肝硬变血浆内毒素与一氧化氮水平的改变及关系的研究

目的研究肝硬变患者血浆内毒素与一氧化氮水平改变及关系．方法应用鲎试剂定量法和高效液相色谱分析法分别检测肝硬变患者４４例（男３２例，女１２例；年龄２５岁～７３岁，平均５０４岁±１１０岁）；ＣｈｉｌｄＰｕｇｈＡ级９例，Ｂ级２０例，Ｃ级１５例；其中有腹水者２７例及健康对照２５例（男１８例，女７例，年龄２４岁～６３岁，平均４６８岁±１２４岁）血浆内毒素和一氧化氮水平．结果肝硬变血浆内毒素及一氧化氮水平（２３７１ＥＵ／Ｌ±８２３ＥＵ／Ｌ，３８７１７ｎｇ／ｍｌ±１０６４１ｎｇ／ｍｌ）明显高于对照组（１５６７ＥＵ／Ｌ±２４６ＥＵ／Ｌ，２９２３０ｎｇ／ｍｌ±５４４９ｎｇ／ｍｌ，Ｐ＜００１）．腹水患者内毒素与一氧化氮水平（２３６９ＥＵ／Ｌ±５３６ＥＵ／Ｌ，４１４６７ｎｇ／ｍｌ±１０７０５ｎｇ／ｍｌ）明显高于无腹水者（１９６９ＥＵ／Ｌ±４５２ＥＵ／Ｌ，３２７１７ｎｇ／ｍｌ±７０２０ｎｇ／ｍｌ，Ｐ＜００５，Ｐ＜００１）．一氧化氮与内毒素呈直线正相关（Ｐ＜００１，ｒ＝０７８２）．结论肝硬变患者血浆内毒素及一氧化氮水平皆升高，且两者呈直线正相关．     

胃癌及消化性溃疡患者胃窦粘膜胃肠激素的变化

目的探讨胃癌及消化性溃疡（ＰＵ）患者胃窦粘膜胃肠激素变化的意义．方法内镜及活检确诊的浅表性胃炎（ＣＳＧ）１０例，胃溃疡（ＧＵ）１５例，十二指肠溃疡（ＤＵ）１２例，胃癌（ＧＣ）６例．胃镜下取胃窦粘膜，用ＲＩＡ法测定胃泌素（Ｇａｓ）、生长抑素（ＳＳ）、Ｐ物质（ＳＰ）的含量，各组间进行比较．结果胃窦粘膜ＳＳ含量在ＧＵ，ＤＵ，ＣＳＧ，ＧＣ组分别为２５１ｐｇ／ｍｇ±１９４ｐｇ／ｍｇ（以下同），４７０±１７９，５３２±２１１及１２９３±５２３。其中ＧＵ组低于其余各组（Ｐ＜００５），而ＧＣ时则显著升高（Ｐ＜００１）．ＳＰ含量在ＤＵ组显著降低，与ＧＵ，ＣＳＧ，ＧＣ比较分别为４７９±１５７ｖｓ７６５±４１５，７８９±３９０及８０１±３４６，Ｐ＜００５；ＧＣ患者Ｇａｓ水平显著高于ＣＳＧ组，为４６４５±２９４４，ｖｓ２７６８±１５７２，Ｐ＜００１．结论胃粘膜中Ｇａｓ，ＳＳ，ＳＰ含量的变化可能在ＰＵ及胃癌的发病机理中起重要作用．     

老年消化性溃疡222例临床特征

目的探讨老年消化性溃疡（ＰＵＡ）的临床及内镜下特点．方法１９８５－１９９４年６０岁以上消化性溃疡（ＰＵ）住院患者２２２例，以同期６０岁以下ＰＵ１００例为对照进行临床内镜分析．结果老年胃溃疡占同期胃溃疡住院人数的构成比已由１９８５年的１０９％递增至１９９４年的２４０％．ＰＵＡ上腹痛、节律性腹痛、反酸、烧心症状发生率依次为５７８％，２２５％，３１５％和１０４％，对照组依次为８７０％，４５０％，４８０％和３８０％（Ｐ＜００１）．并发症发生率ＰＵＡ组为６０８％，对照组为４００％（Ｐ＜００１）．ＰＵＡ直径大于３ｃｍ者占２２５％，对照组为４０％（Ｐ＜００１）．行手术治疗者ＰＵＡ组为２１６％，对照组为１１０％（Ｐ＜００１）．结论ＰＵＡ临床症状不典型，并发症发生率高，巨大溃疡常见，出血难止，手术机率增加     

