肝硬化患者血浆VIP、CCK水平与胆囊排空功能的关系

探讨肝硬化时血浆胃肠激素水平对胆囊运动的影响。用放免法测定肝硬化患者及对照者血浆血管活性肠肽 (VIP)和胆囊收缩素 (CCK)含量 ;用B超测定餐前、餐后胆囊容积及排空率。结果 :肝硬化时血浆VIP、CCK均明显增高 (P <0 0 1,P <0 0 5 ) ;胆囊空腹容积、剩余容积均明显增大 (P <0 0 1,P <0 0 0 1) ,最大排空率较对照组无明显差异 (P >0 0 5 ) ,但Child -PughC级降低 (P <0 0 5 )。肝硬化组胆囊最大排空率与VIP呈负相关 ,胆囊空腹容积及剩余容积与VIP均呈正相关 ,胆囊空腹容积、剩余容积及最大排空率与CCK均无相关。提示肝硬化时VIP增高既抑制胆囊运动 ,又明显降低胆囊张力 ,肝硬化时可能存在对CCK的抵抗。     

肠易激综合征患者血浆脑肠肽水平的变化

脑肠肽作为一类具有神经递质和激素双重功能的小分子多肽,在肠易激综合征（IBS）的发病机制中起重要作用.目的：研究血管活性肠肽（VIP）,神经肽Y（NPY）和神经降压素（NT）水平在IBS患者血浆中的变化及其临床意义.方法：根据RomeⅡ标准纳入IBS患者36例,其中腹泻为主型IBS（D-IBS）24例,便秘为主型IBS（C-IBS）12例,同时纳入正常对照者10名.采用放射免疫测定分别检测受试者血浆VIP、NPY和NT水平.结果：D-IBS患者血浆VIP水平显著高于正常对照组（P＜0.05）,而C-IBS患者血浆VIP水平与正常对照组比较无显著差异（P＞0.05）;D-IBS和C-IBS患者血浆NPY水平均显著低于正常对照组（P＜0.05和P＜0.01）,其中C-IBS患者又显著低于D-IBS患者（P＜0.05）;D-IBS和C-IBS患者血浆NT水平均显著高于正常对照组（P＜0.05）,但两亚型间比较无显著差异（P＞0.05）.结论：IBS患者血浆脑肠肽水平与腹泻或便秘症状有一定的联系,表现为D-IBS和C-IBS患者的血浆NT水平均显著升高,而NPY和VIP水平因IBS亚型的不同而有差异.脑肠肽作为调节胃肠运动功能和感觉功能的重要因素,可能与IBS的发生、发展有必然的内在联系.     

肠易激综合征血浆及乙状结肠粘膜中VIP及SS的含量

目的 :探讨肠易激综合征 (IBS)患者血浆及乙状结肠粘膜中血管活性肠肽 (VIP)、生长抑素 (SS)有无变化 ,以及它们在IBS发病过程中的可能作用和临床意义。方法 :应用放射免疫分析法 (RIA)测定IBS患者血浆及乙状结肠粘膜内VIP、SS的含量 ,并与正常组比较。结果 :便秘型IBS血浆及乙状结肠粘膜中VIP含量显著高于正常组 (P <0 .0 1 ) ,腹泻型显著低于正常组 (P <0 .0 5) ;SS在IBS各组均显著高于正常组 (P <0 .0 5) ,而便秘型又显著高于腹泻型 (P <0 .0 5)。结论 :IBS患者存在VIP、SS含量异常 ,且这些异常可能在IBS发病中起一定的作用 ;不同类型IBS患者VIP及SS含量有显著差异 ,说明不同类型IBS在发病机制上有其不同的病理生理学基础     

肝硬化门脉高压患者血浆SS、VIP及MTL变化的临床意义

目的　研究生长抑素(SS)、血管活性肠肽(VIP)、胃动素(MTL)在门脉高压症中的水平及其作用。方法　应用放射免疫学方法对 62例肝硬化门脉高压症患者、51例正常对照者血浆及 43份门脉高压性腹水进行SS、VIP与MTL的检测。结果　门脉高压症组血浆SS、VIP与MTL水平分别为 58 23±13 5pg/ml, 18 68±4 22pg/ml及 362 95±32 82pg/ml;正常对照组分别为 81 23±31 89pg/ml, 11 96±3 27pg/ml及 202 95±26 42pg/ml,二者差异有显著性(P<0 05)。腹水组分别为 148 03±28 41pg/ml, 14 12±3 64pg/ml及 267 43±29 04pg/ml。腹水SS、MTL高于对照组血浆含量(P<0 05)。腹水VIP与对照组血浆含量差异无显著性。肝硬化腹水患者血浆SS低于无腹水者,而VIP与MTL水平高于无腹水者(P<0 05)。VIP、MTL随着肝功能分级的发展而逐步增加。结论　血浆SS、VIP与MTL在肝硬化门脉高压症的病理生理机制中起着重要作用。     

