促性腺激素释放激动剂辅助诱导排卵的机制和临床应用

促性腺激素释放激动剂（gonadotropin-releasing hormone angonist,GnRHa)是近年来受到重视的诱导排卵药物,相对于传统方案,该方案能预防内源性LH过早波动,避免过早黄素化,促使多个卵泡发育,增加取卵成功率,降低多胎妊娠率及卵巢过度刺激综合征（OHSS）风险,从而提高妊娠率。本文综述和分析了GnRHa诱导排卵的特性及临床意义,为临床给药方案的优化提供重要的参考依据。     

促性腺激素释放激素激动剂(GnRHa)对卵巢巧克力囊肿患者腹腔镜术后的临床疗效及其对卵巢功能的影响

目的探讨促性腺激素释放激动剂(GnRHa)对卵巢巧克力囊肿患者腹腔镜术后的临床疗效及其对卵巢功能的影响。方法选择2011年1月至2012年12月来我院就诊的卵巢巧克力囊肿患者62例,随机分为观察组和对照组,各31例,两组患者均使用腹腔镜手术进行治疗,观察组患者在术后给予GnRHa,比较两组临床疗效及治疗前后临床症状改善情况。结果观察组患者在治疗后1年内有1例复发,总有效率为96.77%,对照组患者中有7例复发,总有效率为77.72%,观察组临床疗效显著优于对照组(P<0.05);经过治疗,两组患者的主要临床症状都有明显的改善,但观察组的改善情况优于对照组(P<0.05);经治疗后两组患者的雌二醇(E2)、孕激素(P)含量明显下降,促卵泡素(FSH)、促黄体素(LH)含量均明显升高,观察组下降或升高的幅度较对照组更明显(P<0.05);经过治疗后,观察组患者中有13例妊娠,妊娠率为41.94%,对照组患者中有5例妊娠,妊娠率为16.13%,观察组患者妊娠率显著高于对照组(P<0.05)。结论 GnRHa可提高卵巢巧克力囊肿患者腹腔镜术后临床疗效,能有效抑制术后复发,改善患者临床症状及卵巢功能,提高妊娠率,值得临床推广。     

左炔诺孕酮宫内缓释系统联合促性腺激素释放激动剂治疗子宫内膜异位症的临床效果

目的：探讨左炔诺孕酮宫内缓释系统联合促性腺激素释放激动剂治疗子宫内膜异位症的临床效果。方法将96例子宫内膜异位症患者分为LNG-IUS组、GnRH-a组及联合组3组,每组各32例,LNG-IUS组与GnRH-a组分别单独采用左炔诺孕酮宫内缓释系统与促性腺激素释放激动剂进行治疗,联合组则联合两种方法进行治疗。结果GnRH-a组与联合组的1年临床总有效率均为100.0%,显著高于LNG-IUS组的87.5%（P〈0.05）。GnRH-a组2年复发率为35.3%,显著高于LNG-IUS组的8.3%和联合组的13.3%（P〈0.05）;GnRH-a组与联合组的2年复发率比较差异无统计学意义（P〉0.05）。随访1年,GnRH-a组与联合组的骨密度与治疗前比较差异有统计学意义（P〈0.05）;随访2年,3组的骨密度与治疗前比较差异无统计学意义（P〉0.05）。结论左炔诺孕酮宫内缓释系统联合促性腺激素释放激动剂治疗子宫内膜异位症的整体效果较两者单独使用时更显著,其联合用药方案可作为临床治疗子宫内膜异位症的首选。     

促性腺激素释放激素激动剂长方案和促性腺激素释放激素抑制剂方案对卵巢功能减退患者促排卵效果和临床妊娠的影响

目的 探讨促性腺激素释放激素激动剂长方案和促性腺激素释放激素抑制剂方案对卵巢功能减退患者促排卵效果和临床妊娠的影响。方法 80例卵巢功能减退患者为研究对象,随机分为观察组和对照组,各40例。观察组采用促性腺激素释放激素激动剂长方案进行治疗,对照组采用促性腺激素释放激素抑制剂方案进行治疗,观察治疗周期结束之后,两组患者促排卵效果(包括获卵数、受精率、种植率、卵裂率)和临床妊娠(包括妊娠率和足月分娩率)情况。结果 两组患者的获卵数、受精数、卵裂数、受精率、种植率、卵裂率比较,差异无统计学意义(P>0.05),但观察组妊娠率和足月分娩率明显高于对照组,差异有统计学意义(P<0.05)。结论 促性腺激素释放激素激动剂长方案比促性腺激素释放激素抑制剂方案对卵巢功能减退患者临床妊娠效果更显著,值得临床推广应用。     

