食管癌木后并发乳糜胸的护理干预

目的：探讨29例食管癌根治术后患者并发乳糜胸的护理方法。方法：给予29例患者生长抑素治疗，同时加强对胸腔引流液的观察，做好呼吸道管理、营养支持、饮食宣教等一系列护理干预措施。结果：除2例经生长抑素治疗无效、行再次开胸结扎胸导管治愈外，其他27例患者应用生长抑素保守治疗均治愈，治愈时间8～21天。结论：应用生长抑素保守治疗食管癌根治术后并发乳糜胸患者，同时配合一系列精心的护理干预措施可以提高乳糜胸的治疗效果。     

Effect of Somatostatin on Pentagastrin-Stimulated Gastric Acid Secretion and Gastric Antral Motility in Dogs with Gastric Fistula

The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and gastric antral motility in conscious dogs with gastric fistula. Infusion of pentagastrin induced motility with a digestive pattern. Somatostatin inhibited dose-dependently the stimulated acid secretion, whereas the effect on antral motility was more complex, acting especially on the amplitude of the contractions. The effects of somatostatin were not altered by using α-and β-adrenergic, dopaminergic, and serotonergic blocking drugs. The dose-response kinetics with seven doses of pentagastrin with and without somatostatin showed inhibition of a competitive type for gastric acid secretion and of a non-competitive type for antral motility with regard to amplitude.     

The protective effects of calcitonin gene-related peptide on gastric mucosa injury of gastric ischemia reperfusion in rats

Gastric mucosa is one of the most vulnerable tissues in human and animal. However, little is known about the effects of calcitonin gene-related peptide (CGRP) on gastric mucosa injuries induced by gastric ischemia reperfusion. The purpose of the present study was to investigate the protective effects and mechanism of CGRP on gastric mucosa injury after gastric ischemia reperfusion in rats. Thirty-six healthy Wistar rats were randomly divided into CGRP-treated, sham-operated, and control groups. Twelve rats were involved in each group. These groups were further divided into 24-h and 48-h subgroups. Gastric ischemia reperfusion injury (GI-RI) rat model was established by a 30-min celiac artery occlusion by an artery clamp, followed by 24?h or 48?h of reperfusion. CGRP (1?μg/ml) at the dose of 3?μg/kg was given intraperiloneally (IP) at the beginning of reperfusion for rats in CGRP-treated group. Saline as vehicle (3?ml/kg body weight), IP, was administered at the beginning of reperfusion for rats in control group. Sham-operated animals were subjected to an operation without GI-RI. Twenty-four hours or 48?h after operation, the samples were taken out and processed for calculating stomach mucous membrane damage index according to Guth method, detecting pathological changes of gastric mucosa tissue by light microscopy and observing the expression of gastrin (Gas) and somatostatin (SST) by immunohistochemical staining. The results showed the following: (i) gastric mucosa with diffuse edema, splinter hemorrhage and erosion, numerous endothelial cells necrosis, mucosa dissociation, and infiltration of inflammatory cells were observed in both control and CGRP-treated animals, especially in the earlier period (24?h) and then gradually healing. CGRP administration could reduce the damage of gastric mucosa. The injury index of gastric mucosa was lower in CGRP-treated group as compared with that in control group (P?<?0.01). (ii) Gas expression in gastric antrum mucosa was lower in CGRP-treated group than that in control group (P?<?0.01). SST expression in gastric antrum mucosa was higher in CGRP-treated group than that in control group (P?<?0.01). It is concluded that CGRP regulated the secretion of Gas and SST and thus alleviated the damage of gastric mucosa induced by ischemia and reperfusion. CGRP might be a potential candidate for clinical therapy on modulating gastric mucosal protection and maintaining gastric mucosal integrity after ischemia and reperfusion of the stomach.     