肝硬化患者血浆及胃粘膜内血管活性肠肽和生长抑素含量的变化及意义

本文采用放射免疫测定法研究了肝硬化（ＨＣ）患者血浆及胃粘膜内血管活性肠肽（ＶＩＰ）和生长抑素（ＳＳ）含量变化及其意义。结果表明：肝硬化患者血浆和胃粘膜内的ＶＩＰ含量（１７４·９９±８８·１１ｐｇ／ｍｌ，１０９．４７±３０．７０ｐｇ／ｍｇ）和ＳＳ含量（５０．８８±１５．８ｐｇ／ｍｌ，３９８．２１±１２５．７３ｐｇ／ｍｇ）均显著高于正常对照组（ＶＩＰ：１０７．４６±９．８ｐｇ／ｍｌ，５８．７４±６．７１ｐｇ／ｍｇ和ＳＳ：２６．８３±５．９２ｐｇ／ｍｌ，２１２．６２±４７．６４ｐｇ／ｍｇ）（Ｐ＜０．０１）。ＨＣ伴溃疡病患者血浆及粘膜中ＳＳ含量显著高于无溃疡的ＨＣ患者（Ｐ＜０．０５）；血浆及胃粘膜中ＶＩＰ的含量与胃、十二指肠粘膜充血程度呈正相关（Ｐ＜０．０５）；重度食管静脉曲张患者ＶＩＰ含量显著高于无食管静脉曲张者（Ｐ＜０．０５）；血浆及胃粘膜内ＶＩＰ和ＳＳ含量与血浆白蛋白呈负相关（Ｐ＜０．０１）和凝血酶原时间延长呈正相关（Ｐ＜０．０１）与腹水的有无及程度关系不密切。提示：在ＨＣ时存在着严重的胃肠激素代谢紊乱，并且它在ＨＣ的病理生理机制和ＨＣ时胃肠功能改变和病理变化中起着重要作用。     

哮喘患者血浆P物质和血管活性肠肽含量变化及其临床意义

用放射免疫分析法测定不同信群血浆ＳＰ，ＶＩＰ浓度及其对治疗的反应，结果：（１）缓解期血浆ＳＰ浓度升高，ＶＩＰ浓度下降，与对照组比较有显著性差异；（２）发作期组治疗前血浆ＳＰ，ＶＩＰ浓度变化较缓解期及正常组比较有显著性差异，（３）发作期组治疗后ＳＰ，ＶＩＰ浓度与治疗前比较有显著性差异，与缓解期组比较无显著性差异，结论：哮喘病人气道粘膜病理学改变致血浆ＳＰ浓度升高，ＶＩＰ浓度下降，与临床症状加重同步，     

急诊重症患者的胃肠功能障碍与胃泌素水平

目的:检测合并胃肠功能障碍的急诊重症患者血胃泌素(gastrin,GAS)水平和对急诊重症患者APACHEⅡ评分进行断面分析,探讨GAS水平在胃肠功能障碍发生早期的临床意义.方法:共84例患者入选,其中胃肠功能受损组23例,胃肠衰竭早期组22例,胃肠衰竭组39例,设同期健康体检者20例为对照组,84例患者在入院第1、3、5天进行血GAS水平检测和APACHEⅡ评分,按评分<15、15-25、>25进行断面分组.结果:除第5天胃肠衰竭组与胃肠衰竭早期组GAS水平两两比较无统计学意义外(q=2.456P=0.086),第1、3、5天各组GAS水平两两比较均有统计学差异,P<0.05;第1、3、5天GAS与胃肠功能障碍严重程度分组有显著相关性(r=0.855、0.895、0.682,P=0.000).按APACHEⅡ评分断面分组GAS水平总体比较有统计学差异,P<0.05;各组GAS水平两两比较均有统计学差异,P<0.05;各组GAS水平与APACHEⅡ评分有显著相关性(r=0.805,P=0.000).结论:急诊重症患者GAS水平与重症患者疾病严重程度相关,GAS水平可以早期提示胃肠功能障碍的存在和判定胃肠功能障碍严重程度.     