肝硬变病程中的肾脏血流动力学变化与肾损害

目的观察肝硬变从代偿期、失代偿期至肝肾综合征肾血流动力学的变化和肾损害的关系．方法肝硬变患者５２例，进行双肾多普勒超声检查，并检测尿中氨基葡萄糖苷酶（ＮＡＧ）活性．其中代偿期和失代偿期各２０例，肝肾综合征１２例．另选健康对照２０例，各组年龄相近．结果代偿期肾动脉内径（Ｄ）为５２ｍｍ±０４ｍｍ，肾血流量（Ｖ）为５０７ｍｌ±１４０ｍｌ，阻力指数（ＲＩ）为０６２±０１２．与对照组无差异（Ｐ＞００５）．失代偿期和肝肾综合征期Ｄ分别为３７ｍｍ±０６ｍｍ和２８ｍｍ±０２ｍｍ，Ｖ分别为１６１ｍｌ±６１ｍｌ和８９ｍｌ±１６ｍｌ，ＲＩ分别为０８４±００９和０９２±００１．比对照组和代偿期有明显变化（Ｐ＜００１）．尿ＮＡＧ在对照组是６４Ｕ±３２Ｕ，代偿期和失代偿期分别为１０３Ｕ±３６Ｕ，３８４Ｕ±２６３Ｕ（Ｐ＜００１）．以大于对照组ｘ±３ｓ为异常，血肌酐、ＢＵＮ均正常的失代偿期中６５％有早期肾损害，并ＲＩ均大于０８．而ＲＩ＞０８的患者中５９１％有早期肾损害．结论肝硬变病程中肾血流动力学变化逐渐加重．失代偿期中有许多亚临床肝肾综合征患者     

内皮素与一氧化氮在肝硬变血流动力学紊乱中的作用

目的研究内皮素、一氧化氮在肝硬变血流动力学紊乱中的作用及关系．方法应用放免法和高效液相色谱法分别检测肝硬变患者４４例，（男３２例，女１２例；年龄５０４岁±１１０岁），其中腹水患者２７例及健康对照２５例（男１８例，女７例；年龄４６８岁±１２４岁）血浆内皮素（ＥＴ）、一氧化氮（ＮＯ）及部分血管活性物质水平．结果肝硬变组血浆ＥＴ及ＮＯ水平（５７０ｎｇ／Ｌ±２５４ｎｇ／Ｌ，３８７２μｇ／Ｌ±１０６４μｇ／Ｌ）明显高于对照组（３３０ｎｇ／Ｌ±１０９ｎｇ／Ｌ，２９２３μｇ／Ｌ±５４５μｇ／Ｌ，Ｐ＜００１）．腹水患者血浆ＥＴ及ＮＯ水平（６７５ｎｇ／Ｌ±２４７ｎｇ／Ｌ，４１４７μｇ／Ｌ±１０７１μｇ／Ｌ），显著高于无腹水患者（４５９ｎｇ／Ｌ±１８３ｎｇ／Ｌ，３２７２μｇ／Ｌ±７０２μｇ／Ｌ，Ｐ＜００１）．ＮＯ与ＥＴ呈直线正相关（ｒ＝０７７２，Ｐ＜００１）．结论肝硬变患者ＥＴ与ＮＯ水平升高，且腹水患者较无腹水者更升高；两者呈直线正相关     

