睾丸去神经对大鼠半去势诱导的睾酮代偿性分泌的影响

在成年大鼠,半去势可以在促性腺激素没有明显改变的情况下导致睾丸静脉血液中睾酮浓度代偿性增加,其机理尚不明了。本研究以成年大鼠为实验动物,检验睾酮的代偿性增加是否受到睾丸去神经的影响。睾丸去神经（ｉｎｆｅｒｉｏｒ ｓｐｅｍａｔｉｃ ｎｅｒｖｅｓ,ＩＳＮ或ＩＳＮ ｐｌｕｓ ｓｕｐｅｒｉｏｒ ｓｐｅｒｍａｔｉｃ ｎｅｒｖｅｓ,ＩＳＮ－ＳＳＮ）手术２周后开始半去势实验,半去势之前和半去势之后６和２４ｈ,     

催乳素对培养的绵羊睾丸间质细胞睾酮分泌的影响

在绵羊睾丸间质细胞体外无血清长期培养的条件下,研究了催乳素对睾丸间质细胞睾酮分泌的调节作用。实验结果表明,催乳素可增强细胞对人绒毛膜促性腺激素(hCG)刺激的反应。催乳素的这种作用呈双相调节。睾酮分泌量显著高于hCG和催乳素单独作用时的总和。在hCG存在下,不同的底物转化为睾酮的量不同。其中雄烯二酮和孕酮转化为睾酮的方式存在着双相性。脱氢表雄酮转为睾酮的量少,不存在双相性,而与其剂量成正比。催乳素在hCG存在下可调节底物转化为睾酮。低剂量的催乳素(1ng/ml)可使一定剂量的孕酮(10～30ng/ml)转化为睾酮的量明显增加,而高剂量的催乳素(>10ng/ml)却明显地抑制孕酮转化为睾酮。催乳素可明显地抑制雄烯二酮转化为睾酮,与剂量无关。可见催乳素对于孕酮和雄烯二酮这两个关键底物转化为睾酮的调节是不同的。催乳素增强hCG刺激睾酮分泌的作用可能部分是通过其促进孕酮转化为睾酮来实现的。     

神经介质C对促胃液素分泌的影响

采用带血管灌流的离体大鼠胃模型,就铃蟾肽类肽能神经介质Ｃ（ＮＭＣ）对促胃液素分泌的影响及其与胆碱能神经的关系,以及铃蟾肽受体拮抗剂（ＢＮ－Ａｎｔ）Ｄ－Ｐｈｅ~６－ＢＮ（６－１３）ＯＭｅ对ＮＭＣ诱导的促胃液素分泌的影响等问题进行探讨。实验结果表明,ＮＭＣ可明显刺激大鼠胃分泌促胃液素（从基础的５５０±１２６ｐｇ／１０ｍｉｎ增加到刺激时的１０６０±１８０ｐｇ／１０ｍｉｎ）,与对照组或自身基础状态比较,差异非常显著（Ｐ＜０．０１）;此效应（净增量）被Ｄ－Ｐｈｅ~６－ＢＮ（６－１３）ＯＭｅ完全消除或被阿托品抵消约６０％（Ｐ＜０．０１）。本实验结果证实,铃蟾肽类肽能神经递质ＮＭＣ是促胃液素分泌的强刺激剂;新近问世的ＢＮ－ＡｎｔＤ－Ｐｈｅ~６－ＢＮ（６－１３）ＯＭｅ具有高效拮抗ＮＭＣ刺激促胃液素分泌的作用;同时揭示,ＮＭＣ的作用机制不仅直接对胃Ｇ细胞、而且还可能通过影响胆碱能神经而发挥效应。     