Effect of glucagon antibodies on plasma glucose,insulin and somatostatin in the fasting and fed rat

Summary A potent high-titre glucagon antibody pool was used to induce a state of acute glucagon deficiency in order to investigate the importance of glucagon in maintaining euglycaemia in the fed and fasted anaesthetised rat. Binding characteristics of the antiserum and evidence of its neutralisation of the biological effects of exogenous glucagon are described. The amount of antibody administered was capable of neutralising up to 12 times the total content of glucagon (approximately 1nmol) in the rat pancreas. The hyperglycaemic response to 1.43 nmol exogenous glucagon was significantly inhibited in the rat by glucagon antibodies given intravenously or intraperitoneally (p < 0.001). However, no changes in plasma glucose occurred in rats fasted 16 h (4.35±0.1 mmol/l or 24 h (4.0±0.05 mmol/l) after antibody administration. The same dose of glucagon antibodies produced no change in plasma glucose (6.1±0.2 mmol/l), immunoreactive insulin (1.85±0.05 g/l) or immunoreactive somatostatin (110±30 ng/l) in rats after antibody administration. Antibody excess, equivalent to a binding capacity for glucagon of 40 nmol/l in the plasma of recipient animals, was demonstrable at all times after passive immunisation. The absence of any affect on glucose concentrations following immunoneutralisation of glucagon suggests that glucagon secretion may not be a major factor in the maintenance of euglycaemia in the rat.     

Altered Gastrin Regulation in Mice Infected with Helicobacter felis

Altered gastrin expression associated with Helicobacter pylori infection may contribute to the pathogenesis of peptic ulcer disease or gastric cancer in man, but gastrin has not been investigated in a murine model of Helicobacter infection. C57BL/6 mice were inoculated with Helicobacter felis and examined after 4–21 weeks for G and D cell numbers, antral gastrin and somatostatin mRNA, and luminal pH. In H. felis-infected mice, gastrin mRNA declined at four and six weeks after infection to 57% and 23%, respectively, of uninfected control values. Concurrently, somatostatin mRNA showed no change at four weeks and a modest 25% decrease at six weeks after infection. Similar reductions were noted in G and D cell numbers, resulting in a decrease in the G/D cell ratio after mice were infected with H. felis. Infected animals also showed a loss of parietal and chief cells, and an increased gastric pH. H. felis infection in C57BL/6 mice leads to an early suppression of G cell number and gastrin mRNA. These changes precede an alteration in somatostatin cell number and mRNA and, coupled with reductions in parietal and chief cells, may contribute both to severe impairment of gastric acid output and the potential for carcinogenic processes.     

Lanreotide-conjugated PEG-DSPE micelles: an efficient nanocarrier targeting to somatostatin receptor positive tumors

Lanreotide is an octapeptide analog of endogenous somatostatin, specifically binding with tumors over-express somatostatin receptor 2 (SSTR2). In this study, we conjugated lanreotide to 1, 2-distearoyl-sn-glycero-3-phosphoethanolamine-N-[methoxy (poly-(ethylene glycol))-2000] (PEG-DSPE), constructed active targeted micelles (lanreotide-PM), characterized their in vitro and in vivo targeting effect, and explored the receptor mediated transportion. The uptake of lanreotide-PM was found to be related to the expression level of SSTR2 in different cell lines and the competitive inhibition phenomenon indicated that the cellular uptake of lanreotide-PM was via a receptor meditated mechanism. In vivo, more lanreotide-PM accumulated in SSTR2 high expression tumor xenografts, endocytosed by the tumor cells, induced more apoptosis of tumor cells, and suppressed tumor growth efficiently. In conclusion, lanreotide–modified micelles containing antitumor drugs provide a promising strategy for the treatment of SSTR-expressing tumors.     