肝硬化患者血浆及胃粘膜内血管活性肠肽和生长抑素含量的变化及意义

采用放射免疫测定法研究了肝硬化（ＨＣ）患者血浆及胃粘膜内血管活性肠肽（ＶＩＰ）和生长抑素（ＳＳ）含量变化及其意义。结果表明：肝硬化患者血浆和胃粘膜内的ＶＩＰ含量和ＳＳ含量均显著高于正常对照组（Ｐ＜０．０１）；ＨＣ伴溃疡病患者血浆及胃粘膜中ＳＳ含量显著高于无溃疡的ＨＣ患者（Ｐ＜０．０５）；血浆及胃粘膜中ＶＩＰ的含量随着胃、十二指肠粘膜充血程度的加剧而升高；并且血浆及胃粘膜内ＶＩＰ和ＳＳ含量与肝功能密切相关。提示：在ＨＣ时存在着严重的胃肠激素代谢率乱，并且它在ＨＣ的病理生理机制和ＨＣ时胃肠功能改变和病理变化中起着重要作用。     

The Effect of Vasoactive Intestinal Polypeptide on Meal-Stimulated Gastric Acid Secretion in Man

The effect of vasoactive intestinal polypeptide (VIP) on meal-stimulated gastric acid secretion was studied in six healthy volunteers. Acid secretion was stimulated by instillation of a 10% solution of peptone, which was adjusted to pH 5.5, circulated through the stomach via a double-lumen gastric tube by a peristaltic pump. The acid secretion was estimated by continuous titration by a pH-stat. The subjects were studied twice on separate days, receiving an intravenous infusion of either VIP (1 μg/kg/h or saline. No effect on acid secretion was found. Mean serum gastrin concentration rose from 42 pmol/l to 150 pmol/l during meal stimulation and was unaffected by infusion of VIP. Plasma VIP concentration during infusion of saline was 6.8 pmol/l and during VIP infusion, 82.8 pmol/l. Plasma VIP concentration was unaffected by the peptone meal.     

Vasoactive Intestinal Peptide-Like Immunoreactive Nerve Fibers in the Pineal Gland of the Sheep

Vasoactive intestinal peptide (VIP)-like immunoreactive nerve fibers were demonstrated by peroxidase antiperoxidase (PAP) immunohistochemistry to be distributed throughout the entire pineal gland of the sheep. VIP-containing fibers were observed along the blood vessels, penetrating into the gland from the pial capsule and also in the capsule itself. Some fibers left the perivascular position and entered the pineal parenchyma, where they were located among pinealocytes. This suggested that the VIPergic fibers might influence both pinealocytes and blood vessels of the gland. The location of VIP-containing fibers in the capsule of the pineal gland indicates that the fibers originate from perikarya located in a peripheral ganglion.     

The Effect of Insulin-Induced Hypoglycemia with and without Atropine on Plasma Vasoactive Intestinal Polypeptide in Man

Plasma vasoactive intestinal polypeptide (VIP) was measured in six healthy male students on 2 separate days after insulin-induced hypoglycemia with and without atropine and on a 3rd day in five of the students after atropine alone. A significant increase in peripheral plasma VIP was observed when atropine was given together with insulin, whereas insulin or atropine alone had no effect on plasma VIP. It is suggested that cholinergic nicotinic receptors may be involved in the increase of VIP after insulin-induced hypoglycemia and that the lack of VIP increase seen after insulin alone may be caused by an inhibitory effect of other gastrointestinal hormones.     