西沙必利对功能性消化不良患者胃动力、胃动素、胃泌素影响的研究

对３０例功能性消化不良（ＦＤ）患者服用西沙必利前后的胃腔内压力、血中胃动素及胃泌素的变化进行检测，并以１１例正常人作对照。结果：①ＦＤ患者胃窦和胃体基础压、胃窦蠕动压及血中胃动素浓度，明显低于正常对照组（Ｐ值分别＜００５，＜００１）；而胃窦蠕动波持续时间、血中胃泌素浓度与正常组无显著差异（Ｐ＞００５）。②服用西沙必利后，ＦＤ患者与正常对照组胃窦和胃体基础压、胃窦蠕动压及血中胃动素浓度，均较服药前明显升高（Ｐ＜００５，Ｐ＜００１）。而胃窦蠕动波持续时间和血中胃泌素浓度，正常组和ＦＤ组服药前后均无显著差异（Ｐ＞００５）。结论：ＦＤ与胃动力障碍有关，西沙必利治疗ＦＤ是合理、有效的     

超声显像预测肝硬变上消化道出血的危险性

目的研究Ｂ超显像预测门脉高压上消化道出血的危险性．方法１９９０年～１９９６年采用Ｂ型超声诊断仪探测１４２例（非出血组１０８例，出血级３４例）肝炎后肝硬变患者肝门静脉、脾门静脉的直径，并与慢性肝炎７５例作为对照．结果肝门静脉、脾门静脉直径与食管胃底静脉曲张发生率有关．肝硬变上消化道出血组肝门静脉（１５１ｃｍ±０２０ｃｍ）、脾门静脉（１１８ｃｍ±０２８ｃｍ）直径明显大于肝硬变非出血组（１１９ｃｍ±０２３ｃｍ，０９４ｃｍ±０１８ｃｍ，Ｐ＜００１）．肝门静脉、脾门静脉直径与上消化道出血率呈正相关（ｒ＝０９９，Ｐ＜００１）．肝门静脉≥１５ｃｍ，脾门静脉≥１１ｃｍ，可作为预测上消化道出血的警戒线．２２例门脉高压患者应用普鲁纳洛治疗，治疗后显示肝门静脉、脾门静脉直径较前缩小．结论应用Ｂ超显像测定静脉直径可预测肝硬变上消化道出血的危险性，亦可作为观察降门脉压力药物疗效的指标．     

乙型肝炎病毒感染与消化性溃疡的关系

目的探讨乙型肝炎病毒（ＨＢＶ）感染与消化性溃疡（ＰＵ）之间的关系及其在ＰＵ形成中的作用机制．方法１９８９１０／１９９５０９因消化道症状而进行内镜检查及血清ＨＢＶＭ检测的３３４例患者，并对结果进行统计学处理分析．结果在３３４例患者中有４６例感染了ＨＢＶ，列为ＨＢＶ感染组，检出ＰＵ１９例（４１３％），其余２８８例列为ＨＢＶ非感染组，检出ＰＵ６６例（２２９％），两组有极显著差异（Ｐ＜００１）．在３３４例患者中有ＰＵ８５例，列为ＰＵ组，血清ＨＢＶＭ阳性率为２２４％，其中胃溃疡（ＧＵ）３１例（３６５％），十二指肠溃疡（ＤＵ）３５例（４１２％），复合性溃疡（ＣＵ）１９例（２２３％），ＧＵ，ＤＵ及ＣＵ血清ＨＢＶＭ阳性率分别为２５８％（８／３１），２２９％（８／３５）及１５８％（３／１９），三组相互间比较无显著性差异（Ｐ＞００５）；其余２４９例列为非ＰＵ组，血清ＨＢＶＭ阳性率１０８％，两组有极显著差异（Ｐ＜００１）．ＰＵ组与全国城市人群标化ＨＢＶＭ阳性率７９％比较有极显著差异（Ｐ＜００１）．结论ＨＢＶ感染与ＰＵ关系密切，是参与ＰＵ发病的一个因素．     

