全身性非特异性免疫反应对大鼠睾丸功能的影响──Ⅱ.激素水平的变化

本实验以ＳＤ雄性大鼠为实验对象，采用碳粒血管内注射的方法，给动物造成一种全身性的非特异性免疫反应状态，以观察在这种状态下睾丸和垂体的激素分泌情况。动物经每天１次，共１０天的碳粒鼠尾静脉注射后，血浆睾酮的水平（０．８９６±０．３５８ｎｇ／ｄｌ，ｎ＝５）明显低于对照组（２．６５６±０．９９３ｎｇ／ｄｌ，ｎ＝７，Ｐ＜０．００５）；血浆ＬＨ（３．６７６±１．３５０ｍＩＵ／ｍｌ，ｎ＝９，４．６２７±２．５３９ｍＩＵ／ｍｌ，ｎ＝１０）两组比较无显著差异（Ｐ＞０．０５）；ＦＳＨ实验组（３．３６２±０．９２６ｍＩＵ／ｍｌ，ｎ＝９）与对照组相比明显降低（４．８９４±１．２３６ｍＩＵ／ｍｌ，ｎ＝１０，Ｐ＜０．０１）。实验组动物睾丸间质内ＡＣＰ阳性反应细胞增多，而β－羟基甾体脱氢酶反应消失。作者认为全身性的免疫反应既可以通过垂体也可以直接的作用于睾丸内的相关细胞，从而影响睾丸的功能。     

弱精症男子与正常人精浆和精子膜尿激酶酶活性的研究

应用琼酯糖－纤维蛋白－平板法和抗人尿激酶多克隆抗体的免疫阻断法，分别测定了２０名正常生育力男子和２２例精子活力低下（弱精症）的男性不育症患者精浆中及精子膜尿激酶型纤溶酶原激活因子（ｕＰＡ）的酶活性。结果：弱精症组精浆ｕＰＡ活性为２１３４±１５８１ＩＵ／Ｌ，正常生育组精浆ｕＰＡ活性为３３６５±１８５９．５ＩＵ／Ｌ，两组间差异有显著性意义（Ｐ＜０．０５）。弱精症组精子膜ｕＰＡ活性为５．１３±３．８２ｍＵ／１０６ｃｅｌｓ，正常生育组精子膜ｕＰＡ活性为１０．１７±６．１８ｍＵ／１０６ｃｅｌｓ，两组间差异有极显著性意义（Ｐ＜０．００５）。精子膜ｕＰＡ活性值与精子活率、活力亦呈线性相关。提示精子膜ｕＰＡ酶活性与精子活力及生育力可能有一定关系。     

不稳定心绞痛与急性心肌梗死血脂变化比较

目的：探讨不稳定心绞痛（ＵＡＰ）和急性心肌梗死（ＡＭＩ）之间血脂变化。方法：对１０９例ＵＡＰ和１４３例ＡＭＩ病人血脂值进行统计学处理分析。结果：ＵＡＰ组ＴＧ（１７１．２±１４６．９）ｍｇ／ｄｌ高于ＡＭＩ值（１３６．９±８４）ｍｇ／ｄｌ（Ｐ〈０．００５）,结论,ＵＡＰ病人ＬＤＬ－Ｃ／ＨＤＬ－Ｃ比值增高可能与其血管病变严重性相关。     

人重组γ-干扰素抗生育效应及其机理研究

本研究以新西兰品系实验兔为动物模型,观察人重组－γ干扰素（ｈｒＩＦＮ－γ）的抗生育效应并探讨其作用机理。实验结果：ｈｒＩＦＮ－γ能降低兔胚泡的着床率,对照组的着床率为８０％,ｈｒＩＦＮ－γ２．５、５．０和１０万ＩＵ３组的着床率分别为３０％、２７％和２７％。检测血清中雌二醇（Ｅ２）水平,对照组为１５７．９±３１．８ｐｍｏｌ／Ｌ,ｈｒＩＦＮ－γ各组均有降低趋势,分别为１０７．３±１９．２、１０６．３±２１．７和１０４．９±１９．８０ｐｍｏｌ／Ｌ;血清孕酮（Ｐ）水平,对照组为５０．５９±７．６２ｎｍｏｌ／Ｌ,ｈｒＩＦＮ－γ各组分别为１０．２１±３．１８、６．２３±１．６４和４．８７±０．２６ｎｍｏｌ／Ｌ。在对卵巢和子宫组织的实验病理学的系统观察发现,ｈｒＩＦＮ－γ剂量为１０万ＩＵ时,呈明显的黄体退化、子宫内膜的发育及内膜上皮和腺体的分泌均被抑制。研究表明ｈｒＩＦＮ－γ对孕兔有一定的抗生育效应,其抗孕作用的主要靶器官可能是卵巢,从而影响子宫内环境,使不利于妊娠     

