肝硬化患者血浆胆囊收缩素及胃动素对胃排空的影响

目的本研究旨在探讨肝硬化患者胃排空功能,并探讨其胃排空作用与空腹血浆胆囊收缩素、胃动素的关系,进而为预防和治疗肝硬化提供参考。方法 将30例肝硬化患者作为试验组,30例健康志愿者作为对照组,采用^13C-辛酸呼气试验法测定肝硬化患者以及对照组的胃固体半排空时间（GET1／2）,同时用放射免疫技术测定患者及对照组的空腹血浆胆囊收缩素（CCK）及胃动素（MTL）水平。结果与健康志愿者组相比,肝硬化患者组GET1／2明显延迟（P〈0．05）;空腹血浆CCIK及MTL水平明显升高,组间差异有统计学意义（P〈0．05）;患者GET1／2与空腹血浆CCK及MTL水平各自呈正相关。结论肝硬化患者胃排空延迟可能与血浆CCK及MTL水平的异常增高相关。推测肝硬化时血浆CCK及MTL水平均明显增高,由此引发胃排空延迟,最终导致营养不良,进而加重患者病情。     

糖尿病大鼠血浆和胃肠组织胃动素、胆囊收缩素和生长抑素含量的变化

糖尿病胃肠功能障碍的发病与胃肠激素紊乱密切相关，而糖尿病时的机体状态对胃肠道内分泌系统亦有显著影响。胃肠激素由胃肠道内分泌细胞产生，其中Mo细胞分泌的胃动素（motilin）可促进餐前胃排空，I细胞分泌的胆囊收缩素（cholecystokinin）可抑制餐后胃排空，D细胞分泌的生长抑素（somatostatin）对胃肠蠕动起抑制作用。但是，这3种对胃肠运动起主要作用的胃肠激素在糖尿病胃肠功能障碍发病中的相关性尚未见报道。本研究旨在探讨胃动素、胆囊收缩素和生长抑素在糖尿病胃肠功能障碍发病中的变化和相互关系。     

胆囊收缩素与功能性消化不良患者胃电活动及胃运动相关性的临床研究

胆囊收缩素 (ＣＣＫ)是一种具有广泛生物活性的脑肠肽 ,能引发胃电节律失常及胃运动功能障碍。我们旨在探讨功能性消化不良 (ＦＤ)患者血浆ＣＣＫ浓度与胃电活动及胃排空运动的相关性。一、资料与方法1.对象 :对照组 15例 ,男 12例 ,女 3例 ,年龄 2 3～ 5 8岁 ,平均 2 9岁 ,均无消化系统疾病及胃肠道症状 ,无腹部手术史。ＦＤ组 2 8例 ,男 2 3例 ,女 5例 ,年龄 2 5～ 5 4岁 ,平均 32岁。受试前 1周禁用影响消化道运动功能的药物。2 .方法 :①胃肌电活动测定 :用ＹＷＣ 4型胃肠电放大仪、30 6 6型多导生理记录仪进行空腹及试餐状态下 ,从肘静…     

NIDDM患者血清胃泌素、血浆胃动素及生长抑素的检测及其意义

ＮＩＤＤＭ患者血清胃泌素、血浆胃动素及生长抑素的检测及其意义朱瑞平，邓长生，夏冰，范幼筠，张颖大约５０％的糖尿病患者可出现早饱、恶心、呕吐及腹胀等胃肠功能紊乱症状［１，２］。近年来国外从胃肠激素方面对糖尿病性胃轻瘫进行了某些探讨，但尚未有准确结论。我...     

消化性溃疡患者血浆促胃液素及胃动素浓度和胃肌电节律的改变

[目的]观察胃溃疡(GU)、十二指肠球部溃疡(DU)患者胃肌电节律紊乱的发生率,及血浆促胃液素(GAS)、胃动素(MOT)在其中的临床意义。[方法]DU患者22例,GU15例,与慢性胃炎20例作对照组行餐前体表胃电图检查,并进行空腹血浆GAS、MOT检测。[结果]根据正常胃慢波百分比,DU组、GU组和对照组胃电节律异常者分别占45.5%、53.3%、20.0%,血浆GAS浓度分别为(73.84±32.25)、(80.45±27.18)及(44.94±27.56)ng/L,DU组和GU组均显著高于对照组(P<0.01),血浆MOT浓度分别为(423.47±315.92)、(610.85±331.66)(、201.19±156.23)ng/L,各组差异均有统计学意义(P<0.05)。[结论]消化性溃疡患者有胃肌电节律改变,可能由血浆GAS、MOT分泌异常所致。     

