奥典肽降低食管曲张静脉压力及减少硬化剂注射针孔出血的临床研究

１０例肝硬化食管静脉曲张患者内镜直视下硬化剂注射针穿刺入曲张静脉内直接测压，继而外周静脉内推注奥曲肽（Ｏｃｔｒｅｏｔｉｄｅ）０．１ｍｇ，测定其后１０分钟曲张静脉内压力变化，２０例患者静脉注射奥曲肽０．１ｍｇ，约１０分钟后行食管曲张静脉内硬化剂注射治疗，观察注射针孔出血情况并与２６例屯硬化剂注射作化比较。结果表明奥曲肽静脉注射后１分钟内，所有患者均有效地降低曲张静脉内压力，１０分钟内平均降低５１％（     

经内镜食管曲张静脉测压及生长抑素和奥曲肽的降压作用 …

目的 测定肝硬化食管曲张静脉内压力（ＩＯＶＰ）,比较生长抑素及奥曲肽降压效应。方法：生长抑素组８例,奥曲肽组１０例,均经内镜作食管曲张静脉穿刺测压,分别静脉内注射生长抑素０．２５ｍｇ及奥曲肽０．１ｍｇ,测压５分钟结果 生长抑素组ＩＯＶＰ降低４９．８％（Ｐ〈０．０１）,奥曲肽组ＩＯＶＰ降低２９．９％,结论 两组患者对生长抑素和奥曲肽均有反应性,能有效降低肝硬化门脉高压患者的ＩＯＶＰ值。     

奥曲肽在内镜粘合剂D-TH治疗食管和胃静脉曲张中的应用

目的 探讨奥曲肽在内镜粘合剂Ｄ－ＴＨ治疗食管和胃静脉曲线中的作用。方法 粘合剂Ｄ－ＴＨ内镜注射治疗前５ｈ起静脉维持滴注奥曲肽０．０２５ｍｇ／ｈ,术前２０＇静脉注射冲击量奥曲肽０．１ｍｇ。内镜直观下注射Ｄ－ＴＨ液治疗肝硬化食管和胃静脉曲线及其出血。结果 Ｄ－ＴＨ治疗７例食管和胃硬化剂治疗均无针孔出知。结论 应用奥曲肽有助于食管和胃静脉曲张及其出血的内镜下Ｄ－ＴＨ硬化治疗,术后维持治疗可有效降低出血率     

善得定诱导下食管静脉曲张硬化剂治疗

善得定诱导下食管静脉曲张硬化剂治疗陆华生李玉明王亚明钱俊波１９９２年８月～１９９４年１０月，我院采用善得定１００μｇ术前１５分钟静脉注射，随之在曲张的食管静脉内注射１％乙氧硬化醇，拔针前注射１单位立止血，观察注射针孔出血及止血效果以及曲张静脉消失率，...     

食管静脉曲张密集结扎术和硬化及结扎联合术的疗效对照观察

比较内镜下食管静脉曲张密集结扎术和内镜下硬化及结扎联合术治疗食管静脉曲张破裂出血的疗效。４２例食管静脉曲张破裂出血病情稳定的病人分为两组，２２例患者接受ＤＥＶＬ，２０例病人行ＥＳ＋ＥＶＬ，两组具有可比性（Ｐ＞０．０５）。第１次治疗，ＤＥＶＬ组每个病人平均结扎１１．３２个点，每根曲张静脉平均结扎２．８３个点；ＥＳ＋ＥＶＬ组首先静脉内注射硬化剂，然后行结扎，第１次治疗平均每根曲张静脉注射硬化剂１．０３次（点），结扎１．０１个点。结果：第１次治疗后，ＤＥＶＬ组食管静脉曲张消失率为５０％，ＥＳ＋ＥＶＬ组为３５％，两组比较无统计学意义（Ｐ＞０．０５）；第１、４、１２及２４周的再出血率，ＤＥＶＬ组为４．５％、４．５％、４．５％、４．５％，ＥＳ＋ＥＶＬ组为１０％、１５％、１５％、２５％，两组无显著差别（Ｐ＞０．０５）。ＤＥＶＬ和ＥＳ＋ＥＶＬ均为治疗食管静脉曲张破裂出血、根除食管静脉曲张的有效方法，ＤＥＶＬ的操作较容易、并发症较少、再出血率较低，内镜下食管静脉曲张密集结扎术将取代内镜下硬化剂注射疗法，成为治疗食管静脉曲张破裂出血的首选方法。     