精液液化不良男子与正常人精浆尿激酶活性的研究

应用琼脂糖－纤维蛋白－平板法和抗尿激酶多克隆抗体的免疫阻断法测定１５名正常生育男子和２０例精液液化不良的不育症男子精浆中尿激酶的活力。结果发现：正常生育组精浆中尿激酶的含量为８４５０±１０５０ＩＵ／Ｌ，液化不良组尿激酶的含量为６４５０±１０５０ＩＵ／Ｌ。与正常生育组比较，尿激酶活性明显降低，两组间差异有极显著性（Ｐ＜０．００１）。提示精浆中尿激酶可能与精液的液化有关联。     

脑室注射γ-氨基丁酸对雄性大鼠下丘脑促性腺激素释放激素含量的影响

本研究观察了不同剂量γ－氨基丁酸（ＧＡＢＡ）对雄性大鼠下丘脑促性腺激素释放激素（ＧｎＲＨ）含量的作用。结果表明，脑室注射５、５０、２５０及５００ｍｍｏｌ／ＬＧＡＢＡ各为２０μｌ，４０分钟后下丘脑ＧｎＲＨ含量分别为３．５７±０．５８、３．７５±０．６６、４．６３±０．６３及５．０７±０．５９ｎｇ／１０ｍｇ湿重组织，均显著高于对照组下丘脑ＧｎＲＨ含量（１．７６±０．２１ｎｇ／１０ｍｇ湿重组织，Ｐ＜０．０５）。脑室注射２５０ｍｍｏｌ／ＬＧＡＢＡ２０μｌ后２０、４０、６０、１２０及２４０分钟下丘脑ＧｎＲＨ含量依次为２．２４±０．２９、４．６３±０．６３、５．１１±０．３８、４．２０±０．４０及３．９８±０．９１ｎｇ／１０ｍｇ湿重组织。ＧＡＢＡ受体拮抗剂荷包牡丹碱（ｂｉｃｕｃｕｌｉｎｅ，Ｂｉｃ）可阻断ＧＡＢＡ对下丘脑ＧｎＲＨ含量的促进作用。     

基因重组人白细胞介素—2的I期临床观察

１７例急性肿瘤病人接受了基因重组人白细胞介素－２的Ｉ期临床试验，静脉用药的毒性反应主要包括发展，寒战，低血压、流感样症状、恶心、呕吐、毒性反应与剂量有关。剂量限制毒性反应为寒战。静脉用药最大耐受量为０．９，１０＾６ＩＵ／ｍ＾２，单次剂量为１．８０×１０＾６ＩＵ，故推荐临床静脉用药剂量搂０．２－－０．４×１０＾６ＩＵ／ｍ＾２。     

高血压病的胰岛素与内皮素变化

应用放射免疫法同明检测了３０例高血压患者的胰岛素空腹（ＦＩＮＳ）与内皮素（ＥＴ）。结果：（１）正常对照组的ＦＩＮＳ、ＥＴ分别为６．７３±２．８３ｍＵ／Ｌ、４０．３±１０．６２ｎｇ／Ｌ。高血压病组成１５．６２±８．３６ｍＵ／Ｌ、６２．３６±１０．８２ｎｇ／Ｌ。两组相比Ｐ＜０．０１；（２）高血压病患者的ＦＩＮＳ与ＥＴ有一一的相关性，ｒ值为０．３６，Ｐ＜０．０５，作者认为胰岛素、内皮素相互影响，相互促进     