肝硬化患者血浆胃动素水平的动态观察

以放射免疫法检测35例肝硬化患者的血浆胃动素(MTL)水平。肝硬化组入院时血浆MTL水平显著高于对照组。待肝肾功能明显发转、腹水基本消退后,血浆MTL水平则较入院时显著降低。研究结果提示血浆MTL水平的动态变化可能与肝硬化的病理生理过程有密切关系。     

糖尿病大鼠胃肠功能障碍与胃动素、胆囊收缩素、生长激素相关性研究

Wistar雄性大鼠30只,体重180～220g,随机分为糖尿病模型(DM)组与正常对照(NC)组各15只.DM组不予降糖药控制血糖,12周时检测两组胃排空、小肠传输功能与血浆胃动素、胆囊收缩素、生长激素.DM组大鼠胃内残留率明显增多、小肠推进率下降及胃肠激素紊乱.由此推测糖尿病胃肠功能障碍与胃肠激素的紊乱密切相关.     

肝硬化病人血浆胃动素水平的变化及其临床意义

目的 探讨肝硬化病人空腹血浆胃动素水平的变化及其与肝功能损害的关系。方法 应用放免法检测肝炎肝硬化病人、慢性胆炎病人和正常人空腥血浆胃动素,并进行比较。结果 肝硬化病人平均空腥血浆胃动素水平的变化及异常率（〉３１２ｎｇ／ｍｌ为异常）均明显高于慢性肝炎和正常人,且ＣｈｉｌｄＣ级〉Ｂ级〉Ａ级。肝硬化进空腹血浆胃动素水平与血浆白蛋白呈负相关,与血清总胆红素呈正相关。结论 肝硬化病人空腹血浆胃动素水平明显     

胆石症患者胆囊对胆囊收缩素的敏感性

在胆固醇性胆结石的发病机制中,胆囊功能的改变可能具有重要性。胆固醇性胆结石患者,餐后胆囊排空增快,胆囊排空与胆囊收缩素(CCK)的释放有关。作者等曾报道胆石症病人餐后血清CCK浓度与对照组之间无明显差别。本文目的即针对上述情况,研究胆石症病人与正常人的胆囊对CCK的敏感性有无差异。所用方法为闪烁扫描法。研究对象为18例口服胆囊造影示胆囊内有透光结石和18例有消化不良症状而胆囊造影肯定正常的对照者。18对中13对是女性,5对是男性,结石组平均年龄53岁,对照组为54岁。应用~(99m)锝标记的N-(2,6-diethylphenyl-carbamoylmethyl) iminodiacetate(简称~(99m)Tc-HIDA)进行动态胆囊闪烁扫描术,以测定胆囊对胆囊收缩素的敏感性。患者空腹静脉注入10μCi~(99m)Tc-HIDA/kg体重,应用连接小型计算机的γ照相机,记录胆囊对放射核素的摄取。90分钟后,静脉滴注CCK,开始滴注率为0.005mu/kg/min(用等渗盐水稀释),以后逐渐递增至0.01、0.03及0.06mu/kg/min。每种滴注率持续12分钟后换滴盐水6分钟,再增加滴注率。资料贮存于磁盘,备以后分析。根据胆囊区的放射     

Plasma cholecystokinin and somatostatin levels in chronic pancreatitis patients

BACKGROUND/AIMS: The existence of a negative-feedback mechanism between pancreatic enzyme secretion and intraduodenal proteases and the role of cholecystokinin in its mediation in humans is debatable. The presence of such a feedback mechanism in chronic pancreatitis patients with exocrine enzyme deficiency possibly leads to an increase in cholecystokinin plasma levels. Somatostatin has been used in many studies in the therapy of pain in chronic pancreatitis and plays a role in the regulation of cholecystokinin levels, however data on its plasma levels are still lacking. METHODOLOGY: Basal and the postprandial cholecystokinin and somatostatin levels in 30 patients with chronic pancreatitis (11 with severe chronic pancreatitis and 19 with mild chronic pancreatitis) were measured 14 days after discontinuation of enzymatic substitution therapy and then were compared with the levels taken from 25 healthy subjects. RESULTS: The cholecystokinin postprandial plasma levels were significantly higher in patients with chronic pancreatitis when compared with those of healthy individuals (P < 0.01). Basal, somatostatin, cholecystokinin and postprandial somatostatin levels were not significantly higher than those in healthy subjects. There was no correlation between basal and postprandial levels of cholecystokinin and somatostatin in our study. CONCLUSIONS: The cholecystokinin postprandial plasma levels were significantly higher in all patients with chronic pancreatitis when compared with healthy individuals, which suggests the role of cholecystokinin in the feedback control of pancreatic secretion.     