去甲肾上腺素对刺激隐神经诱发大鼠体感皮层单位放电的调制

本实验观察微电泳去甲肾上腺素（ＮＡ）及肾上腺素能体拮抗剂育亨宾和心得安对刺激隐神经引起的大鼠大脑皮层体感Ⅰ区诱发单位放电（ＳＩ－ＳＥＵＤ）的影响。用计算机对ＳＩ－ＳＥＵＤ作放电点过程分析和标准化互协方差函数（ＮＣＣＶＦ）处理,小剂量（５－３５ｎＡ）ＮＡ对ＳＩ－ＳＥＵＤ主要起抑制作用,大剂量主要起易化作用,中等剂量作用不显著。ＮＡ对强的ＳＩ－ＳＥＵＤ主要起抑制作用,对弱的则主要起易化作用;提示ＮＡ可     

大鼠睾丸金属结合蛋白含量对睾酮合成速率的影响

通过观察具有不同睾丸金属结合蛋白（ｔｅｓｔｉｓｍｅｔａｌｂｉｎｄｉｎｇｐｒｏｔｅｉｎ,ＴＭＢＰ）含量的对照和缺锌后补锌大鼠安静时和力竭性游泳后不同时间睾丸和血清睾酮和锌含量变化,以探讨ＴＭＢＰ含量对睾酮合成速率的影响．实验结果证实了如下推测：ＴＭＢＰ含量不同,睾酮合成的速率也不同,高起始含量ＴＭＢＰ的状况下,睾丸睾酮的合成加快．这一结果提示：ＴＭＢＰ可能参与睾酮的合成．     

增产菊胺酯对小鼠睾丸间质细胞-氧化氮合酶和3β-羟基甾体脱氢酶影响的酶组织化学研究

本文用ＮＡＤＰＨ－黄递酶法研究了ＮＯＳ在小鼠睾丸的分布与活性,用ＮＢＴ法研究了３β－ＨＳＤＨ的活性,以探讨新型植物生长调节剂增产菊胺酯的生殖毒作用机理。光镜观察和图像分析表明,ＮＯＳ主要存在于睾丸间质细胞,而支持细胞和生精细胞未见或仅见弱阳性反应产物。进一步观察表明,随着剂量的增加,ＮＯＳ和３β－ＨＳＤＨ活性均明显减弱,睾丸内睾酮含量也随之减少。结果提示,增产菊胺酯可能由此而引起生殖功能的损伤     

大鼠睾丸中S-100蛋白生后发育变化的免疫细胞化学研究

本文应用免疫细胞方法,研究大鼠生后４天、７天、１４天、３０天、２个月和３个月睾丸中Ｓ－１００蛋白的分布和变化规律。结果表明：Ｓ－１００蛋白染色反应位于睾丸间质细胞,直到生后３０天才出现阳性细胞,数量少,着色浅,而２月龄和３月龄大鼠睾丸Ｓ－１００蛋白阳性细胞数量多,着色深。提示Ｓ－１００蛋白可能参与间质细胞的合成和分泌睾酮过程。     

睾酮对雄家猫附性器官金属硫蛋白的诱导

睾丸切除后,家猫前列腺背叶、腹叶及尿道球腺内的金属硫蛋白（ｍｅｔａｌｏｔｈｉｏｎｅｉｎ,ＭＴ）分别下降至正常家猫的２１２％（Ｐ＜００１）、８８４％（Ｐ＞００５）和１８５％（Ｐ＜００１）,而在腹叶影响较小。睾丸切除后注射芝麻油,前列腺背叶及尿道球腺ＭＴ均未得到恢复。但若在睾丸切除后连续３ｄ注射１０μｇ／ｋｇｂｗ睾酮,两者依次恢复至６９３％和５９４％。随睾酮注射剂量增加（５、１０、１５、２０、２５μｇ／ｋｇｂｗ）,血浆睾酮的浓度、前列腺背叶及尿道球腺ＭＴ含量增高。血浆睾酮与前列腺背叶及尿道球腺ＭＴ呈正相关（Ｐ＜００１）。这些结果表明,睾酮诱导前列腺背叶及尿道球腺ＭＴ,其最适剂量为２０μｇ／ｋｇｂｗ。     