重视食管胃静脉曲张出血的临床研究

我国各种病因的肝硬化食管胃静脉曲张出血患者众多，临床死亡率高。内镜治疗的多种方法能有效地控制出血，消除曲张静脉，降低再出血率。加强肝硬化食管胃静脉曲张出血的基础和临床研究，有利于选择合理的治疗方案，提高治疗效果。一、食管曲张静脉测压肝硬化食管和（或）胃静脉曲张破裂时往往出血量大，控制急性出血至关重要。应用血管活性药物能有效降低门静脉压力，在众多药物中，生长抑素及其类似物奥曲肽、特利加压素等的有效率约为７０％～９０％。为研究曲张静脉内压力与破裂出血的关系以及探索血管活性药物降压的有效性和相关机理，…     

奥曲肽与硬化剂注射对急性食管静脉出血治疗效果的多中心随机对照研究

硬化剂疗法与血管活性药物已广泛应用于食管静脉曲张出血的治疗,奥曲肽虽也很常用,但其临床疗效仍未定论。本实验旨在对比评价奥曲肽与硬化剂疗法的疗效。病人和方法　将来自英国4所医院的150例急性食管静脉出血病人随机分为硬化剂治疗组与奥曲肽治疗组。对77例硬化剂治疗组于入院后给予急诊内镜检查,每条曲张静脉注射油酸乙醇胺2～3ｍｌ,硬化剂注射后若仍有持续性渗血则给予气囊压迫,但不超过12小时,12小时后仍需重复插入气囊压迫或有复发性出血,定为治疗失败。奥曲肽组73例于急诊内镜检查确诊后即给予奥曲肽50μｇ/ｈ静脉点滴,持续48ｈ。…     

食管硬化剂治疗与门脉高压性胃病

本文前瞻性观察９６例食管胃底静脉曲张出血硬化剂治疗者门脉高压性胃病（ＰＨＧ）的发生率。硬化剂治疗前ＰＨＧ１０例（１０．４％）。１％乙氧硬化醇注射２２７次（４０例注射１次），５６例平均注射３．３３次，其中曲张静脉消退或明显减轻３９例（８８．５％）。结果１例原轻度ＰＨＧ发展成重度ＰＨＧ并大出血，１０例硬化剂注射后（平均８．２５个月）发生ＰＨＧ（１７．８％），每例硬化剂注射平均３．７２次，静脉内注射４９．６ｍｌ，静脉旁１２．５ｍｌ，其中２例发生ＰＨＧ性出血。本研究结果表明，硬化剂治疗后部分患者可发生ＰＨＧ或使原ＰＨ６加重甚至发生出血。作者就ＰＨＧ出血的机理及治疗进行了探讨     

巴曲酶重度曲张静脉内注射预防硬化治疗针孔出血的临床研究

巴曲酶重度曲张静脉内注射预防硬化治疗针孔出血的临床研究吴云林，李荣洲，陈和阳，房长兴门脉高压患者常伴有明显的食管及／或胃底静脉曲张，部分病人出现曲张静脉突发破裂大出血，临床死亡率高。目前国际上普遍应用硬化剂注射作紧急止血或曲张静脉择期治疗，对止血和曲...     

三腔单囊管压迫胃底静脉前后食管曲张静脉压力的变化

目的: 研究肝硬化食管静脉曲张患者在放置三腔单囊管压迫胃底静脉前、后食管曲张静脉压力的变化.方法:8例肝硬化食管静脉曲张患者在单胃囊三腔管牵引下, 采用50 g/L鱼肝油酸钠行食管静脉内注射. 在单胃囊三腔管牵引前、后测曲张静脉的压力变化情况, 并观察注射后针孔出血情况.结果: 单胃囊三腔管压迫胃底静脉前、后食管曲张静脉内的压力改变有显著性差异(t = 5.55, P<0.005). 经单胃囊三腔管压迫后再予以硬化剂注射治疗后, 未发生涌血, 2例为少量渗血, 其余无出血.结论:硬化治疗时, 改良的三腔单胃囊管牵引可有效降低食管曲张静脉内的压力, 使硬化治疗的疗效更确切、简便、安全.     

