新生儿胎粪中肠三叶因子的意义探讨

目的探讨新生儿胎粪中肠三叶因子（ITF）的影响因素。方法收集我院出生新生儿的胎粪和血清标本,根据胎龄和Apgar评分将研究对象分为正常足月对照组、早产儿组和窒息组。采用高效液相色谱法测定胎粪中ITF的含量,采用ELISA法测定血清中胃动素（MOT）、胃泌素（GAS）和生长抑素（SS）。结果①胎粪中ITF的含量与胎龄的相关系数r为0.526,P为0.002。②早产儿组和窒息儿组胎粪中ITF含量均明显低于对照组,差别有统计学意义。③胎粪中ITF含量与血清中MOT、GAS及SS浓度的相关系数分别为-0.692,-0.361,0.213,P值分别为0.042,0.150,0.251。④对照组胎粪中ITF含量男性为（3.793±0.381）ng/g,女性为（4.108±0.429）ng/g,差异无统计学意义（P=0.129）。⑤所有研究对象中无1例坏死性小肠结肠炎（NEC）发生,但早产儿组有4例发生明显的喂养不耐受;窒息组有2例出现轻微的喂养不耐受。结论早产、窒息儿粪便中的ITF含量低于正常足月儿,推测肠道ITF分泌不足可能是导致早产儿和窒息儿容易发生肠道粘膜损害的原因之一。但进一步的系统研究非常必要。     

静脉营养治疗24例极低体重儿成功报告

极低体重儿 (ＶＬＢＷＩ)生后喂养困难 ,长期不能摄入足够营养 ,易发生各种并发症 ,死亡率高。我科新生儿重病监护病房自 1994年对ＶＬＢＷＩ进行全静脉营养 (ＴＰＮ)部分静脉营养 (ＰＰＮ)治疗 ,成活 2 4例 ,现总结如下。临床资料1.一般资料 :男 13例 ,女 11例。日龄 30分钟 - 13小时。胎龄 2 9- 37周 ,平均 33.2周。体重 10 0 0 - 15 0 0ｇ ,适于胎龄儿 10例 ,。小于胎龄儿 14例、住院天数 18- 6 2天 ,平均 2 9天。2 .出生情况及相关因素 :3胞胎 1例 ,双胞胎 3例 ,母亲重度妊高征及产时窒息各 7例 ,羊水吸入 8例 ,入院时体温<35℃ 17例。3…     

小于胎龄儿胎盘11β-HSD2及脐血皮质醇的研究

目的检测小于胎龄儿(SGA)的胎盘11-β羟基类固醇脱氢酶2型及脐血皮质醇水平,初步探讨足月小于胎龄儿的发生机制。方法足月SGA新生儿20例(其中母亲正常妊娠的SGA新生儿10例为SGA1组,母亲有妊高症、或羊水少、或胆汁淤积症妊娠的SGA新生儿10例为SGA2组),正常妊娠的足月AGA新生儿10例为对照组。采用RT-PCR法检测人胎盘组织11β-HSD2基因mRNA的表达水平,采用化学发光法检测脐血皮质醇浓度。结果 1)胎盘11β-HSD2mRNA的表达水平与新生儿出生体重具有显著正相关(r=0.554,P<0.01);2)SGA组11β-HSD2 mRNA表达水平显著低于对照组(0.054±0.016 vs 0.082±0.026);SGA1组与SGA2组胎盘11β-HSD2 mRNA表达水平无差异;3)SGA组脐血皮质醇含量显著低于对照组(169.05±83.77nmol/l vs 327.90±179.19)nmol/l,P<0.05;SGA1组与SGA2组脐血皮质醇含量有差异。结论足月小样儿的发生与胎盘11β-HSD2活性下降有关,足月小样儿妊娠晚期脐血皮质醇浓度较适于胎龄儿低,与胎盘11β-HSD2的活性无关,可能主要与小于胎龄儿的HPA轴未成熟有关。     

窒息新生儿缺氧缺血性心肌损害Q-T离散度与血清CK-MB的早期变化及意义

目的探讨窒息新生儿缺氧缺血性心肌损害(HIM)患儿早期Q-T离散度(Q-Td)和血清肌酸激酶同工酶B(CK-MB)的变化,为临床提供早期诊断和治疗依据.方法对66例HIM患儿发病24h内、72h内和治疗7d后的Q-Td和CK-MB值进行检测,并与30例无窒息新生儿对照比较.结果 HIM组与对照组比较:HIM组发病24h内Q-Td与CK-MB即明显升高,72h内达到高峰(P<0.01).经7d治疗后,HIM患儿Q-Td与CK-MB均显著下降,但足月小于胎龄儿(SGA)HIM组下降欠理想,且足月小于胎龄儿HIM组并发症多,多数有循环不良表现,预后差(P<0.05).结论 Q-Td与CK-MB相结合作为HIM的早期特异性敏感指标,对早期诊断及治疗HIM有益.     