Gastrointestinal transit and anorectal manometry in children with colonic substance P deficiency

BACKGROUND AND AIMS: Severe intractable constipation in children may be associated with a reduction of substance P (SP)- containing fibers in colonic circular muscle. The aim of this study was to characterize gastrointestinal transit (GIT), anorectal manometry (ARM) and electromyographic (EMG) changes in these children. METHODS: Seromuscular laparoscopic biopsies of the colon were obtained from 35 children with severe constipation. Immunofluorescent staining for SP and vasoactive intestinal peptide (VIP) were then performed on these specimens. The cohort of patients studied included a SP-deficient group (SPD, n = 25) who had reduced numbers of SP-immunoreactive nerve fibers. The other group consisted of patients with normal staining for both SP and VIP (SPN, n = 10). Gastrointestinal transit studies (gastric emptying, orocecal and colonic transit) suitable for analysis were available for 17 patients (SPD, n = 9 and SPN, n = 8). The colon was divided into segments and radioactivity counts in each segment were expressed as a percentage of the total colonic count at each time point (6, 24, 32 and 48 h). The geometric center (GC), ARM, EMG, clinical and demographic data characteristics of both groups of patients were compared. RESULTS: There were no differences in demographic data, gastric emptying, orocecal transit or geometric center of transit in the colon between the two patient groups. The ARM and EMG studies suggested that the SPN group have a higher mean threshold volume of balloon distension required to initiate a rectoanal inhibitory reflex, and a higher incidence of anismus; however, this did not reach statistical significance. CONCLUSIONS: These data suggest a trend that the SPN patients have a greater problem with obstructive defecation and abnormal rectal sensation than those with SPD. We were unable to confirm any defect in colonic transit in the SPD patients compared with the SPN group.     

反流性食管炎患者血浆血管活性肠肽、胃动素变化及其意义

测定反流性食管炎患者血浆血管活性肠肽、胃动素浓度,及下食管括约肌压力,以探讨反流性食管炎的发病机制。方法：采用液体灌注体外传感器法测定２８例反流性食管炎患者下食管括约肌压力。采用放射免疫法测定其血浆ＶＩＰ及胃动素浓度。     

Vagal Control of the Release of Somatostatin,Vasoactive Intestinal Polypeptide,Gastrin-Releasing Peptide,and HC1 from Porcine Non-Antral Stomach

We studied the secretion of somatostatin and HO and the release of vasoactive intestinal polypeptide (VIP) and gastrin-releasing peptide (GRP) from isolated, vascularly perfused, porcine non-antral stomach. Electric vagus stimulation increased acid secretion and the release of VIP and GRP and inhibited somatostatin secretion as determined in the venous effluent. Atropine abolished the HC1 response and reversed the somatostatin inhibition to a three-fold increase, whereas GRP and VIP responses were unchanged. Both intra-arterial carbachol (10′⁶M) and GRP (10′⁸M) increased acid secretion and inhibited somatostatin secretion. VIP (10^_8M) increased somatostatin secretion and had no effect on acid secretion. By immunohistochemistry, somatostatin was localized to both open-type and closed-type cells equally spread in the various parts of the gastric glands without particular relation to the parietal cells. Numerous GRP- and VIP-immunoreactive nerve fibers were seen between the glands. It is concluded that the fundic and antral secretion of somatostatin, investigated in a previous study, are differently regulated. The relation of fundic somatostatin release to acid secretion seems to be complex.     

Release of Vasoactive Intestinal Polypeptide (VIP) by Intraduodenal Stimuli

The effect of intraduodenal infusion of amino acids, glucose, fat, HCl, ethanol, or saline on plasma VIP concentration was investigated in 7 normal subjects, 5 post-vagotomy patients, and 12 anaesthetized pigs. Furthermore, the concentrations of VIP in plasma after ingestion of a mixed meal were measured in 6 normal subjects. In normal subjects the median peripheral concentration of VIP in the basal state was 4.3 pmol × 1-¹ (range 0-12.0). No significant changes occurred after amino acids, glucose, saline, or ingestion of a meal. In contrast infusion of HCl, fat, or ethanol resulted in a rise in plasma VIP concentration in all the subjects studied. The peak values (medians and ranges) after HCl, fat, or ethanol were 9.8 (5.9-12.6), 7.5 (2.4-10.2), and 12.6 (7.8-16.8) pmol × 1-¹, respectively. Truncal vagotomy did not change the response of HCl. The results from measurements in portal plasma of pigs confirmed the findings in peripheral plasma of normal subjects and showed that the levels of VIP in portal plasma are 1.6-2.9 times higher than the levels of VIP in arterial plasma. The pH threshold to release of VIP was pH 1.1-2.1, and the effect of HCl was not abolished by ganglionic blockade.