电刺激大鼠苍白球对黑质I型神经元的影响

采用细胞外记录方法,分别观察了黑质（ＳＮ）Ｉ型神经元对刺激苍白球（ＧＰ）内侧部及外侧部的反应。实验共记录了９６个Ｉ型神经元。刺激ＧＰ的内侧部,有５７个（５９．３８％）神经元顺行抑制。刺激ＧＰ的外侧部,有８６个（８９．５８％）神经元被顺行抑制;２个（２．０８％）被逆行激活,被逆行激活的神经元产生的诱发电位潜伏期恒定且短（分别为８．０和８．５ｍｓ）。被顺行抑制的神经元中,有的产生抑制、兴奋交替出现的振     

大鼠和小鼠睾丸表皮生长因子表达的免疫组织化学定位观察

为了了解大鼠和小鼠睾丸是否产生ＥＧＦ及其细胞定位,本实验用ＥＧＦ单克隆抗体对大鼠和小鼠睾丸进行了免疫细胞化学定位研究,结果显示：（１）出生后,大鼠和小鼠睾丸即开始产生ＥＧＦ,分泌活动主要位于睾丸间质细胞。（２）至性成熟期,少数精原细胞、精母细胞及个别圆形精子细胞和管周肌样细胞也产生ＥＧＦ,使生精小管尤其是血睾屏障管腔小室侧的ＥＧＦ分泌增加。（３）在本实验中,睾丸支持细胞未见明显ＥＧＦ阳性染色。结果表明,大鼠和小鼠睾丸是可以产生ＥＧＦ的,间质细胞是其主要的ＥＧＦ分泌细胞。进入性成熟期后,少数精原细胞、精母细胞及个别圆形精子细胞和管周肌样细胞也产生ＥＧＦ。大鼠和小鼠睾丸在发育过程中ＥＧＦ分泌量呈上升趋势,至性成熟期达分泌高峰     

Synthesis and aromatization of 19-norandrogens in the stallion testis

The results of the measurement of 19-nortestosterone in the testiscular artery and vein of the stallion, the very low levels of this steroid in the peripheral blood of geldings and the similar patterns of increase in the peripheral levels of 19-nortestosterone and testosterone after hCG stimulation, show that 19-nortestosterone, like testosterone, is essentially synthesized in the testis. This testicular origin was confirmed by the ability of testicular tissue to synthesize 19-norandrogens from [4-14C]androgens in vitro. 19-Nortestosterone was 50% conjugated in the peripheral blood and almost entirely conjugated after biosynthesis in vitro. The sequence of appearance of steroids in the peripheral blood after a single injection of 10,000 IU hCG suggests that, in the equine testis, 19-norandrogens are produced by a specific C10-19 desmolase (estrene synthetase), stimulable by hCG. 19-Nortestosterone was aromatized into estradiol-17 beta by stallion testicular microsomes. The affinity of the aromatase for 19-nortestosterone was very low compared to that for testosterone. At low and presumably physiological levels, and at a high testosterone/19-nortestosterone ratio, testosterone did not inhibit 19-nortestosterone aromatization by more than 53%. Thus, 19-nortestosterone may be aromatized in vivo in the testis in spite of the endogenous concentrations of androgens. However, the low velocity of 19-nortestosterone aromatization by testicular microsomes at roughly physiological concentrations suggests that 19-norandrogen aromatization may only participate slightly in the testicular estrogen production. These results suggest that in the equine testis, two aromatizing enzyme systems may exist: one which aromatizes both androgens and 19-norandrogens, and a minority system more specific for 19-norandrogens.     