新生儿血清瘦素水平变化与IGF-Ⅰ、生长激素等相关因素的分析

目的探讨新生儿血清瘦素来源及其与胰岛素样生长因子-Ⅰ(IGF-I)和生长激素的关系.方法采用放射免疫法检测80例新生儿静脉血和脐血瘦素水平,根据不同胎龄新生儿出生体重值分为大于胎龄儿组28例,适于胎龄儿组36例,小于胎龄儿组16例;采用Rohrer's指数=出生体重(g)×10/身长(cm)3估测新生儿营养状态.结果早产儿血清瘦素水平明显低于足月儿(0.66±1.03ng/ml vs 3.59±2.16ng/ml,P＜0.01=;适于胎龄儿血清瘦素水平(3.06±0.96ng/ml明显低于大于胎龄儿(4.03±2.22ng/ml),而高于小于胎龄儿(1.13±1.98ng/ml);足月新生儿血清瘦素水平与Rohrer's指数、新生儿体重、胎龄、血清IGF-Ⅰ、生长激素水平呈显著正相关.结论新生儿体内瘦素主要来源于自身脂肪组织,它反映新生儿的生长营养状态,推测瘦素可能通过IGF-Ⅰ、生长激素共同调节新生儿的生长发育,在胎儿和新生儿生长发育中起重要作用.     

新生儿血清瘦素水平变化与IGF—I、生长激素等相关因素的分析

目的　探讨新生儿血清瘦素来源及其与胰岛素样生长因子 -I(IGF -I)和生长激素的关系。方法　采用放射免疫法检测 80例新生儿静脉血和脐血瘦素水平 ,根据不同胎龄新生儿出生体重值分为大于胎龄儿组 2 8例 ,适于胎龄儿组 36例 ,小于胎龄儿组 16例 ;采用Rohrer’s指数 =出生体重 (g)× 10 /身长 (cm) 3 估测新生儿营养状态。结果　早产儿血清瘦素水平明显低于足月儿 (0 .6 6± 1.0 3ng/mlvs 3.5 9± 2 .16ng/ml,P <0 .0 1=;适于胎龄儿血清瘦素水平 (3.0 6± 0 .96ng/ml明显低于大于胎龄儿 (4.0 3± 2 .2 2ng/ml) ,而高于小于胎龄儿 (1.13± 1.98ng/ml) ;足月新生儿血清瘦素水平与Rohrer’s指数、新生儿体重、胎龄、血清IGF -I、生长激素水平呈显著正相关。结论　新生儿体内瘦素主要来源于自身脂肪组织 ,它反映新生儿的生长营养状态 ,推测瘦素可能通过IGF -I、生长激素共同调节新生儿的生长发育 ,在胎儿和新生儿生长发育中起重要作用     

益生菌联合小剂量红霉素治疗极低出生体重儿喂养不耐受疗效分析

目的：探讨益生菌联合小剂量红霉素治疗极低出生体重儿喂养不耐受的临床疗效。方法将40例胎龄28~36w喂养不耐受的极低出生体重儿,随机分为两组,对照组20例在常规治疗的同时给予小剂量红霉素治疗,治疗组20例在对照组治疗的基础上加用益生菌,记录每次胃残余量、喂奶量、临床症状及消失时间,达全胃肠喂养时间,出院时间。每日记录体重,计算体重增长速度,并观察其体重恢复至出生体重时间。结果治疗组患儿腹胀消失时间、恢复出生体重时间、达全胃肠营养及出院时间与对照组比较,差异均有统计学意义(<0.05);治疗组平均增加体重量与对照组比较有统计学意义(<0.05)。结论口服小剂量红霉素联合益生菌治疗极低出生体重儿喂养不耐受明显优于单纯给予小剂量红霉素组,益生菌可明显提高极低出生体重儿喂养耐受性,增加耐受奶量,且安全有效,值得临床推广应用。     