梗阻性黄疸对肝脏血流动力学的影响

目的探讨梗阻性黄疸对肝脏血流动力学的影响．方法采用彩色多普勒血流显象仪对２０例梗阻性黄疸患者的肝固有动脉和门静脉血流进行定量测量，并与２０例正常人进行对比分析．结果梗阻性黄疸患者肝固有动脉的峰值流速（ｃｍ／ｓ，９２±１５ｖｓ６９±１９，Ｐ＜００５）、血流量（ｍＬ／ｍｉｎ，７１４±３６３ｖｓ３０５±１２１，Ｐ＜００１）显著高于正常人；门静脉血管内径（ｃｍ，１２５±０２４ｖｓ１０４±０１９，Ｐ＜００１）及门脉充血指数（ｃｍ×ｓ，０１４１±００１３ｖｓ０１１９±００１３，Ｐ＜００１）明显高于正常人．但门静脉血流量及峰值流速则低于正常人．结论彩色多普勒血流显象仪探讨梗阻性黄疸时肝脏血流动力学改变的较理想非创伤性方法，根据其有效循环血容量的改变可初步判断梗阻性黄疸的预后     

奥曲肽预防ERCP术后高淀粉酶血症及胰腺炎的疗效

目的探讨奥曲肽对内镜逆行胰胆管造影（ＥＲＣＰ）术后高淀粉酶血症及胰腺炎的预防作用．方法行ＥＲＣＰ患者２７６例，随机分为两组：预防组１６７例，分别于术前３０ｍｉｎ及术后４ｈ内ｓｃ奥曲肽０１ｍｇ；对照组１０９例，ＥＲＣＰ术前后分别予生理盐水１ｍＬｓｃ．两组患者术前后均不用其他任何抑制胰腺分泌及预防胰腺炎药物．并分别于术前、术后２ｈ，２４ｈ作血清淀粉酶测定，同时观察胰腺炎的发生情况．结果预防组ＥＲＣＰ术后２ｈ，２４ｈ血淀粉酶（Ｕ／Ｌ）分别为２４６±２２４和２５２±２９１；明显低于对照组（４９９±５９７和４６６±５５９，Ｐ＜００１）；预防组发生胰腺炎７例（４２％），对照组发生９例（８３％，Ｐ＜００１）．结论小剂量奥曲肽能有效地预防ＥＲＣＰ术后的高淀粉酶血症及胰腺炎     

Prophylactic effect of somatostatin on stress ulcer formation in rats

The aim of the present study was to investigate the effect of somatostatin (growth-hormone release-inhibiting hormone) on ulcer formation during immobilisation stress. This was done in male Albino-rats to study the effect of somatostatin on number and size of ulcers, to calculate ulcer index, to measure pH-value of gastric juice as well as plasma levels of gastrointestinal hormones. Rats treated with somatostatin before and during stress exposition had only the third part of the ulcers compared with the untreated animals. Total ulceration area was less than the tenth of the untreated rats. Normal corticoid plasma levels during stress exposition were found in the lower range of normal values in somatostatin treated rats. Decrease of plasma gastrin during stress exposition exceeded the gastrin decrease of somatostatin treated rats. Rise of plasma glucagon was completely inhibited during somatostatin application. Results of serum glucose paralleled those seen in glucagon.     

非静脉曲张性急性上消化道出血血清胃泌素检测及其临床意义

目的:了解非静脉曲张性急性上消化道出血血清胃泌素变化及其临床意义。方法:A组:急性非静脉曲张性上消化道出血34例;B组:活动期消化性溃疡29例;C组:慢性胃炎30例。采用放免法检测血清胃泌素。结果:A组血清胄泌素为97.94±22.75ng/L,95％可信限(95％CI)为92.08～103.80ng/L;B组胃泌素52.31±9.94ng/L,95％CI 48.70～55.94ng/L;C组胃泌素35.15±11.95ng/L,95％ CI 30.88～39.42ng/L。A组胃泌素显著高于B、C组(P<0.01),B组胃泌素也明显高于C组(P<0.05)。结论:胃泌素增多与消化道出血相关。     