膀胱上疝1例报告

患者,女,７２岁,因腹痛、腹胀、呕吐,排便,排气停止２４ 小时,加重２小时急诊入院。查体：一般状态可,急性面容,Ｔ３７．８℃,Ｐ ９４次／分,ＢＰ １７／１０ｋＰａ（１３０／８０ｍｍＨｇ）。腹部膨隆,在中上腹可见肠型,未触及包块、肝、脾肋下未触及,全腹有压痛、反跳痛和肌紧张,移动性浊音（±）,可闻及气过水声及金属音。 ＷＢＣ２４．０×１０９／Ｌ,Ｎ０．９,Ｌ０．４０,ＲＢＣ３．９０×１０１２／Ｌ,Ｈｂ１２０ｇ／Ｌ,ＰＣ １３０×１０９／Ｌ。腹部Ｘ线透视见多处液气平面;腹腔穿刺抽出淡红色混浊样液体约２…     

连续性肾脏替代疗法在治疗多器官功能障碍综合征中的应用

病史摘要 患者,男性,４１岁,因腹部外伤ｌｈ后入院。查体：体温３６．２℃,脉搏１２８次／ｍｉｎ,呼吸２０次／ｍｉｎ,ＢＰ ８０／６０ｍｍＨｇ。胸廓无畸形及压痛,两肺呼吸音清。心率１２８次／ｍｉｎ,律齐,无杂音。腹稍饱满,剑突下、左上腹明显压痛,伴肌紧张;肝区无叩痛,肝肋下未及;脾肋下未及,左季肋部无压痛,但有叩痛。肛指检查阴性。辅助检查：血常规：Ｈｂ ８０ｇ／Ｌ,ＷＢＣ １０．４ × １０~９／Ｌ,Ｎ ０．７６,Ｌ ０．２４;Ｐｌｔ１０~３ × １０~９／Ｌ。肝功能：正常。肾功能：ＢＵＮ１４．２ ｍｍｏｌ／Ｌ…     

Spectrum of the pulsatile characteristics of LH release in normal men

To assess the spectrum of LH pulse characteristics in normal men, blood samples from 36 individuals were drawn at 20-minute intervals for 8 hours. The subsequent immunoactive LH concentrations were analyzed by computer algorithms to delineate the frequency and amplitude characteristics of pulsatile LH secretion. The absolute range for LH pulse frequency estimated by a modified threshold method was 1-6 pulses/8 hr, with a mean (+/- SEM) of 3.36 +/- 0.17 (median -3)pulses/8 hr. The distribution differed significantly from a Gaussian pattern. The mean LH pulse amplitude expressed as a percent increase above nadir was 92.1 +/- 6.1 (median-91.5%). When LH pulse amplitude was defined as an increment (mIU/ml) above nadir, the mean value was 5.13 +/- 0.4 (median -4.8) mIU/ml. These two expressions of amplitude were positively correlated (P less than 0.01), while the incremental (mIU/ml) pulse amplitude correlated inversely with pulse frequency (P less than 0.01). To examine the influence of more intensified rates of venous sampling on the spectrum of LH pulse properties, blood was sampled at 4-minute intervals for 8 hours in a subgroup of 13 men. Under these conditions, estimated LH pulse frequency was significantly higher, with a mean of 10.31 +/- 1.87 (median -9) pulses/8 hr compared with 20-minute sampling in the same individuals (P less than 0.001). Although the estimates of LH pulse frequency at 4-minute and 20-minute sampling intervals were significantly correlated (P less than 0.01), the dispersion of the LH pulse frequency estimates was considerably larger at more rapid rates of sampling. There was an absolute range of 2-20 pulses/8 hr for the 4-minute sampling, and 1-6 pulses/8 hr for the 20-minute sampling in the same individuals. This increase in LH pulse frequency and the broader dispersion of the range of frequencies estimated at 4-minute compared with 20-minute sampling intervals were confirmed using either another pulse detection algorithm, or separate criteria designed to adjust false-positive error rates in relation to sampling intensity. It was concluded that eugonadal men exhibit a broad spectrum of pulsatile LH characteristics, and the range of LH pulse attributes is even greater at more intensive rates of venous sampling. The results of this study in normal men demonstrate that a wider dispersion of physiologic LH pulse characteristics must be recognized in man.(ABSTRACT TRUNCATED AT 400 WORDS)     

Fasting‐induced Changes in Ovulation Rate,Plasma Leptin,Gonadotropins, GH,IGF‐I and Insulin Concentrations During Oestrus in Ewes

