饲予克山病病区粮对大鼠胰岛β细胞分泌功能及胰岛素、C肽分泌贮备的影响

应用免疫组织化学及放免分析方法,对饲予克山病病区粮大鼠胰岛的形态与机能研究结果表明:低硒的克山病病区粮可引起大鼠血清胰岛素、C肽水平明显下降,胰岛内C肽和胰岛素分泌贮备显著减少,并出现胰岛β细胞萎缩、变性等形态学损害。在病区粮内补一定剂量硒或维生素E(VE)可明显提高血清胰岛素、C肽水平,增加β细胞分泌贮备,提示硒和VE缺乏引起的过氧化损害可能是胰岛受损的主要机制。本研究结果提示克山病基本病因可引起胰岛的原发性损害,其作为克山病发病过程中的重要环节,可能对心肌坏死的发生发展起一定作用。     

硒和维生素E对克山病病区粮喂饲大鼠心肌损伤的影响

本实验在克山病病区粮食中补充硒和维生素E(VE)或单独补充硒喂饲大鼠,和单纯喂饲病区粮大鼠比较,联合补充硒和VE可明显减轻亚硝酸钠引起的大鼠心肌损伤;硒加VE组大鼠红细胞高铁血红蛋白还原酶活性明显升高,其可使亚硝酸盐氧化血红蛋白形成的高铁血红蛋白迅速还原,从而减轻机体缺氧状态;硒和VE可使大鼠心肌脂质过氧化产物丙二醛含量明显减少,减轻了病区粮喂饲大鼠心肌损伤;硒加VE使大鼠血清甲状腺激素(T_3、T_4)和心肌呼吸酶(CCO、SDH)活性维持在低水平,表明其纠正了病区粮喂养大鼠心肌能量代谢紊乱,使代偿增加的血清T_3、T_4和心肌CCO、SDH活性降低。和病区粮组大鼠比,单纯加硒组大鼠除心肌谷胱甘肽过氧化物酶活性升高外,其心肌损伤未明显减轻。 上述结果提示,联合补充硒和VE在预防克山病发病上可能会有更好效果。     

克山病病区粮喂养大鼠心肌内心钠素含量变化及硒和维生素对其影响

本文用低硒的克山病病区粮喂养大鼠,证明其心肌中心钠素(ANP)含量明显增高,而在补充硒、维生素E(VE)后均可使其含量下降,并且具有一定的量效关系,尤其是硒和VE的联合补充使心肌中ANP含量明显降低,接近饲非病区粮和常规食水平。表明二者对心脏内产生和释放ANP具有明显的影响,据此推论硒和VE的联合缺乏可能就是造成病区粮饲养动物心肌内ANP含量增加的主要原因。     

克山病病区粮喂饲大鼠维生素E营养状态评价及补充硒和维生素E的影响

克山病病区粮,或在其中补充硒或维生素E(VE)喂饲大鼠21～22周,以非病区粮组大鼠为对照。结果表明:病区粮组大鼠心、肝、脾、肾、骨骼肌、肾上腺和胰腺形态改变不明显;病区粮组大鼠心重:体重比值高于非病区粮组和补充硒或VE组大鼠;病区粮组大鼠24小时尿中肌酸排泄量高于非病区粮组在补充VE组大鼠尿中没有检出肌酸;病区粮组大鼠和非病区粮组大鼠红细胞体外过氧化氢溶血率相同,但都处于高水平,补充硒可明显降低溶血率,补充VE则溶血率更进一步降低。综合上述结果得出结论,病区粮喂养大鼠体内VE储存不能满足其需要。     