Helicobacter pylori and gut hormones

Helicobacter pylori infection has been found to decrease the expression of antral somatostatin and to increase the release of the acid-stimulating hormone gastrin. The reversal of these changes in gut hormones by the eradication of H. pylori, and in-vivo and in-vitro studies in animals either infected with H. pylori or exposed to H. pylori-related materials may support the somatostatin-gastrin link theory in the pathophysiology of H. pylori infection. The following mechanisms have been proposed to explain the H. pylori infection-associated changes in gut hormones; (1) ammonia produced by H. pylori and monochloramine, (2) effect on somatostatin receptor subtype-2, (3) action of lipopolysaccharide from H. pylori on somatostatin receptor, (4) inflammatory cells and mediators, and (5) bacterial strain diversity. H. pylori infection can alter gastric acid secretion in both directions. The elevated acid secretion in patients with duodenal ulcer is decreased by H. pylori eradication, and is accompanied by the normalization of gut hormones in patients whose H. pylori-induced gastritis is limited to the antrum with hyperacidity. Corpus gastritis and the subsequent development of mucosal atrophy induced by H. pylori result in decreased acid secretion, although the mechanism underlying H. pylori-induced atrophy in some subjects remains unclear. Hypoacidity enhances corpus atrophy and increases gastrin secretion, mediated via a physiological suppression of somatostatin release, features that are also observed in H. pylori infection. Therefore, the capacity of acid secretion and distribution of gastritis or atrophy should be taken into consideration when we discuss the affect of H. pylori on gut hormones. Received: October 1, 2001 / Accepted: November 30, 2001     

Effect of <Emphasis Type="Italic">gsp</Emphasis> oncogene on somatostatin receptor subtype 1 and 2 mRNA levels in GHRH-responsive GH3 cells

Growth hormone releasing hormone (GHRH) signals via G protein-coupled receptors (GHRH-R) to enhance intracellular Gαs/adenylyl cyclase/cAMP signaling, which in turn has positive effects on GH synthesis and release, as well as proliferation of the GH-producing cells of the anterior pituitary gland. Some GH-producing pituitary tumors express a constitutively active mutant form of Gαs (gsp oncogene). It has been reported that these tumors are more responsive to octreotide therapy. In this study we used a rat GH-producing cell line (GH3) stably transfected with the human GHRH-R cDNA (GH3-GHRHR cells) as a model to study the effects of gsp oncogene on somatostatin (SRIH) receptor subtype 1 and 2 (sst1 and sst2) mRNA levels. Transient transfection of gsp oncogene in GH3-GHRHR cells for 48 h increased intracellular cAMP levels and GH release. Phosphodiesterase (PDE) 4, sst1 and sst2 mRNA levels were increased by G protein mutation as assessed by real-time RT-PCR. Increased PDE mRNA levels in gsp-transfected cells may be a compensatory mechanism to the constitutive activation of cAMP-dependent pathway by G protein mutation and is consistent with reports of higher PDE expression in human pituitary tumor that express gsp. Our data suggest that higher expression of sst1 and sst2 mRNA induced by the gsp oncogene may be a mechanism by which gsp-positive tumors show a greater response to SRIH. GH3 cells permanently transfected with GHRH-R can be used for in vitro studies of actions of GHRH.     

健脾通腑方序贯联合生长抑素治疗急性胰腺炎对TREM-1水平和胰腺功能的影响分析

【】目的 分析健脾通腑方序贯联合生长抑素治疗急性胰腺炎对髓样细胞触发受体-1(TREM-1)水平和胰腺功能的影响。方法 回顾性选取2015年12月至2018年1月我院收治的急性胰腺炎患者106例,根据治疗方法不同分为对照组和观察组。对照组患者采用常规治疗联合生长抑素治疗,观察组患者加用健脾通腑方序贯治疗,分析两组患者治疗后的临床效果。结果 治疗前,两组患者中医症状积分水平比较,差异无统计学意义(P>0.05)。治疗后,观察组患者中医症状积分水平低于对照组,差异有统计学意义(P<0.05)。治疗前,两组患者TREM-1、内皮素(ET)、C反应蛋白(CRP)、胰腺功能指标水平比较,差异无统计学意义(P>0.05)。治疗后,观察组患者正铜蓝蛋白(CP)、胰岛素(INS)水平高于对照组,TREM-1、ET、CRP、胰蛋白酶原-2(TPS-2)、脂肪酶(LIP)水平低于对照组,差异有统计学意义(P<0.05)。观察组患者中转手术率低于对照组,血淀粉酶恢复时间、腹痛缓解时间及住院时间短于对照组,差异有统计学意义(P<0.05)。结论 健脾通腑方序贯联合生长抑素治疗急性胰腺炎可降低患者TREM-1、ET、CRP水平,改善患者胰腺功能,缩短住院时间。