胸腺因子D对老龄大鼠垂体-性腺轴内分泌激素的影响

目的　探讨胸腺因子 D对垂体 -性腺轴内分泌衰老的延缓作用。 方法 　雌、雄 2 1月老龄 SD大鼠各随机分成两组 ,一组隔日背部皮下注射胸腺因子 D2 mg· kg- 1 ,另一组及 6月青龄雌、雄对照注射等量生理盐水 ,连续处理 3个月后 ,用放射免疫法测定腺垂体组织、血清 FSF、L H和血清 E2 、T。结果 　与雄性青龄对照组相比 ,雄性老年血清 L H升高 ,血清 T和 E2 下降 ,给药后 ,这些老年性改变可部分得到改善 ,而腺垂体组织FSH和血清 FSH、L H、E2 、T在各雌性大鼠间无差异。结论 　胸腺因子 D可逆转老龄雄性大鼠垂体 -性腺轴内分泌激素的老龄性改变 ,从而延缓衰老     

孕马血清促性腺激素(PMSG)的提取与纯化研究

本试验对孕马血清采用50％乙醇分级沉淀——0.25 mol/L,pH5.2乙酸缓冲液(含一定量乙醇)抽提——HPO-3调pH值至5.0——0.25mol/L,pH5.2、40％乙醇乙酸缓冲液抽提,得到了生物活性为976～1267 IU/mg的PMSG粗提物;对粗提物用CM Sepharose CL-6B进行柱层析,得到了生物活性为2450～2589 IU/mg的PMSG精制品。     

长方案促性腺激素启动时间对体外授精-胚胎移植结局的影响

黄体期长方案是体外授精-胚胎移植(in vitro fertility and embryo transfer,IVF-ET)的首选方案.其优势在于: 降低黄体生成素(LH)峰提前发生率; 降低周期取消率; 更为精确地调控卵泡发育; 便于患者的取卵安排.然而该方案在临床应用中还有不完善的地方,为了寻求更为完善的方法,生殖同仁们尝试着不同的改良方法,从长针长方案,到短针长方案,从月经来潮第3天统一启动促性腺激素(Gn),到现在根据卵泡大小酌情开始运用Gn,目的就是为了在提高妊娠率的同时尽可能降低患者的用药时间,用药总量及花费.     

体外培养子宫腺肌病在位内膜细胞促性腺激素释放激素受体的表达

目的研究促性腺激素释放激素受体(GnRH-R)在子宫腺肌病在位内膜组织中的表达,探讨GnRH-R与子宫腺肌病的关系,为临床治疗子宫腺肌病提供理论依据。方法分离腺上皮细胞及间质细胞进行体外培养,应用免疫组织化学的方法检测上述细胞中GnRH-R的表达,分析其在子宫腺肌病的表达。结果Gn-RH-R在子宫腺肌病在位内膜腺上皮细胞100%表达,增殖期和分泌期表达差异无统计学意义(P>0.05),基质细胞无表达。结论GnRH-R在子宫腺肌病在位内膜腺上皮细胞有表达,在基质细胞无表达。     

(+),(-)和(±)棉酚在雌大鼠抗早孕作用的研究

妊娠第6～9天大鼠,分别ig(±)和(-)棉酚80mg·kg^-1·d^-1和40mg·kg^-1·d^-1,结果有明显的抗早孕作用。然而(+)棉酚40mg·kg^-1·d^-1对大鼠生育无明显影响。(-)棉酚30μg·ml^-1能抑制体外培养黄体细胞孕酮的分泌。(+)棉酚10μg·ml^-1能促进黄体细胞分泌孕酮。hCG1IU·ml^-1能明显刺激体外培养颗粒细胞孕酮的分泌。(±)棉酚10和30μg·ml^-1皆能明显降低颗粒细胞对hCG的反应性。     