Functional arterio-venous anastomoses between the testicular artery and the pampiniform plexus in the spermatic cord of rams

Blood flow to the testis, haemoglobin oxygen saturation and testosterone concentration in arterial and venous testicular blood vessels were studied in Texel rams in the breeding and non-breeding season. Blood flow in the proximal and distal testicular artery was measured electromagnetically. The mean flow in the proximal testicular artery was 18.5 ml/min and in the distal testicular artery 7.5 ml/min, and there was no detectable seasonal influence. Haemoglobin oxygen saturation and testosterone concentration were measured in the saphenous artery and vein, the distal testicular artery and vein, and in the proximal testicular vein. The haemoglobin oxygen saturation in the proximal testicular vein was significantly higher than in the distal testicular vein in both seasons. The mean testosterone concentration was significantly lower in the proximal testicular vein than in the distal testicular vein in both seasons. Based on haemoglobin oxygen saturation and testosterone data, it was calculated that between 28 and 46% of the testicular arterial blood was bypassing the testis and was directly flowing through arterio-venous anastomoses towards the pampiniform plexus in the spermatic cord of conscious rams. In anaesthetized rams 55 and 64% of the blood was flowing directly from the testicular artery to the pampiniform plexus based on blood flow data. Transfer of testosterone and oxygen by passive diffusion from the testicular artery to the pampiniform plexus and vice versa in the spermatic cord was not detected.     

Regulation of 3 beta-hydroxysteroid dehydrogenase activity by human chorionic gonadotropin, androgens, and anti-androgens in cultured testicular cells

delta 5-3 beta-Hydroxysteroid dehydrogenase is a key enzyme for testicular androgen biosynthesis and a marker for the Leydig cells. The hormonal regulation of this enzyme was studied in cultured rat testicular cells. Human chorionic gonadotropin (hCG) increased testosterone production in vitro while time course studies indicated a biphasic action of the gonadotropin on 3 beta-hydroxysteroid dehydrogenase activity. An initial stimulation (51%) of the enzyme was detected between 3 and 12 h of culture when medium testosterone was low. This is followed by an inhibition of 3 beta-hydroxysteroid dehydrogenase activity on days 2 and 3 of culture when medium testosterone was elevated. Concomitant treatment with a synthetic androgen (R1881) inhibited 3 beta-hydroxysteroid dehydrogenase activity and testosterone production in hCG-treated cultures while an anti-androgen (cyproterone acetate) increased 3 beta-hydroxysteroid dehydrogenase activity and testosterone biosynthesis. Addition of 10(-5) M spironolactone, an inhibitor of 17 alpha-hydroxylase, blocked the hCG stimulation of testosterone production but increased medium progesterone. In the absence of the secreted androgen, hCG stimulated 3 beta-hydroxysteroid dehydrogenase activity in a time- and dose-related manner. Furthermore, hCG stimulation of 3 beta-hydroxysteroid dehydrogenase activity and progesterone accumulation in spironolactone-supplemented cultures was decreased by concomitant treatment with R1881 but was not affected by cyproterone acetate. The inhibitory effect of R1881 was blocked by the anti-androgen. In the absence of hCG, treatment with testosterone, dihydrotestosterone, or R1881, but not promegestone, alone also inhibited 3 beta-hydroxysteroid dehydrogenase activity while the inhibitory effect of testosterone was blocked by cyproterone acetate. Thus, hCG stimulates 3 beta-hydroxysteroid dehydrogenase activity in cultured testicular cells. The androgenic steroidogenic end products, in turn, inhibit this enzyme. The hormonal regulation of 3 beta-hydroxysteroid dehydrogenase activity may be important in the ultrashort loop autoregulation of androgen biosynthesis.     

Heritable testicular hypoplasia in Nguni (Bos indicus) bulls: vascular characteristics and testosterone production.

