选取经内镜检查和黏膜胆汁酸浓度确诊的40例胆汁反流性胃炎患者和20例无胆汁反流性胃炎患者,评估幽门螺杆菌(H.pylori)检出率,行组织病理学评分,并分析胃黏膜胆汁酸浓度与组织病理学评分的相关性。结果:与无胆汁反流性胃炎患者相比,胆汁反流性胃炎患者H.pylori检出率无明显差异;胃窦、胃体黏膜组织胆汁酸含量显著升高(P0.05);胃窦黏膜慢性炎症和肠化生评分显著升高(P0.05),胃体黏膜慢性炎症、炎症活动性、萎缩和肠化生评分均显著升高(P0.05)。胆汁反流性胃炎患者胃窦、胃体组织病理学改变均与胆汁酸浓度相关(P0.05)。结论:以胃黏膜胆汁酸浓度评估的胆汁反流与胃黏膜病理损伤严重程度呈正相关。与无胆汁反流性胃炎相比,胃内胆汁反流主要加重胃体部组织病理学损伤。     

Clinical research on the relation of chronic gastritis and intragastric bile acids

Intragastric bile acids on fasting for 1 hour have been determined by radioimmunoassay and thin-layer chromatographic scanning in 102 cases of chronic gastritis. The results showed that all of intragastric conjunction bile acids were higher in chronic atrophic gastritis group than those in chronic superficial gastritis group. Both of their intragastric bile acids and nitrite levels increased significantly in patients whose gastric mucosa appeared acute inflammation, glandular atrophy and moderate or severe intestinal metaplasia. These findings suggest that bile acids may be implicated in premalignant histological changes of gastric mucosa such as chronic atrophic gastritis. Determining intragastric bile acids will reflect the degree and injurious effect of duodenogastric reflux.     

胆汁反流性胃炎患者幽门螺杆菌感染及其胃粘膜病理学表现研究*

目的 探讨胆汁反流性胃炎（BRG）患者幽门螺杆菌（Hp）感染及其胃粘膜病理学变化。方法 我院诊治的BRG患者618例和无胆汁反流的慢性浅表性胃炎（CSG）患者1486例,采用¹⁴C-尿素呼气试验、血清抗-Hp抗体检测和对组织切片行硼酸亚甲蓝染色三种方法对受试者进行Hp感染诊断,常规行胃镜检查,参照新悉尼系统标准,将组织学上胃黏膜慢性炎性反应、炎性反应活动性、萎缩和肠上皮化生的严重程度分为无、轻、中和重4个等级。结果 BRG患者Hp感染率为32.7%（202/618）,而CSG组患者为40.6%（603/1486）,两组间无显著性差异（P>0.05）;在202例Hp阳性的BRG患者中,胃粘膜轻、中、重度炎症反应发生率分别为10.9%、61.4%和27.7%,显著重于416例Hp阴性患者的40.4%、51.7%和7.9%（P<0.05）,胃粘膜淋巴滤泡形成、肠化生和活动性炎症发生率分别为15.4%、5.4%和16.8%,也显著重于Hp阴性患者的2.7%、10.8%和0.7%（P<0.05）;603例Hp阳性的CSG患者胃粘膜轻、中、重度炎症反应发生率分别为29.2%、59.4%和11.5%,与883例Hp阴性患者的34.1%、54.0%和11.9%比,无显著性差异（P>0.05）,胃粘膜淋巴滤泡形成、肠化生和活动性炎症发生率分别为10.4%、1.8%和8.5%,与Hp阴性患者的7.8%、1.0%和5.0%比,也无显著性差异（P>0.05）;观察胃粘膜病理学轻度、中度和重度炎症情况发现,117例内镜下胃粘膜III级BRG患者炎症程度显著重于200例I级或301例II级患者（P<0.05）。结论 BRG患者无论是胃镜下表现还是胃粘膜组织病理学变化都存在明显的病变,胆汁反流和Hp感染是引起胃粘膜炎症反应的重要因素。     

Duodenogastric bile reflux after gastric bypass: a cholescintigraphic study

In this exploratory study, we examined the occurrence of duodenogastric bile reflux to the excluded stomach after Roux-en-Y gastric bypass, a standard surgical therapy for morbid obesity. We studied 22 unselected patients (median age 44, 20 females) 18 months postoperatively. BMI at surgery and cholescintigraphy was 45 and 29 kg/m², respectively. Mebrofenin labeled with 200 MBq ^99mT was injected intravenously and the fate of radioactivity followed for 90 min. Bile flow was enhanced with cholecystokinin. We found scintigraphic evidence of duodenogastric bile reflux in 36% of the patients. The tracer remained in the excluded stomach throughout the study period. In conclusion, our investigation indicates that in more than one third of the patients undergoing gastric bypass, the gastric mucosa in the excluded stomach is exposed to the potential deleterious effects of bile.     

M3受体在人胃和食管组织中的表达

目的研究发现石胆酰牛磺酸及其他一些胆汁酸是M3受体的部分激动剂，而胆汁反流到胃和食管又是一个普遍现象。本研究旨在探索胃、食管黏膜的M3受体表达情况。方法分别使用羊和兔抗人M3受体的多克隆IgG抗体A和B，采用免疫组化，在11例人胃和食管的不同部位黏膜对M3受体进行定位。结果使用抗体A发现胃泌酸腺表面黏液细胞、小凹细胞、颈部细胞和壁细胞，及食管鳞状上皮的棘层细胞表现为细胞质染色，使用抗体B发现除上述细胞的胞质染色外，人胃壁肌层平滑肌细胞表现为胞膜和胞质共同染色。结论研究揭示M3受体表达于人胃泌酸腺表面黏液细胞、小凹细胞、腺颈部细胞、壁细胞和食管鳞状上皮的棘层细胞。