灵芝多糖肽拮抗吗啡的免疫抑制作用的体外试验

目的··:研究灵芝多糖肽(GPP)对吗啡所致免疫抑制的拮抗效应。方法··:采用中性红法检测小鼠腹腔巨噬细胞吞噬功能;采用[3H]TdR参入法测定淋巴细胞增殖反应;分别采用胸腺细胞增殖法和依赖IL-2和HT-2细胞株测定IL-1和IL-2生成。结果··:体外GPP50-800μg·ml-1可以不同程度地翻转高浓度吗啡所致的巨噬细胞吞噬功能降低,IL-1/IL-2产生减少及淋巴细胞增殖功能减退,使之恢复正常。结论··:提示GPP直接地使遭受抑制的免疫细胞的功能得以恢复,产生功能性拮抗作用。     

3,5-甾二烯化合物的合成及抗早孕活性

以18-甲基-17β-羟基-17α-乙炔基-雌甾-4-烯-3-酮(18-甲基炔诺酮),17β-羟基-17α-乙缺基-雌甾-4-烯-3-酮(炔诺酮),17β-羟基-17α-乙炔基-雄甾-4-烯-3-酮(妊娠素)和17a-羟基孕甾-4-烯-3,20二酮(17α-羟基黄体酮)为原料,经NaBH,还原、脱水、双键转位和酯化等反应合成一系列3,5-甾二烯化合物,用¹HNMR和MS证明了它们的结构。动物筛选结果表明,17β-丙酰氧基-17α-乙炔基-雌甾-3,5-二烯(IV_b2有明显的抗早孕活性。中断早期妊娠的作用似与其雌激素活性有关。     

IN VIVO AND IN VITRO EFFECTS OF ATRIAL NATRIURETIC PEPTIDE ON RENIN RELEASE

1. This study investigated the effect of atrial natriuretic peptide on renin release from the kidney. The in vitro direct effect was examined in the animal experiment using renal cortical slices of rat, and the in vivo effect was observed in the human infusion study. 2. In the in vitro experiments, alpha-human atrial natriuretic peptide (alpha-hANP) ranging 10(-9) to 10(-6) mol/L did not change the basal renin release rate from the renal cortical slices (-9% at 10(-6) mol/L, NS). Isoproterenol (10(-6) mol/L) increased renin release by 40% (P < 0.001), whereas angiotensin II (10(-6) mol/L) suppressed it by 48% (P < 0.001). However, alpha-hANP did not affect the stimulative effect of isoproterenol or the inhibitory effect of angiotensin II. 3. Also in the human study, infusion of 25 ng/kg per min alpha-hANP failed to change the plasma renin activity in normotensive subjects (-4%) or patients with essential hypertension (+5%), or even in patients with raised renin levels such as renovascular hypertension (+10%) or congestive heart failure (-13%). 4. These results put forth negative views on the direct involvement of atrial natriuretic peptide in renin release from the juxtaglomerular apparatus.     

促渗剂对布洛芬透皮吸收速率的影响

以简单小室法研究了布洛芬分别在不加助渗剂、加１％月桂氮　酮、加１％尿素、加１％月桂氮　酮及１％吐温－８０时渗过离体小白鼠皮肤的吸收效果。结果表明，月桂氮　酮有显著的吸收促进作用，尿素次之。吐温－８０则有抑制作用。     