Gastrin and somatostatin cells in dyspeptic patients with and without duodenal ulcer: A quantitative study based on multiple biopsy specimens

The numbers of immunoreactive gastrin and somatostatin cells in gastric and duodenal mucosal biopsy specimens from dyspeptic patients with duodenal ulcers and dyspeptic controls without ulcers were calculated using a morphometric method. The levels of gastrin and somatostatin in the tissue were also measured by the radioimmunoassay. The results showed no significant difference in the number of G cells and the level of gastrin in the tissue between the ulcer and non-ulcer groups. However, the number of D cells and the level of somatostatin in the tissue in ulcer patients were remarkably reduced in comparison with those in non-ulcer patients (P less than 0.01 and P less than 0.05, respectively). The G:D cells and gastrin:somatostatin ratios in ulcer patients were much higher than those in the non-ulcer control group. It is considered that the reduction of D cells and the relative lack of somatostatin in duodenal ulcer patients might have a role in the mechanism of the duodenal ulceration.     

Antral release of gastrin and somatostatin in duodenal ulcer and control subjects.

Organ culture was used to compare gastrin and somatostatin release from cultured antral mucosa obtained from duodenal ulcer and non-ulcer (control) subjects. In response to dibutyryl cyclic AMP (DBCAMP) cultured antral mucosal explants from patients with a history of duodenal ulcer released a greater proportion of antral gastrin into the medium than did antral mucosal explants from non-ulcer subjects. Somatostatin release from antral mucosa from duodenal ulcer patients was substantially less than somatostatin released by antral explants from non-ulcer subjects. In the non-ulcer subjects there was a direct positive correlation between the amounts of antral somatostatin and gastrin released into the culture medium (r = 0.64, less than p 0.01). In the duodenal ulcer patients, however, there was no correlation between gastrin release and somatostatin release from antral mucosa ( r = 0.09; p greater than 0.2). Results of these studies identify enhanced gastrin release in response to stimulation and decreased release of somatostatin from antral mucosa of duodenal ulcer patients. These alterations in paracrine relationships of antral somatostatin and gastrin in duodenal ulcer subjects may contribute, at least in part, to the pathogenesis of duodenal ulcer disease.     

The influence of Helicobacter pylori infection on gastrin and somatostatin values present in serum

BACKGROUND/AIMS: Recent studies on the role of Helicobacter pylori in pathogenesis of duodenal ulcers have focused on the mechanism by which H. pylori infections causes exaggerated gastrin release. METHODOLOGY: We compared the gastrin and somatostatin serum values between two groups of patients; 37 H. pylori-positive ones and 29 H. pylori-negative ones. We applied radioimmunoassay technique to determine the gastrin and somatostatin values in serum. H. pylori was confirmed by urease test and by histopathological color according to Giemsa. RESULTS: The level of gastrin in the serum of Helicobacter pylori-positive patients with chronic gastritis were significantly higher in relation to H. pylori-negative patients. The somatostatin concentration in the sera of H. pylori-positive patients with duodenal ulcer (16.27 +/- 9.49 pg/mL) were less in comparison with those without duodenal ulcer (23.25 +/- 13.59 pg/mL). CONCLUSIONS: The results suggest that H. pylori infection suppresses the somatostatin secretion.     

血清胃泌素诊断结直肠肿瘤的价值

目的研究结直肠肿瘤患者血清胃泌素水平与病情的相关性．方法经纤维结肠镜下活组织病理检查和／或术后病理确诊的结直肠腺瘤２８例和结直肠癌患者４６例，在排除有可能影响血清胃泌素水平的其它情况后，用ＲＩＡ法检测空腹血清胃泌素及ＣＥＡ含量．结果以胃泌素≥１００ｎｇ／Ｌ作为结直肠腺瘤的诊断指标，其敏感性、特异性和诊断效率分别为７５％，８１％和７８９％，以胃泌素≥１３０ｎｇ／Ｌ作为结直肠癌的诊断指标，其敏感性、特异性和诊断效率分别为７００％，９１９％和７９３％；而ＣＥＡ≥１５μｇ／Ｌ，则分别为３２０％，９４４％和４８５％．以胃泌素≥１３０ｎｇ／Ｌ作为癌肿与腺瘤的鉴别诊断指标，其敏感性、特异性和诊断效率都是７００％；而ＣＥＡ≥１５μｇ／Ｌ，则分别为３００％，９００％和４８６％．在早期结直肠癌患者，胃泌素≥１００ｎｇ／Ｌ者占７７８％，明显高于便血率（４５５％）．结论血清胃泌素对结直肠肿瘤的诊断和鉴别诊断优于ＣＥＡ，可作为结直肠癌的普查手段．     