The biased unilateral occurrence of heritable gonadal hypoplasia was investigated by examining the gross- and microanatomy of the testicular artery and vein, testicular blood flow and testicular testosterone secretion in normal Nguni bulls and in Nguni bulls showing unilateral left, unilateral right and bilateral hypoplasia of the testis. A high incidence of branching of the testicular artery was found ipsilateral to hypoplastic testes. The branching occurs a short distance from the dorsal aorta: one branch proceeds to the testis, the other to the ipsilateral kidney. The association between arterial branching to the kidney and ipsilateral hypoplasia of the testis held for both unilaterally left and unilaterally right hypoplastic bulls. Variations in the anatomy of the testicular vein occurred in both normal and hypoplastic bulls but there was no specific association between the variations and ipsilateral hypoplasia. The lumen diameter of the testicular artery or branch correlated with testis mass. Wall thickness of the artery ipsilateral to hypoplastic testes was not different from that in normal bulls, discounting hyperplasia of the endothelium. Total blood flow to the testis correlated with testis mass. The secretion rate of testosterone from hypoplastic testes was lower than that of normal testes but there was no difference when compared on a unit mass basis.     

Regulation of testicular steroidogenesis by gonadotropin-releasing hormone agonists and antagonists

Clinical and experimental studies are described on the effects of a gonadotropin-releasing hormone (GnRH) agonist (A) and antagonist (Ant.) on testicular endocrine function. Testicular effects of long-term gonadotropin suppression by GnRH-A were assessed during treatment of prostatic cancer patients. The testis tissue removed after 6 months of A treatment had less than 5% of the testosterone(T)-producing capacity in comparison to testis tissue removed from untreated control patients. However, the LH receptors (R) and responsiveness of T output to LH stimulation in vitro were unchanged. FSH-R decreased by 70%. Hence, despite suppression of gonadotropins and testicular androgen production during long-term GnRH-A treatment the responsiveness to exogenous gonadotropins is maintained. The testicular effects of a gonadotropin suppression induced with GnRH-Ant. and testicular GnRH-R blockade were studied in rats. Besides decreases of gonadotropins and testicular T, systemic Ant. treatment decreased testicular Prl-R, but had no effect on LH-R or FSH-R. Bromocriptine-induced hypoprolactinemia, in contrast, decreased LH-R but had no effect on Prl-R. The results indicate reciprocal regulation of LH-R and Prl-R, and that testicular steroidogenesis and LH-R are under differential regulation, the former by LH, the latter by Prl. In another study, testicular GnRH-R, and consequently the action of a putative testicular GnRH-like factor, were blocked by unilateral intratesticular infusion of Ant. (1 week, Alzet osmotic pumps). The treatment resulted in 90% occupancy of testicular GnRH-R in the Ant.-infused testes, and this was associated with decreased levels of R for LH, FSH and Prl, and of T. The results indicated that the testicular GnRH-R have a physiological function in subtle stimulation of Leydig cell functions.     

Androgens and oestrogens in normal and cryptorchid stallions.

Total androgens, testosterone and total oestrogens were measured in twenty-one intact, nine unilaterally cryptorchid, three bilaterally cryptorchid stallions and four geldings. Total oestrogens were significantly higher (P less than 0-005) and total androgens significantly lower (P less than 0-05) in the bilateral cryptorchid compared to other groups. There was a significant (P less than 0-025) day and night variation in total androgen levels. Thyroidectomized and intact animals showed a marked decrease in total androgen as well as testosterone levels during the winter period thus showing an effect of season on androgenic function of the testis. Disappearance rate of total and androgens following castration was extremely rapid and levels were undectable within 12 hr. Sexual stimulation appeared to increase total androgen levels. Testosterone, androstenedione, dihydrotestosterone, androstandiols, and androstenediol were identified in spermatic vein blood. Dihydrotestosterone was measured in fluid from the cauda epididymidis.     