内、外环境硒营养水平与克山病发病关系的研究

目的 探讨克山病病区内、外环境硒水平以及与克山病发病的关系。方法 分别采集病区、非病区水，以及居民食用粮和病区、非病区人群头发、血清及尿样，用荧光法测定样品硒含量；并观察全省40年克山病病情动态变化，观察硒水平与克山病发病的关系。结果 克山病病区水硒、土壤硒含量低于非病区；居民食用粮（小麦、玉米、瓜干）硒含量显著低于非病区（P〈0．01）；克山病病区水、土中硒含量与当地粮食中硒含量成正相关关系。克山病患者发硒、血清硒、尿硒含量均显著低于病区健康人和非病区健康人（P〈0．01），病区健康人的血清硒、尿硒水平低于非病区健康人，发硒也有降低趋势。从1976～2004年克山病病区居民食用小麦、玉米硒含量逐渐增高，克山病患者头发、血清及尿液硒含量逐渐增高，克山病患病率逐渐降低。结论 克山病发生于低硒地区，病区居民机体硒营养水平与克山病患病率之间呈一定的负相关关系。缺硒可能是克山病发生的地区性条件致病因素。     

补大剂量锌对饲克山病病区粮大鼠红细胞膜锌、铜含量及脂质过氧化的影响

以前作者曾报道过,克山病病区粮中补加200ug/g的锌和/或0.lug/g的硒,可显著增加大鼠红细胞膜锌含量,同时脂质过氧化强度也得到了一定程度的抑制。本文则报道在克山病病区粮中补加2000ug/g的锌,对大鼠红细胞膜锌、铜含量及脂质过氧化的影响。1 材料和方法 实验动物选用Wistar纯种大鼠,共分4组:1.非病区粮对照;2.病区粮对照;3.病区粮补 Zn(Zn-     

急性脑血管病患者下丘脑-垂体-性腺轴及泌乳变化的探讨

目的观察急性脑血管病患者下丘脑一垂体一性腺轴的变化.方法用放免法测定急性脑血管病患者血中PRL、LH、FSH、E2、T.结果PRL、LH、FSH、E2明显增高,P、T下降.结论急性脑血管病影响下丘脑-垂体-性腺轴的功能变化.     

急性脑血管病患者下丘脑-垂体-性腺轴及泌乳素变化的探讨

目的　观察急性脑血管病患者下丘脑—垂体—性腺轴的变化。方法　用放免法测定急性脑血管病患者血中 PRL、LH、FSH、E2、T。结果　PRL、LH、FSH、E2明显增高 ,P、T下降。结论　急性脑血管病影响下丘脑—垂体—性腺轴的功能变化。     

克山病病区粮及硒补充对小鼠免疫功能的影响

用克山病病区粮和在病区粮中补加不同水平硒的饲料喂养 C_(57)BL/6J 断乳小鼠7周,病区粮组小鼠脾脏免疫特异玫瑰花形成细胞(RFC)数、溶血空斑形成细胞(PFC)数、脾脏淋巴细胞介导的体外绵羊红细胞溶血反应均明显低于非病区粮组,病区粮补硒各组小鼠的上述免疫反应虽     

男性肝硬化失代偿期患者垂体及性腺激素水平变化

报告35例男性肝硬化失代偿期患者血清FSH、LH、PRL、E_2、T测定结果,并与50例正常健康人对照。结果显示血清PRL显著升高(P<0.001),E_2升高(P<0.05),T显著降低(P<0.001),FSH、LH近于正常水平(P>0.05)。提示肝硬化失代偿期患者存在下丘脑—垂体—性腺轴功能障碍。     

Effects of starvation in rats on serum levels of follicle stimulating hormone, luteinizing hormone, thyrotropin, growth hormone and prolactin; response to LH-releasing hormone and thyrotropin-releasing hormone.