早期足量静脉营养对极低出生体重儿宫外生长和酸碱平衡的影响研究

目的探讨早期足量静脉营养对极低出生体重儿宫外生长及酸碱平衡状态的影响。方法 2010年1月～10月在我院新生儿重症病房住院的存活极低出生体重儿160例,按入院先后顺序将患儿随机分为两组:治疗组80例和对照组80例,治疗组即早期足量静脉营养组,对照组即传统静脉营养组,两组其他治疗均相同,均按需给予电解质、维生素和微量元素,均尽早经口或间断经胃管微量肠道喂养,不能经口喂养者给予非营养性吸吮,肠道内营养热卡达90～100 kCal/(kg.d)时停静脉营养,每天计算热卡,称体重,每天监测多次微量血糖,计算体重下降幅度及恢复出生时体重的平均时间,计算经胃肠达到摄入标准的平均时间,两组患儿出院时EUGR的发生率。各组患儿均于治疗第1d、第4d及第7d留取桡动脉血60μl进行血气分析,记录pH、BE、氧分压、二氧化碳分压、碳酸氢根离子等指标变化。结果治疗组与对照组比较,治疗组极低出生体重儿平均住院时间和生理性体重下降持续时间缩短(P<0.05),体重下降幅度低(P<0.01),每天体重增长快于对照组(P<0.01),过渡到全肠道营养的时间缩短(P<0.01),节约住院费用(P<0.01)。治疗组生后第3天热卡明显高于对照组(P<0.05),出院时EUGR的发生率38.8%低于对照组72.5%(P<0.05)。在治疗的第4d,治疗组的pH值、HCO3-浓度和负离子间隙(BE)均降低(P<0.05),容易发生代谢性酸中毒,体重越低,越容易发生酸碱平衡紊乱(P<0.05)。结论早期足量静脉营养可促进极低出生体重儿的宫外生长,减少极低出生体重儿EUGR的发生率。早期足量静脉营养能够引起代谢性酸中毒发生,早产儿酸碱平衡紊乱主要发生在治疗第四天。早期足量静脉营养可缩短极低出生体重儿的住院时间,每个患儿可节约4000～5000元开支。     

早期微量喂养联合静脉营养治疗极低出生体重儿35例

极低出生体重儿(VLBW),常出现喂养困难、喂养不耐受使营养物质缺乏,导致宫外发育迟缓、营养不良性贫血,甚至出现各种并发症、酸碱失衡、电解质紊乱而危及生命,病死率较高。我科采用早期微量喂养(MEN)联合静脉营养(PN)治疗极低出生体重儿35例取得满意效果,报告如下。资料与方法1.一般资料2005年2月~2006年2月我院出生并收治的极低出生体重儿35例,其中男28例,女7例,胎龄(29~34)周,出生体重900~1000g 2例,1000~1200g 14例,1200~1500g 19例,平均体重(1230±210)g。2.方法无重度窒息及感染史者于生后12h开始微量喂养,24h后开始静脉营养治疗。…     

健康小儿胃肠内分泌功能的研究

目的探讨健康小儿胃肠内分泌功能。方法采用放射免疫分析法测定空腹和摄入液体实验餐后60m in时外周血胃泌素(Gas)、胃动素(MTL)、生长抑素(SS)水平。结果健康小儿餐后与餐前比较,Gas及MTL无明显差异(P>0.05),SS水平则明显升高(P<0.01)。结论Gas、MTL和SS水平的变化反应了健康小儿胃肠激素餐后分泌前整个过程。     

Postnatal development of intestinal endocrine cell populations in the water buffalo