Effects of hemicastration at various ages and of oestradiol-17 beta on plasma concentrations of gonadotrophins and androgens, testicular growth and interstitial cell responses in prepubertal lambs

The effect of the removal of one testis from cross-bred lambs at 1, 4, 8 or 12 weeks of age on plasma FSH, LH and testosterone was studied until 16 weeks of age. Hemicastration at all ages elicited a significant increase in plasma FSH compared to controls without a corresponding change in plasma LH or testosterone. The raised FSH after hemicastration at 1 or 4 weeks of age was suppressed to control levels between weeks 7 and 8; such a suppression was not observed in the 4 weeks following hemicastration at 8 or 12 weeks of age. The weight of the remaining testis had increased compared with the control by 12 weeks of age after hemicastration at 1 week (+ 69%), 4 weeks (+ 13%) and 8 weeks (+ 40%); hemicastration at 12 weeks of age also resulted in growth of the remaining testis at 16 weeks (+ 82%). The total androgen production of interstitial cells in response to ovine LH stimulation in vitro did not differ significantly between lambs of 1 and 12 weeks of age, or in animals of 4, 8 and 12 weeks of age after hemicastration at 1 week of age. Subdermal implantation of oestradiol-17 beta into 1-week hemicastrated lambs at the time of operation or at 6 weeks of age increased plasma oestradiol concentrations by approximately 2-4-fold, prevented the FSH and testicular growth responses to hemicastration and suppressed plasma LH and testosterone to levels lower than those in control lambs. The total androgen response of interstitial cells from the remaining testis of oestradiol-implanted lambs at 12 weeks of age was significantly reduced. We suggest that the pituitary-testis axis varies in sensitivity during the prepubertal period although the interstitial cellular response of the testis to LH stimulation remains constant.     

Effect of testosterone on testicular steroidogenesis in the hypogonadal (hpg) mouse

Previous studies have shown that androgens have direct inhibitory effects on steroidogenesis in active Leydig cells. It is not clear what effect androgens have on inactive Leydig cell either through direct action on the cell itself or indirectly through stimulation of Sertoli cell activity. The hpg mouse has undetectable levels of circulating gonadotrophins and the gonads fail to develop post-natally. The effect of androgen treatment on testicular steroidogenesis and morphology was examined in these animals. Treatment with testosterone propionate for two weeks significantly increased testicular and seminal vesicle weight. Seminiferous tubules showed marked development in androgen-treated animals, indicating increased Sertoli cell activity, but the abnormal Leydig cell morphology of the hpg testis was unchanged. Androgen production per testis in vitro was low in control hpg animals and remained unaffected by treatment with androgen. Similarly, the pattern of [3H]pregnenolone metabolism was not significantly affected by androgen treatment. The androgen content of the testis was higher in androgen-treated animals but this could be accounted for by uptake of administered steroid from the circulation. It is concluded that androgens have no direct trophic effect on Leydig cells and that stimulation of Sertoli cell activity is not, in itself, sufficient to affect Leydig cell function.     

Limitations imposed by testicular blood flow on the function of Leydig cells in rats in vivo

Testis blood flow per testis closely follows testis weight in rats made aspermatogenic by a single exposure of the testis to 43 degrees C for 30 min or 500 rad (5 Gy) of irradiation from a caesium source, or following ligation of the efferent ducts. Aspermatogenesis following these treatments was associated with only minor changes in the concentrations of testosterone in peripheral blood before stimulation with human chorionic gonadotrophin (hCG), and a reduced responsiveness to hCG when testis weight had fallen after heating. The concentrations of testosterone in testicular venous blood was normal or above normal during aspermatogenesis resulting from heat or irradiation, and only slightly reduced following efferent duct ligation. Consequently testosterone production (defined as the product of plasma flow and the veno-arterial concentration difference for testosterone) was markedly reduced during aspermatogenesis, both before and after stimulation with hCG. It appears that the reduced blood flow limits the amount of testosterone leaving the testis, and while the Leydig cells are capable under some circumstances of compensating partially for this fall by increasing the concentration of testosterone in the testicular venous blood, this compensation is not complete when there are severe reductions in blood flow. Therefore one can conclude that the mass of the tubules is the main determinant of testis blood flow and the Leydig cells must manage with what the tubules require.