Effect of intragastric pH on antral gastrin and somatostatin release in anaesthetised, atropinised duodenal ulcer patients and controls.

The synchronous change in the antral release of gastrin and somatostatin into a vein draining the stomach was studied during acidic and alkaline intragastric pH in six anaesthetised duodenal ulcer patients and six controls after atropinisation. No differences in the basal secretion of gastrin and somatostatin were observed among the two groups. Alkaline as well as acidic intragastric pH had no effect on the antral release of somatostatin in duodenal ulcer patients and controls. In contrast, alkaline intragastric pH was associated with a significantly higher antral gastrin release in duodenal ulcer patients than in controls. Acidic intragastric pH was associated with a significantly smaller inhibition of antral gastrin release in duodenal ulcer patients than in controls. These results suggest that atropinised anaesthetised duodenal patients release gastrin abnormally in the presence of acidic or alkaline intragastric pH and that any inverse relationship between antral gastrin and somatostatin release is uncoupled under these conditions.     

Gastrin, somatostatin, G and D cells of gastric ulcer in rats

AIM: To investigate the relationship among gastrin, somatostatin, G and D cells in gastric ulcer and in its healing process in rats. METHODS: Fourty-nine Wistar rats were divided into 7 groups. The gastric ulcer model was induced by acetic acid successfully. The gastrin and the somatostatin in rat plasma, gastric fluid and antral tissue were measured by radioimmunoassay(RIA). G and D cells in antral mucosa were analyzed with polyclonal antibody of gastrin and somatostatin by immunohistochemical method and Quantimet 500 image analysis system. RESULTS: In gastric ulcer, the level of gastrin in plasma, gastric fluid, and antral tissue increased, that of somatostatin declined, and the disorder gradually recovered to the normal level in the healing process. Immunohistochemical technique of G and D cells in antral mucosa demonstrated that the number of G cells increased and that of D cells decreased, both areas of G and D cells declined, the ratio of number and area of G/D increased in gastric ulcer, and the disorder gradually recovered in the healing process. CONCLUSION: In gastric ulcer, the increased gastrin secreted by G cells, the declined somatostatin secreted by D cells, and the disordered G/D cell ratio can lead to gastrointestinal dysfunction.     

Effect of systemic gastric acid stimulation and intragastric pH changes on synchronous antral gastrin and somatostatin release in anesthetized,nonatropinized duodenal ulcer patients and controls

The synchronous changes in antral gastrin and somatostatin release in anesthetized, nonatropinized duodenal ulcer patients and control subjects were investigated by serial intraoperative blood sampling from the right gastroepiploic vein. The mean basal antral plasma gastrin and somatostatin concentrations of the two groups did not differ significantly. The significantly greater gastric acid secretory response to systemic gastric acid stimulation (pentagastrin stimulation) in duodenal ulcer patients compared with that of control subjects was not linked to any difference in antral somatostatin release pattern. The decrease in antral plasma gastrin release was significantly lower after acid instillation and the increase was significantly higher after alkali instillation in duodenal ulcer patients compared with those of controls, indicating an abnormal gastrin response to intragastric pH changes in duodenal ulcer patients, which was again not found to be coupled to any significant difference in antral somatostatin release. The results suggest that an abnormal somatostatin-mediated inhibition of gastrin release and/or gastric acid secretion does not exist in duodenal ulcer patients.