EFFECT OF EXERCISE ON PLASMA ADRENOMEDULLIN AND NATRIURETIC PEPTIDE LEVELS IN MYOCARDIAL INFARCTION

1. We investigated the effect of exercise on plasma adreno-medullin, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) concentrations and studied the relationship between these peptides and haemodynamic parameters in nine patients with old myocardial infarction (MI) and in eight normal subjects. 2. The exercise protocol consisted of two fixed work loads (40 and 80 W) for 4 min each and venous blood samples were taken at rest, during each exercise stage and after exercise while monitoring the mean arterial pressure (MAP) and heart rate (HR). In MI, pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), left ventricular end-diastolic pressure (LVEDP) and cardiac output (CO) were measured throughout exercise. 3. Adrenomedullin levels did not significantly increase with exercise. Adrenomedullin levels correlated with PAP and PCWP at rest (P < 0.05). Atrial natriuretic peptide levels correlated with PAP, PCWP and LVEDP throughout exercise (P < 0.05) but, on multiple regression analysis, PCWP correlated only with ANP (P < 0.01). Brain natriuretic peptide levels correlated with LVEDP throughout exercise (P < 0.01) and its increment correlated closely with basal BNP levels at rest (P < 0.01). 4. These results suggest that adrenomedullin does not respond to the acute haemodynamic changes of exercise, whereas ANP responds to it and PCWP is the major stimulus factor. Brain natriuretic peptide responds to exercise in proportion to the basal synthesis of BNP in patients with left ventricular dysfunction and LVEDP may play a role in increasing BNP during exercise.     

人参皂甙对小脑生长锥影响的体外培养观察

自吉林人参根部制备的总皂甙(Rx),按每毫升培养液含50,100,200μg的浓度,对新生(P-O)B_6C_3小鼠的小脑进行Maximow器官——组织型培养,总数达120片。在体外培养第2,3,5天分别在相差显微镜下进行活体观察,对生长锥的长度和密度作进一步的观察和测量,同时结合神经染色和扫描电镜的观察与记录,结果显示实验组在生长锥的生长趋势较对照组明显,尤以100μg/ml组最为显著,具有统计学意义。本研究结果提示人参皂甙对神经组织的生长和神经网络的建立具有促进作用。     

EFFECT OF ATRIAL PEPTIDE ON COLLECTING DUCT FUNCTION

1. The effects of synthetic rat atrial natriuretic peptides (ANP) on diffusional 22Na+, 36Cl- and tritiated water (THO) permeability of in vitro microperfused rat papillary collecting ducts and the effect in vivo of ANP on stop-flow sodium concentrations in the terminal segment of rabbit nephrons were studied. 2. The addition of 4 x 10(-8) or 4 x 10(-7) mol/l ANP to the medium or perfusion solution did not alter diffusional 22Na+ or 36Cl- permeability of microperfused rat papillary collecting ducts. 3. The basal diffusional THO permeability of papillary collecting ducts was not altered when 4 x 10(-7) mol/l ANP was present in the medium and did not inhibit the increment in diffusional THO permeability induced by vasopressin or reduce the permeability to water in a duct previously stimulated by vasopressin. 4. The administration of ANP (2 micrograms/kg bodyweight) to rabbits in water diuresis did not alter systemic blood pressure but induced a marked natriuresis and increases in urine flow and potassium excretion. This natriuresis was not associated with alterations in stop-flow sodium reabsorptive capacity or sodium permeability of the collecting tubules and ducts. 5. Previously reported in vivo clearance data suggest that ANP causes, at least in part, a natriuresis by altering sodium transport in the medullary collecting ducts. In this study, however, a direct effect could not be demonstrated and it is possible that the medulla needs to be functioning in its normal environment for such effects to be demonstrated.     

EFFECT OF ATRIAL NATRIURETIC PEPTIDE ON COLLECTING DUCT FUNCTION EVALUATED BY STOP-FLOW IN RABBITS

1. The effect of a low dose of a synthetic atrial natriuretic peptide (ANP), rat atriopeptin II (23 amino acids), on stop-flow sodium concentrations was examined in rabbits in water diuresis. 2. Atrial natriuretic peptide (2 micrograms/kg body weight) was injected intravenously as a bolus either before or after the commencement of stop-flow. 3. Atrial natriuretic peptide induced a significant natriuresis within 2 min of injection. This natriuresis was associated with smaller increases in urine volume and potassium excretion. Atrial natriuretic peptide did not alter blood pressure. 4. Atrial natriuretic peptide did not significantly alter stop-flow sodium concentrations. 5. These findings indicate that ANP does not directly alter sodium transport across medullary collecting ducts. 6. It is proposed that ANP acts via a mediator to alter sodium movement across terminal segments of the nephron.