The aim of this experiment was to study the changes in the hormonal status and ovulation rate (OR) evoked by starvation during the follicular phase of the oestrous cycle in ewes. To achieve this goal, 12 female crossbreed sheep were synchronized and then half of them were fasted from the 12th to the 16th day of the oestrous cycle. On the 16th day, analysis of hormones and insulin‐like growth factor‐I (IGF‐I) were performed in 10‐min intervals. Then, on the 6th day of the following oestrous cycle, the OR in all ewes was determined by laparoscopy. Fasting reduced significantly (P < 0.05) the OR in ewes (1.25 ± 0.50) in comparison with control (1.75 ± 0.50). The drop in the OR was coincident with a significant (P < 0.001) decrease in the plasma concentration and pulse amplitude of leptin (0.29 ± 0.08 ng/ml versus control 0.53 ± 0.14 ng/ml), the plasma level of luteinizing hormone (LH) (0.19 ± 0.06 IU/l versus 0.25 ± 0.09 IU/l in control; P < 0.05) and the mean frequency of LH pulses (2.0/h versus 2.5/h in control). Fasting resulted also in a significant (P < 0.05) decrease in the plasma concentration and pulse amplitude of follicle stimulating hormone (FSH) in comparison with the control. Simultaneously, a significant (P < 0.001) drop in the IGF‐I concentration in the fasted ewes (4.78 ± 0.91 ng/ml) was found in comparison with control (7.63 ± 1.85 ng/ml). Also the level of insulin were significantly (P < 0.001) lower in the fasted (178.99 ± 39.08 pm /l respectively) than in the control sheep (302.66 ± 49.01 pm /l respectively). Meanwhile, a double increase in the growth hormone (GH) pulses frequency and an augmentation in its plasma concentrations as a result of starvation was found. The obtained results shows that the acute fasting exerts an inhibitory effect on the ovulation rate in ewes coincident with suppression in leptin, FSH and LH secretion and changes in signalization mediated by GH.     

Nature of alpha subunit secretion in men: circadian rhythms, pulsatile release and secretory profiles

Alpha subunit complements LH as a marker of the activity of the hypothalamic GnRH pulse generator. To characterize episodes of alpha subunit release and to determine if a circadian pattern of alpha subunit secretion is present in man, spontaneous alpha subunit pulsatility was analyzed in six healthy young men by blood sampling every 5 min for 24 h. The resulting alpha subunit concentration time series were analyzed by two statistically based independent peak detection methods, and subjected to Fourier transformation to assess underlying circadian rhythms. Cross-correlation analyses and multiple parameter deconvolution were used to estimate the concordance of spontaneous and exogenous GnRH-stimulated LH and alpha subunit secretion. These analyses revealed that two independent discrete peak detection algorithms yielded similar estimates of spontaneous alpha subunit pulse frequency, namely, 21 +/- 1.1 (Cluster) and 21 +/- 1.5 (Detect) alpha subunit peaks/24 h. Sampling intensity markedly influenced the estimate of endogenous alpha subunit pulse frequency, inasmuch as estimates from 5-min sampling were significantly greater than those of 10-min or 20-min sampling. Fourier transformation unmasked a significant circadian alpha subunit rhythm in all six men, with maximal concentrations at 0836 h and an average amplitude of 28% of the 24-hr mean hormone concentration. Cross-correlation analysis of spontaneous glycoprotein release revealed that serum LH and alpha subunit concentrations were highly cross-correlated when considered simultaneously, but not at various lags. Finally, deconvolution analysis of exogenous GnRH-stimulated glycoprotein release disclosed distinct half-times of alpha subunit and LH clearance with virtually simultaneous underlying secretory bursts. These data indicate that human alpha subunit is secreted in both a circadian and a discrete pulsatile fashion at a pulse frequency that is significantly underestimated at conventional sampling rates. The approximately hourly alpha subunit interpulse interval (68 +/- 4.6 min) is similar to that reported earlier for LH in peripheral blood and for testosterone in gonadal vein blood in healthy men. Moreover, cross-correlation analysis of endogenous GnRH-driven alpha subunit and deconvolution analysis of exogenous GnRH-stimulated alpha subunit and LH secretion suggest that these glycoproteins are secreted virtually simultaneously, but have significantly different endogenous clearance properties. The remarkably similar in vivo pulse frequencies for alpha subunit, LH, and testosterone in man suggest that the release of these three hormones is coordinately regulated.     