The frequency and distribution of 11 endocrine cell populations were studied in the intestine of differently aged buffalo, grouped on the basis of diet: 2-d-olds (suckling), 5-mo-olds (weaning) and 5-y-olds (ruminant adult diet). The endocrine cell populations were identified immunocytochemically using antisera against 5-hydroxytryptamine (5-HT), somatostatin, gastrin, cholecystokinin (CCK), COOH-terminal octapeptide of gastrin/CCK, neurotensin, motilin, gastric inhibitory polypeptide (GIP), secretin, glucagon/glicentin (GLU/GLI) and polypeptide YY (PYY). In adult buffalos the regional distribution of endocrine cells is similar to that of other adult ruminants. During postnatal development, these cell types showed the following changes in their frequency and distribution: (1) 5-HT, neurotensin and gastrin/CCK immunoreactive cells (i.c.) showed a decrease in frequency with age; (2) somatostatin i.c. frequency remained stable with age; (3) motilin, GIP, secretin and CCK i.c. showed a slight increase in frequency with age; (4) GLU/GLI and PYY i.c. decreased in frequency with age in the small intestine, caecum and proximal colon and an increase in frequency in the rectum. It was hypothesised that the endocrine cell types, whose presence and localisation is substantially stable in all examined ages, probably contain substances that are strictly necessary for intestinal function. In contrast the hormones contained in the cell populations that decreased with age, are probably involved in physiological needs during the milk and weaning diet or play a role in intestinal growth.     

Influence of suckling and feeding on insulin, gastrin, somatostatin and VIP levels in peripheral venous blood of lactating sows

Blood samples were collected in peripheral venous blood of seven lactating sows, when their piglets were suckling. In four of the experiments samples were also taken when the sows were fed a meal. Gastrin, insulin, somatostatin and VIP levels were measured by radioimmunoassay. Insulin levels increased by approximately 100% for about 10 min in response to suckling, in some experiments even before the suckling occurred, i.e. when the sows saw, heard and smelled their piglets. In four of the sows suckling caused a biphasic twofold increase in gastrin levels - one immediate peak which lasted for a few min and a second peak of longer duration (about 30-60 min), whereas gastrin levels remained unchanged in three animals. Somatostatin levels usually reflected gastrin levels in a reciprocal way. Thus, a biphasic decrease of somatostatin levels occurred in the high gastrin responders. In contrast, somatostatin levels increased in the experiments, in which gastrin levels did not change. Immediate and short-lasting (a few minutes long) increases of VIP levels were also induced by suckling. Large litters and long suckling periods appeared to be related to greater changes of the levels of all the peptides measured. Feeding influenced insulin, gastrin and somatostatin levels in the same way as did suckling from both a qualitative and a quantitative point of view. In contrast, VIP levels were not increased by feeding. The possible functional effects of the suckling-induced release of gastrointestinal hormones and possible mechanisms of their release are discussed.     

Plasma levels of somatostatin following a test meal in dogs. Initial atropine resistant vagally mediated decrease of somatostatin levels and increase of gastrin and insulin levels

Plasma levels of somatostatin like immunoreactivity (SLI), below referred to as somatostatin levels, were measured in peripheral plasma of conscious dogs. Basal somatostatin levels averaged 49 +/- 10 pM. Somatostatin as well as gastrin and insulin plasma levels were measured before and after feeding with and without prior atropinization. During the first 10 min after feeding somatostatin levels fell from 49 +/- 10 to 23 +/- 9 pM, whereas gastrin and insulin levels rose from 9 +/- 2 and 140 +/- 14 pM to 48 +/- 11 and 370 +/- 91 pM respectively. Atropine 0.01 or 0.1 mg/kg did not inhibit these responses. After the initial decrease, somatostatin level rose again and peaked at around 60 min after feeding (110 +/- 24 pM). This secondary rise was completely abolished by atropine in both doses tried. Gastrin and insulin levels remained elevated throughout the experiments with and without atropine. It is suggested that gastrin release and HCl secretion are inhibited by a tonic outflow of gastric somatostatin during basal conditions. The process of feeding induces an atropine resistant, vagally mediated decrease in somatostatin release from the gastrointestinal tract and this decreased output of somatostatin facilitates initiation of meal-related endocrine and exocrine gastric secretions.     

Plasma levels of somatostatin following a test meal in dogs Initial atropine resistant vagally mediated decrease of somatostain levels and increase of gastrin and insulin levels

Plasma levels of somatostatin like immunoreactivity (SLI), below referred to as somatostatin levels, were measured in peripheral plasma of conscious dogs. Basal somatostatin levels averaged 49±10 pM. Somatostatin as well as gastrin and insulin plasma levels were measured before and after feeding with and without prior atropinization. During the first 10 min after feeding somatostatin levels fell from 49±10 to 23±9 pM, whereas gastrin and insulin levels rose from 9±2 and 140±14 pM to 48±11 and 370±91 pM respectively. Atropine 0.01 or 0.1 mg/kg did not inhibit these responses. After the initial decrease, somatostatin levels rose again and peaked at around 60 min after feeding (110±24 pM). This secondary rise was completely abolished by atropine in both doses tried. Gastrin and insulin levels remained elevated throughout the experiments with and without atropine. It is suggested that gastrin release and HCI secretion are inhibited by a tonic outflow of gastric somatostatin during basal conditions. The process of feeding induces an atropine resistant, vagally mediated decrease in somatostatin release from the gastrointestinal tract and this decreased output of somatostatin facilitates initiation of meal-related endocrine and exocrine gastric secretions.     