蚯蚓纤溶活性成分的抗凝及溶血栓作用

家兔静往蚯蚓纤溶成分F2，观察其整体抗凝、促纤溶及溶血栓作用。与给药前比较，给药后20分钟凝血时间明显延长（P＜0．05），给药后20min及1h凝血酶原时间明显延长（皆P＜0．05），给药后4h及5h血浆纤维蛋白原含量明显降低（皆P＜0．01），给药后1，2，3小时血浆代球蛋白溶解活性均见升高趋势，给药后24h，血栓模型的检重明显减轻（P＜0．05）。     

川芎嗪对大鼠脑梗塞区细胞Ca~(2 )影响的实验研究

本实验用雄性大白鼠24只随机分成三组:A组(n=8)为对照组,在MCAO前30分钟静注蒸馏水;B组(n=8)在MCAO前30分钟静注川芎嗪lmg/kg;C组(n=8)在MCAD后40分钟静注川芎嗪lmg/kg。用钙离子选择性微电极观察脑梗塞区细胞外Ca~(2 )动态变化。结果显示B组脑梗塞区细胞外Ca~(2 )下降明显低于A组(P<0.05);C组给药前后自身对照脑梗塞区细胞外Ca~(2 )回升不显著(P>0.05)。提示缺血前30分钟用药川芎嗪能预防脑缺血区细胞外Ca~(2 )进入细胞。     

Postprandial gall bladder motility and hormone release during intermittent and continuous subcutaneous octreotide treatment in acromegaly.

Repeated daily injections of the somatostatin analogue, octreotide (SMS201-995, Sandostatin) are an effective treatment for acromegaly, but lead to gall stone formation in about 50% of cases during longterm treatment. This is probably because of impaired gall bladder contraction. This study examined whether the timing of intermittent injections in relation to meals, or alternatively, continuous 24 hour subcutaneous octreotide infusion (CSOI) might avert adverse effects on gall bladder contraction. In six patients with active acromegaly, gall bladder volume, plasma cholecystokinin (CCK), and pancreatic polypeptide (PP) were measured in the fasting state and after consumption of a fatty meal. Measurements were made on five separate days: (a) without treatment, (b) 45 minutes after 100 micrograms octreotide given subcutaneously, (c) four hours after 100 micrograms octreotide given subcutaneously, (d) eight hours after 100 micrograms octreotide given subcutaneously, and (e) during CSOI of 300 micrograms/24 h for two weeks. Without treatment, postprandial gall bladder contraction was 86.2 (2.1%). Fasting gall bladder volume increased after octreotide injection and was almost doubled during CSOI. Octreotide injections impaired postprandial gall bladder contraction as well as CCK and PP release for at least four hours. Eight hours after injection and during CSOI, postprandial gall bladder contraction was partly restored (43.4% and 50.8% respectively). Postprandial CCK release was normal at eight hours after injection but very low during CSOI. PP release was suppressed by each mode of octreotide treatment. This study indicates that octreotide injections impair postprandial gall bladder contraction for at least four hours. Eight hours after injection and during CSOI, gall bladder contraction is partly restored.     