Deconvolution analysis of bioassayable LH secretion and half-life in men with idiopathic oligoasthenospermia

To further investigate the nature of neuroendocrine disturbances of the hypothalamo-pituitary-gonadal axis in idiopathic male infertility, we studied 12 infertile men with oligoasthenozoospermia and 13 euspermic controls, matched for age and body mass index, by blood withdrawal at 10-min intervals for 8 h to analyse pulsatile release of bioactive LH (b-LH). The rat interstitial cell testosterone (RICT) bioassay was used in conjunction with a recently validated multiparameter deconvolution algorithm, to estimate the endogenous half-life of b-LH, its secretory burst frequency, amplitude, duration and mass. Oligoasthenospermic men exhibited significant ( p < 0.05) alterations within the LH axis; namely: (1) a prolonged half-life of b-LH (92 min in euspermic men, 127 min in oligoasthenospermic men); (2) a reduced b-LH secretory burst amplitude (2.2 ± 1.2 IU/l/min in euspermic men, 1.7 ± 0.8 IU/l/min in oligoasthenospermic men); (3) a lower bioactive/immunoactive (b/i) ratio for LH secretory burst amplitude (14 in euspermic men, 4 in oligoasthenospermic men); (4) a reduced b/i ratio in the mass of LH secreted per burst (5.4 in euspermic men, 4.1 in oligoasthenospermic men) and (5) decreased coordinate release of b-LH and testosterone in infertile men, as assessed by cross-correlation analysis. These disturbances differ from the neuroendocrine dysregulation described in other states of male hypogonadotrophism.     

Pulsatile bioactive luteinizing hormone secretion in men with chronic renal failure and following renal transplantation

We have measured plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone (To) by radioimmunoassay (RIA) and bioactive LH (B-LH) by in vitro bioassay at 10-min intervals over 6 h in men treated by haemodialysis for renal failure and in men after renal transplantation. Eleven normal male volunteers acted as controls. Immunoreactive LH (I-LH) and FSH levels were elevated (p less than 0.03) in uraemia (mean +/- SE; 10.0 +/- 1.0 and 4.6 +/- 0.7 IU/l for LH and FSH, respectively) and following renal transplantation (8.1 +/- 1.2 and 5.3 +/- 0.5 IU/l) compared to controls (C) 4.9 +/- 0.5 and 2.7 +/- 0.4 IU/l) whereas B-LH [17.3 +/- 2.5, 14.8 +/- 1.8 and 12.9 +/- 1.3 IU/l in dialysis (D), transplant (T) and C groups, respectively] levels were normal. Prolactin levels were elevated (p less than 0.03) in the D group (median 348, range 162-1,780 mU/l) compared to the T group (161, 91-206 mU/l) and controls (163, 124-312 mU/l) whereas total To levels (mean +/- SE; 17.3 +/- 4.8, 15.5 +/- 1.3 and 19.6 +/- 2.1 nmol/l in the D, T and C groups, respectively) were similar as was the free To index. B-LH (median frequency, 2 and range 1-3 pulses/6 h) and I-LH (median frequency, 2 and range 1-2 pulses/6 h) was pulsatile in all the C group but B- and I-LH pulses were absent in 2 of the 5 subjects treated by dialysis. Following renal transplantation B-LH pulses were detected in all subjects, whilst I-LH pulses were absent in 1 subject.(ABSTRACT TRUNCATED AT 250 WORDS)     

Luteinizing hormone pulsatility in men with damage to the germinal epithelium

Bioactive-LH (B-LH) was measured in plasma by in-vitro bioassay and immunoactive-LH (I-LH) by immunoassay at 10 min intervals for 6 h in five men after standard chemotherapy for Hodgkin's disease. Eleven normal men acted as controls. Follicle-stimulating hormone (FSH) was markedly raised in the treated patients (mean +/- SEM; 12.8 +/- 2.8 vs. 2.7 +/- 0.4 IU l-1, P less than 0.006) reflecting damage to the germinal epithelium. Bioactive (27.4 +/- 2.8 vs. 12.9 +/- 1.3 IU l-1) and I-LH (9.6 +/- 2.0 vs. 4.9 +/- 0.4 IU l-1) were elevated (P less than 0.006) in the patient group whilst testosterone levels (24.0 +/- 3.8 vs. 19.6 +/- 2.4 nmol l-1) were normal. The testosterone I-LH ratio, a putative index of Leydig cell dysfunction, was negatively correlated with FSH levels (r = -0.85, P less than 0.02). Bioactive and I-LH pulse peak amplitude were elevated, as were pulse maxima (P less than 0.05). In contrast, B-LH pulse frequency was similar between the patients (2 pulses per 6 h) and controls (median 2, range 1-3 pulses per 6 h) as was the I-LH pulse frequency (median 2, 1-2 pulses per 6 h in both groups). The mean B:I LH ratios were similar (2.94 +/- 0.09 vs. 2.63 +/- 0.14) in both groups, although the inter-pulse B:I ratio was increased (P less than 0.007) in the patient group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pulsatile secretion of gonadotropins and prolactin in male marathon runners. Relation to the endogenous opiate system