鹅胃肠内分泌细胞的免疫组织化学定位

应用６种胃肠激素抗血清，对鹅胃肠各段的内分泌细胞分布进行了免疫组织化学定位。腺胃显示有较多促胃泌素释放肽和生长抑素细胞。肌胃有较多促胃泌素释放肽、生长抑素和胃泌素细胞，少量胰多肽细胞。幽门部有大量的生长抑素细胞，密集的胃泌素细胞，偶见胰多肽细胞。小肠内有胃泌素、胰多肽和生长抑素细胞，细胞类型和数量由前段向后段逐渐减少。未检出胃动素和抑胃肽细胞。     

扬子鳄胚胎视网膜发育的免疫组化研究

目的:检测6种激素在孵育第8天至孵出时扬子鳄胚胎视网膜的表达及变化。方法:免疫组织化学方法。结果:(1)生长抑素(SS)在孵育第8～30天有表达,第12天数量最多,30天以后消失;(2)5-羟色胺(5-HT)从孵育第24天开始表达,第30～40天数量最多,孵出时数量减少;(3)转化生长因子β_1(TGFβ_1)从孵育第40天开始表达,孵出时增多;(4)神经丝蛋白(NFP)阳性细胞和纤维在所检测的各个发育阶段均有表达,P53和P物质在各期胚胎视网膜均未检出阳性细胞。结论:视网膜的发育是个渐进的过程,不同激素在扬子鳄胚胎视网膜中的表达规律不同。     

胎儿小肠生长抑素、胃泌素及血管活性肠肽免疫反应细胞的个体发生

目的：探讨生长抑素（SS）、胃泌素（Gas）、血管活性肠肽（VIP）免疫反应（IR）细胞在胎儿小肠中的个体发生及其分布。方法：免疫组织化学方法和图像分析技术。结果：SS-IR细胞和Gas-IR细胞于11周即可见于小肠三段绒毛上皮和尚未分化完全的肠腺细胞间。随着胎龄增长,SS-IR细胞数量和细胞内SS由少至多,其中以十二指肠细胞最多,回肠最少。Gas-IR细胞和细胞内的Gas在十二指肠中随胎龄增长逐渐增多;21周后空肠中则有所减少,回肠中则消失。VIP-IR细胞数量少,整个胎期细胞数量、形态及免疫染色强度均未见明显变化。结论：SS、Gas和VIP在胎儿小肠的内分泌细胞中表达,提示内分泌激素在胎儿小肠的发育过程中起调节作用。     

新生儿缺氧缺血性脑病患者血浆ET、SS测定的临床意义

目的:探讨了新生儿缺氧缺血性脑病患者血浆内皮素(ET)和生长抑素(SS)水平的变化及临床意义.方法:应用放射免疫分析对63例新生儿缺氧缺血性脑病患者进行了血浆ET和SS检测,并与35名正常健康新生儿作比较.结果:病儿组血浆ET水平显著高于正常儿组,而SS水平则显著低于正常儿组(P＜0.01).结论:新生儿缺氧缺血性脑病的发生发展与ET和SS水平的变化密切相关.     

离体大鼠胃扩张时胃泌素生长抑素分泌的变化及机制探讨

目的：探讨胃扩张时胃泌素，生长抑素分泌的变化以及胃内神经，体液调节机制在其中的可能作用。方法：用带血管灌流的离体大鼠胃，从胃腔灌注生理盐水造成胃扩张模型，经血管注入神经递质或相应拮抗剂等，观察上述指标变化。结果：胃扩张引起容量依赖性的胃泌素分泌减少及生长抑素分泌增加；从胃动脉注入河豚毒或阿托品，上述效应分别被阻断５０％和４０％Ａ左右；注入生长抑素拮抗剂ｃｙｃｏ「７－ａｍｉｎｏｈｅｐｔａｎｏｙｌ－Ｐ