Plasma betatrophin levels in patients with liver cirrhosis

AIM: To investigate the plasma levels of betatrophin in patients with cirrhosis.METHODS: Forty patients diagnosed at the clinic with liver cirrhosis according to biological, ultrasonographic,or histological criteria were included.The severity of cirrhosis was classified according to Pugh's modification of Child's classification and MELD score. Insulin resistance(IR) was assessed by the Homeostasis Model Assessment. A total of 20 patients showed a MELD score higher than 14. The control group consisted in 15 sex-and aged-matched subjects.Fasting blood samples were obtained for subsequent analysis. Serum insulin was determined by Liaison automated immune chemiluminiscence assay(DiaSorin S.p.A.) using a sandwich assay. The sensitivity of the assay was 0.2 μU/mL. The intra and interassay variation coefficients were 4% and 10%,respectively. The normal values were between 2 and17 μU/mL. Human active betatrophin was analyzed by specific quantitative sandwich ELISA(Aviscera Bioscience). The sensitivity of the assay was 0.4 ng/mL, and the intra and interassay reproducibility were 6% and 10%, respectively.RESULTS: Plasma betatrophin levels were significantly increased in patients with cirrhosis compared with those in healthy subjects(P = 0.0001). Betatrophin levels were also associated with disease severity, being higher in Child-Pugh C patients compared to Child-Pugh B(P 0.0005) and in patients who displayed a MELD score higher than 14 points compared to patients with lower punctuation(P = 0.01). In addition, we found a positive correlation between plasma betatrophin levels and the severity of cirrhosis according to Child-Pugh classification(r = 0.53; P 0.01) or MELD score(r = 0.45; P 0.01). In the overall cohort, a moderate correlation between serum betatrophin and plasmatic bilirrubin(r= 0.39; P 0.01) has been observed, as well as an inverse correlation between betatrophin and albumin(r =-0.41; P 0.01) or prothrombin time(r =-0.44;P 0.01). Moreover, insulin resistance was observed in82.5% of the cirrhotic patients. In this group of patients,betatrophin levels were significantly higher than those in the group of patients without IR(P 0.05).CONCLUSION: Plasma betatrophin is increased in patients with cirrhosis. This increase is related to the severity of cirrhosis, as well as with the emergence of insulin resistance.     

Plasma and platelet serotonin levels in patients with liver cirrhosis

AIM： To analyze the relationship between plasma and platelet serotonin levels and the degree of liver insufficiency. METHODS： The prospective study included 30 patients with liver cirrhosis and 30 healthy controls. The degree of liver failure was assessed according to the Child-Pugh classification. Platelet and platelet poor plasma serotonin levels were determined. RESULTS： The mean plasma serotonin level was higher in liver cirrhosis patients than in healthy subjects （215.0 ±26.1 vs 63.1 ± 18.1 nmol/L; P 〈 0.0001）. The mean platelet serotonin content was not significantly different in patients with liver cirrhosis compared with healthy individuals （4.8 ± 0.6; 4.2± 0.3 nmol/platelet; P 〉 0.05）. Plasma serotonin levels were significantly higher in ChildPugh grade A/B than in grade C patients （246.8 ± 35.0 vs 132.3 ± 30.7 nmol/L; P 〈 0.05）. However, platelet serotonin content was not significantly different between Child-Pugh grade C and grade A/B （4.6 ± 0.7 vs 5.2 ± 0.8 nmol/platelet; P 〉 0.05）. CONCLUSION： Plasma serotonin levels are significantly higher in patients with cirrhosis than in the controls and represent the degree of liver insufficiency. In addition, platelet poor plasma serotonin estimation is a better marker for liver insufficiency than platelet serotonin content.     

Evidence of somatostatin as a humoral modulator of motilin release in man. A study of plasma motilin and somatostatin during intravenous infusion of somatostatin, secretin, cholecystokinin, and gastric inhibitory polypeptide

In six healthy persons receiving graded intravenous infusions of synthetic somatostatin the plasma motilin concentrations decreased significantly (p less than 0.05) already with doses giving physiological plasma somatostatin levels, and a rebound of plasma motilin was observed after cessation of infusion of pharmacological somatostatin doses. After an intravenous secretin infusion (280 pmol/kg-h) producing pharmacological plasma secretin concentrations, a comparable plasma somatostatin increase was observed together with a substantial decrease in plasma motilin (p less than 0.05). Infusion of cholecystokinin in a pharmacological dose and of gastric inhibitory polypeptide (GIP) in doses giving plasma GIP levels in the physiological range had no effect on plasma somatostatin or motilin. Circulating plasma somatostatin may be a physiological modulator of the motilin release, and the plasma motilin fall seen during infusion of pharmacological doses of secretin may possibly be explained by the secretin-induced somatostatin release occurring simultaneously.     