We tested the hypothesis that sustained, strenuous physical training alters the neuroendocrine regulation of pulsatile gonadotropin and/or prolactin secretion in men. Blood was sampled at 20-minute intervals over 8 hours in five endurance-trained men after a 10-15 mile run in the middle of the active training season, and in 11 nonendurance trained normal controls. In these two groups, basal patterns of physiologically pulsatile secretion of LH, FSH, and prolactin (PRL) were not significantly different in relation to the following parameters: mean serum concentration of each of the three hormones (N = 25 samples); areas under the hormone concentration vs. time curves; fractional, incremental, and absolute pulse amplitudes; and pulse frequency, or periodicity. To test for enhanced suppressive effects of endogenous opiates in trained male marathon runners, subjects were administered the potent opiate-receptor antagonist, naltrexone (1 mg/kg). This antagonist significantly stimulated pulsatile LH secretion by increasing mean serum LH values from 10.94 to 13.58 mIU/ml (P = 0.007); area under the LH concentration vs. time curve increased from 5370 to 6510 mIU/ml X 8 hours (P = 0.05) and, pulse frequency rose from 2.8 to 4.9 pulses/8 hours (P = 0.006). Naltrexone also enhanced pulse frequency of FSH secretion from 3.4 to 5.4 pulses/8 hours (P = 0.009), but did not alter serum prolactin concentrations. None of these responses differed significantly from those in normal sedentary controls.(ABSTRACT TRUNCATED AT 250 WORDS)     

Impact level of dihydrotestosterone on the hypothalamic-pituitary-leydig cell axis in men

Dihydrotestosterone (DHT) the physiologically most potent androgen cannot be aromatised into oestrogen. DHT is used as a treatment for idiopathic gynaecomastia. In order to investigate the different sites of action of DHT on the hypothalamic-pituitary-testicular axis, two groups of adult men were studied. Group I included 10 gonadotropin-releasing hormone (GnRH)-deficient men who were evaluated before and during a pulsatile infusion of GnRH alone for 2 weeks and then in association with DHT given transdermally at doses used in the treatment of gynaecomastia for further two weeks. Luteinizing hormone (LH) pulsatility was assessed at the end of each step of the study. Plasma LH levels were measured every 15 min. Plasma testosterone (T), DHT, oestradiol (E2), free alpha-subunit (FAS) of glycoproteic hormones and LH bioactivity were measured on pooled plasma samples. Group II included 12 healthy men in whom plasma T, DHT and E2 were measured before and then 24, 48 and 72 h after the injection of 5000 IU hCG alone or in combination with either DHT or the pure anti-androgen nilutamide. Two weeks separated each of the 3 hCG testing. In group I, except for bioactive/immunoreactive (B/I) LH ratio which was unchanged, GnRH treatment induced significant rises (p < 0.01) in all plasma hormone levels, LH pulse amplitude and frequency. During treatment with GnRH+DHT, plasma DHT levels increased up to 16.8 +/- 2.5 nm, while plasma hormone levels, B/I LH ratio, LH pulse amplitude and frequency were similar to those obtained with GnRH alone. In group II, the peak of hCG-induced T rise was not modified by either DHT or nilutamide. In contrast, DHT reduced by 50% (p < 0.01) the E2 peak in response to hCG. These data show that DHT exerts no direct action on the pituitary to retroregulate LH secretion and to modify either B/I LH ratio or FAS secretion. Its reducing effect on LH secretion is likely mediated at the hypothalamic level. DHT does not appear to have a physiological influence on Leydig cells steroidogenesis. Administered at therapeutic doses, DHT directly reduces testicular aromatase activity that combined with its antigonadotropic effect leads to the gain in the symptomatic treatment of gynaecomastia.     