Octreotide administration,under particular temporal conditions,enhances the responses of growth hormone to growth hormone-releasing hormone in normal subjects

OBJECTIVE Somatostatin not only inhibits basal and GHRH-stimulated GH secretion but might also enhance pituitary GH responsivity to GHRH under different temporal conditions. We investigated whether octreotide, a long-acting somatostatin analogue, has any positive actions on GHRH-induced GH release in normal human subjects. DESIGN The study consisted of three protocols. At 0800 hours, after fasting overnight, all subjects received 1 μg/kg GHRH l.v. bolus at 0 minutes. In each protocol, either octreotide (200 μg s.c.) or placebo were given respectively 8, 12, or 16 hours prior to GHRH challenge. SUBJECTS Three groups of eight normal volunteers (four female and four male in each group), aged 18–35 years, were randomly assigned to each protocol. MEASUREMENTS Growth hormone was measured by IRMA. Samples for GH assay were taken at ?30 and 0 minutes and then at 15-minute intervals up to 120 minutes. RESULTS When placebo or octreotide were administered 8 hours before GHRH, peak GH levels were respectively (mean ± SE, mU/l) 56·2 ± 16·6 and 60·8 ± 11·4 (NS). Also, when placebo or the somatostatin analogue were administered 16 hours prior to GHRH, peak GH levels were comparable (61·0 ± 7·4 vs 58·8 ± 7·4, NS). However, in the group receiving placebo or octreotide 12 hours prior to GHRH, the GH responses to GHRH were clearly enhanced by octreotide administration (peak GH levels, mU/l, 55·6 ± 21·6 vs 104·0 ± 17·4, P < 0·02). This enhancement of GH responses was observed in all subjects. CONCLUSIONS Octreotide administration did not affect GH responses to GHRH when given either 8 or 16 hours prior to GHRH. However, octreotide enhanced GHRH-induced GH release when administered 12 hours prior to GHRH. It thus appears that, under particular temporal conditions, octreotide may act positively on GH secretion in man.     

Effect of octreotide on gastrointestinal pressure profiles in health and in functional and organic gastrointestinal disorders.

The somatostatin analogue, octreotide, restores normal pressure profiles in disorders of upper gut motility. This study aimed to evaluate the acute effects of octreotide in five healthy subjects and in 50 consecutive patients with functional (n = 22) or organic (n = 28) dysmotility. Antroduodenojejunal manometry was performed during three hours' fasting, for two hours after a standard meal, and 30 minutes after subcutaneous injection of 50 micrograms octreotide. Antral motility, before and after octreotide, and characteristics of spontaneous migrating motor complexes and octreotide induced activity fronts were compared. Octreotide inhibited antral motility and induced a small intestinal activity front followed by motor quiescence in all healthy subjects and patients. The duration and propagation velocity of activity fronts were greater than those of spontaneous migrating motor complexes. Thirty per cent of activity fronts began simultaneously at different levels of small bowel, and in 20%, a second, normally propagated activity front developed within 30 minutes of octreotide injection. Octreotide induces rapidly propagated, long activity fronts, even in patients with neuropathology, and this may initially facilitate the intestinal propulsion of chyme. Propulsion may not occur, however, if octreotide induces simultaneous activity fronts or if the activity front is followed by prolonged quiescence. Inhibition of antral motility suggests that octreotide may not be effective in gastroparesis.     

Effects of a slow-release formulation of the new somatostatin analogue lanreotide in TSH-secreting pituitary adenomas