Plasma cholecystokinin levels in patients with chronic pancreatitis

Using a sensitive and specific radioimmunoassay for cholecystokinin (CCK) we have measured plasma CCK levels in patients with and without chronic pancreatitis. All patients suffered from steatorrhea. The basal plasma values in patients with chronic pancreatitis (n = 10) were significantly higher compared with a control group of 40 normal subjects. After ingestion of a test meal peak plasma levels of CCK were significantly higher than in controls, but the integrated CCK release did not differ from the normal subjects. The findings indicate a close relationship between plasma CCK concentration and exocrine pancreatic function.     

Plasma human atrial natriuretic peptide levels in patients with liver cirrhosis

Plasma levels of human atrial natriuretic peptide (hANP) were investigated in patients with liver cirrhosis, and the relationships between plasma hANP levels and the following factors were studied: presence of ascites, serum and urine electrolytes, plasma renin activity, angiotensin I and II, aldosterone, catecholamines, prostaglandin derivatives, conventional liver function tests and circulating blood volume. Plasma hANP level was significantly (P less than 0.05) elevated in patients with ascites (mean = 58.6 pg/mL, s.e.m. = 8.8) compared with cases without ascites (mean = 36.6 pg/mL, s.e.m. = 2.6). With the disappearance of ascites, the level fell to normal in most cases. Urine sodium excretion was positively correlated with plasma hANP in patients without ascites, but not in patients with ascites. The plasma hANP level was disproportionately high for the rate of urinary Na excretion in cirrhotics with ascites. The plasma hANP level was not correlated with any of the other factors such as blood volume, renin-angiotensin-aldosterone levels, catecholamines and liver function tests. These results suggest that plasma hANP levels are elevated in cirrhotic patients especially with ascites, but the natriuretic response of the kidney to this raised hANP level can be impaired in patients with liver cirrhosis and ascites.     

老年非溃疡性消化不良患者血清胃泌素、血浆胃动素及生长抑素的检测及其意义

本文采用放射免疫法对３１例老年非溃疡性消化不良（ＮＵＤ）患者和２０例对照者在空腹状态下进行了血清胃泌素、血浆胃动素及生长抑素的测定。结果显示：老年人ＮＵＤ组胃泌素浓度为８５．７２±２２．０３ｐｇ／ｍｌ，较对照组的９０．４２±１５．０６ｐｇ／ｍｌ，差异无显著性（Ｐ＞０．０５）；胃动素浓度为４２７．７４±９５．８５ｐｇ／ｍｌ，较对照组的５４５．７３±１１５．８０ｐｇ／ｍｌ，差异有显著性（Ｐ＜０．０５）；生长抑素浓度为６９．４７±１８．７５ｐｇ／ｍｌ，较对照组的５４．７６±１３．３２ｐｇ／ｍｌ，差异有显著性（Ｐ＜０．０５）。提示胃动素，生长抑素在老年人ＮＵＤ发病机理中起一定作用，而胃泌素则无明显作用。     

不同肝功能分级肝硬化患者血小板参数、胃电参数及胃肠激素水平比较

目的比较不同肝功能分级肝硬化患者血小板参数、胃电参数及胃肠激素水平。方法选取2012年2月-2013年1月于岑溪市人民医院进行诊治的48例肝硬化患者作为观察组,同时期体检的48名健康人员作为对照组,将两组人员的血小板参数、胃电参数及胃肠激素水平进行比较,并对观察组中不同Child-Pugh分级者的上述指标进行比较。结果观察组的PLT和PCT均低于对照组,PDW、MPV及P-LCR均高于对照组,餐前及餐后的胃电幅值、胃电频率和正常慢波节律比均低于对照组,餐前及餐后的血清GAS、VIP、MTL均高于对照组,并且Child-Pugh分级高者波动大于分级低者,差异有统计学意义(P均0.05)。结论肝硬化患者血小板参数、胃电参数及胃肠激素存在明显的异常波动,且Child-Pugh分级越高者波动越大。