Physiologic attributes of the luteinizing hormone pulse signal in the human. Cross-validation studies in men

The performance of two new statistically based, independently formulated, endocrine peak detection methodologies (Cluster and Detect) were tested on the same large set of physiologic LH pulsations. Serum LH concentrations were determined in blood samples withdrawn at 5-minute intervals for 24 hours in eight healthy young men. The subsequent comprehensive LH time series were subjected to Cluster and Detect analysis, each constrained to an alpha level of 0.01 or 0.05. Under both circumstances, computer estimates of physiologic LH pulse frequency by the two separate algorithms were statistically indistinguishable. Moreover, the two distinct methodologies were concordant not only in relation to the original 5-minute sampling series but also with respect to the constituent 10-, 15-, 20-, 30-, and 45-minute sampling data. The cross-validation of these two mathematically independent methodologies has permitted delineation of the detailed spectrum of spontaneous LH pulse properties within individual men and among different males under basal physiologic conditions.     

Primary gonadal failure in men selectively amplifies the mass of follicle stimulating hormone (FSH) secreted per burst and increases the disorderliness of FSH release patterns: reversibility with testosterone replacement

The neuroendocrine mechanisms by which primary gonadal failure in men increases mean serum FSH concentrations (castration-like response) are not known. To investigate the testosterone-dependent mechanisms of the FSH castration response: (i) blood was sampled at 10-min intervals for 24 h for later FSH assay in seven normal middle-aged men and in six patients with primary testicular failure, during testosterone withdrawal and after 6 weeks of parenteral testosterone replacement; (ii) using a specific two-site IRMA, serum FSH concentrations were measured, since this assay correlates well with an in-vitro Sertoli cell bioassay; (iii) multiparameter deconvolution analysis was then applied to estimate the frequency, amplitude, duration, and mass of underlying FSH secretory bursts, and the half-life of endogenous FSH, and (iv) approximate entropy was calculated to quantify the relative orderliness of FSH release over 24 h. Mean (+/- SEM) 24-h serum FSH concentrations were 3.9 +/- 0.8 IU/L in control subjects and 39 +/- 10 IU/L in unreplaced hypogonadal patients (p = 0.034). Deconvolution analysis revealed similar estimated mean FSH half-lives of 346 +/- 40 min (control) and 321 +/- 47 min (untreated patients), and indistinguishable FSH secretory burst frequencies, namely, 20 +/- 0.95 (normal) and 21 +/- 1.3 (patients) pulses per 24 h. In contrast, the daily production rate of FSH was markedly increased in testosterone-withdrawn hypogonadal men at 117 +/- 25 vs. 9.3 +/- 1.8 IU/L/day (control) (p < 0.01). This was due to a 10-fold higher calculated maximal rate (amplitude) of FSH secretion achieved within each FSH release episode (normal 0.078 +/- 0.02 vs. gonadal failure 0.74 +/- 0.087 IU/L/min, p < 0.01), yielding a 10-fold increase in the mass of FSH secreted per burst (control 0.53 +/- 0.06 vs. patients 5.3 +/- 0.81 IU/L, p < 0.01). In contrast, the mean half-duration of FSH secretory bursts was unaltered in unreplaced hypogonadal men at 8.2 +/- 2.2 min (control) vs. 7.0 +/- 1.0 min (patients). Approximate entropy (ApEn), a scale- and model-independent statistic designed to quantify the orderliness or regularity of hormone release, revealed greater irregularity of serum FSH concentrations in the hypoandrogenic state: ApEn = 1.8 +/- 0.025 (testosterone-withdrawn) vs. 1.6 +/- 0.037 (control) (p < 0.05). Parenteral testosterone replacement for 6 weeks significantly decreased mean serum FSH concentrations by reducing the daily FSH secretion rate and FSH secretory burst amplitude and mass, and concomitantly restored the orderliness of FSH release patterns. Testosterone treatment did not change FSH secretory burst half-duration, number, interburst interval, or half-life. It is concluded that primary gonadal failure in men evokes FSH hypersecretion which is marked by more disorderly FSH release patterns and a selectively amplified mass of FSH secreted per burst. These hypergonadotrophic mechanisms are, to a significant extent, testosterone-suppressible.