OBJECTIVE Somatostatin analogues have been proposed for the treatment of thyrotrophinomas. However, this treatment requires several s.c. injections a day to be effective. The present study had the following aims: (i) appraisal of the efficacy of a single dose of two somatostatin analogues (lanreotide and octreotide) to acutely inhibit TSH secretion of TSH-secreting pituitary adenomas; (ii) assessment of the efficacy of a single injection of a slow release formulation of lanreotide (SR-L) in reducing TSH and thyroid hormone secretions in the same cases; and (iii) evaluation of the effects of SR-L used for 3–6 months on hormone secretion and tumour size. PATIENTS Four patients with hyperthyroidism linked to a TSH-secreting pituitary adenoma found on pituitary magnetic resonance imaging (MRI) and subsequently proved by immunohistochemistry were studied. METHODS in the first step of the study the patients received in a random order, vehicle, 150 μg octreotide and 500 μg lanreotide as a single s.c. injection. Measurements of plasma TSH, free T4 (fT4), free T3 (fT3) and free alpha subunit (fAS) levels were carried out before injection and then every other hour for 8 hours. In the second part of the study, after a basal blood sample (0800 h), each patient received 30 mg lanreotide as an l.m. injection of SR-L. Blood was sampled 2 hours later and then three times a week for 3 weeks in order to measure plasma TSH, fT4, fT3 and lanreotide levels using radioimmunoassays. The patients then received one SR-L injection twice or in one case three times a month for 3–6 months. Plasma TSH, fT4 and fT3 levels were measured monthly and a pituitary MRI was performed at the end of the treatment with SR-L. RESULTS 500 μg lanreotide acutely reduced plasma TSH and fAS levels to the same extent as 150 μg octreotide. Two hours after a single i.m. injection of SR-L plasma lanreotide levels reached 7·8±0·6 μg/l and then progressively decreased, being 1·8 ± 0·2 μg/l on day 2 and 1·1 ± 0·3 μg/l on day 14 after the injection. Plasma TSH level decreased from basal value (mean ± SEM 4·4 ± 1·2 mlU/l) within 2 hours (2·5 ± 0·8 mlU/l) and further declined to 0·8 ± 0·2 ml/Ul on day 2 following the injection. Depending on the patient, plasma TSH levels were reduced for a period of 6–15 days. Plasma fT4, fT3 levels were normalized on day 2 and remained in the normal range for a period of time of 9–20 days. During long-term treatment, abdominal cramps and diarrhoea appeared, leading to interruption of the treatment in one patient. The treatment was well tolerated in the other three patients. Plasma TSH and thyroid hormone levels progressively decreased during the treatment. No change in adenoma volume was observed after 3–6 months of therapy. CONCLUSIONS This study shows that (i) lanreotide is able to inhibit acutely TSH secretion in thyrotrophinomas and that a single s.c. injection of 500 μg lanreotide is as effective as 150 μg octreotide; (ii) SR-L appears to be able to reduce plasma TSH and to normalize fT4 and fT3 levels for 9–20 days in patients with thyrotrophinomas; (iii) this effect is maintained throughout the treatment using two or three SR-L injections monthly for months. These results suggest that SR-L could be used as a treatment of thyrotrophinomas and avoids the drawbacks of the modes of administration of other somatostatin analogues used in such cases.     

心脉宁抗凝血作用的观测

目的 :探讨心脉宁对凝血时间、凝血酶原时间和优球蛋白溶解时间的影响。方法 :小鼠 30只 ,心脉宁混悬液灌胃 ,末次给药后 30 min自内眦以毛细玻璃管取血 ,记录凝血时间。家兔 2 4只 ,iv心脉宁溶液后 30 min颈动脉取血 ,测定凝血酶原时间。豚鼠 32只 ,心脉宁混悬液灌胃 ,末次给药后 30 m in于心内取血 ,测定优球蛋白溶解时间。结果 :与对照组比较 ,不同浓度的心脉宁可延长凝血时间和凝血酶原时间 ,并缩短优球蛋白溶解时间。随心脉宁浓度的增加 ,凝血时间随之延长 （P<0 .0 5或 相似文献   

Influence of octreotide (SMS 201-995) and insulin administration on the course of blood pressure after an oral glucose load in hypertensive elderly subjects

Pretreatment with a somatostatin analogue, octreotide (SMS 201-995), prevents postprandial blood pressure reduction in the elderly. We hypothesized that this beneficial effect on blood pressure is caused by an octreotide-induced suppression of insulin secretion. We studied the effects of octreotide and insulin administration on the course of blood pressure after oral glucose loading in 10 healthy hypertensive old persons (mean age 73 +/- 3 years). Octreotide was given in a dose of 50 micrograms subcutaneously (sc) (time = -30 minutes). Insulin was given sc in a dose of 0.3 U/kg body weight (time = -10 minutes) and glucose was given orally in a dose of 75 g in 300 mL water (time = 0 minutes). Plasma insulin concentrations remained essentially unchanged after placebo and rose to a maximum level of 58 +/- 6 mU/L following insulin administration. The course of blood pressure was not different following glucose loading with high or low plasma insulin levels. These data indicate that the effects of octreotide on postprandial blood pressure reduction in the elderly are unrelated to the inhibition of insulin secretion.