Adult male Sprague-Dawley rats averaging 300 g each were subjected to complete food removal for 7 days (acutely starved), 7 days complete food removal followed by 2 weeks of 1/4 ad libitum food intake (chronically strved), 7 days complete food removal and 2 weeks of 1/4 ad libitum intake followed by ad libitum feeding for 7 days (refed), or fed ad libitum throughout (controls). Serum LH, FSH, TSH, PRL, and GH levels were measured by radioimmunoassays for each group of rats. The in vivo response to the combination of synthetic LHRH and TRH also was tested in each group of rats. Circulating LH, TSH, GH, and PRL were significantly depressed in acutely and chronically starved rats, and FSH was lowered only in acutely starved rats. After 7 days of refeeding, serum levels of LH and FSH were significantly greater than in ad libitum fed controls, PRL returned to control levels, and TSH and GH increased but were still below control levels. After LHRH + TRH injection serum LH and TSH were increased significantly in all groups of rats, FSH and PRL rose in acutely but not in chronically starved rats, and GH was not elevated in any group. The increases in serum LH, FSH, TSH and prolactin in response to LHRH + TRH injection in acutely or chronically starved rats were equal to or greater than in the ad libitum fed controls. These data indicate that severe reductions in food intake result in decreased release of at least 5 anterior pituitary hormones, and this is due primarily to reduced hypothalamic stimulation rather than to inability of the pituitary to secrete hormones.     

Release of dynorphin-like immunoreactivity from rat adenohypophysis in vitro during inhibition of anterior pituitary hormone secretion from individual cell types

LHRH has previously been found to be the only known hypothalamic releasing factor which can specifically stimulate the release of the opioid dynorphin and other proenkephalin B-derived peptides from the rat adenohypophysis in vitro. In the present study the mechanisms that regulate dynorphin release were further characterized. It was examined whether or not dynorphin release from the adenohypophysis in vitro is altered during inhibition of the secretion of various anterior pituitary hormones. Rat anterior pituitary quarters were incubated in vitro and hormone release into the incubation medium was measured by RIAs. Somatostatin, dopamine, T3, dexamethasone, and 5 alpha-dihydrotestosterone were used to inhibit the secretion of GH, PRL, TSH, ACTH/beta-endorphin, or LH/FSH, respectively. GH, PRL, or beta-endorphin release was inhibited without affecting the simultaneous release of dynorphin A-(1-13)-like immunoreactivity (Dyn A1-13-IR). Concentrations of T3, somatostatin, or dopamine which were effective in suppressing the evoked and/or basal release of TSH, GH, or PRL, respectively, produced no effect on Dyn A1-13-IR release caused by high potassium concentration (40 mM) or LHRH (500 pM). The LHRH-induced release of LH and FSH was inhibited by the glucocorticoid dexamethasone or the androgen 5 alpha-dihydrotestosterone. Under these conditions, Dyn A1-13-IR release was also reduced. However, whereas LH release was completely blocked by 5 alpha-dihydrotestosterone, FSH and Dyn A1-13-IR release was reduced only by 50%. The release of FSH and Dyn A1-13-IR in vitro from anterior pituitary glands taken from rats, castrated 3 weeks before, was enhanced to a similar extent (about 2.5-fold); the simultaneous enhancement of LH release was significantly (P less than 0.005) greater (about 5-fold). We conclude that the mechanisms which regulate the release and/or biosynthesis of dynorphin and other proenkephalin B-derived peptides of the adenohypophysis are similar to those of the gonadotropins but different from those of any other anterior pituitary hormone, and may be more closely related with FSH release than LH release. These data support the view that dynorphin of the normal rat adenohypophysis may be localized in at least a subpopulation of gonadotrophs.     

The impact of euglycemia and hyperglycemia on stimulated pituitary hormone release in insulin-dependent diabetics

To study the influence of different blood glucose (BG) concentrations on the release of pituitary hormones, the effect of the simultaneous iv administration of LRH (200 micrograms), TRH (400 micrograms), and arginine (30 g/30 min) upon the serum concentrations of LH, FSH, TSH, PRL, and GH was determined in six male insulin-dependent diabetics. BG concentration was clamped by feedback control and an automated glucose-controlled insulin infusion system at euglycemic (BG 4-5 mmol/liter) or hyperglycemic (BG, 14-18 mmol/liter) levels. Increments in serum concentrations of LH, FSH, TSH, and PRL were similar in the euglycemic and hyperglycemic steady states, whereas the GH response to arginine was suppressed during the hyperglycemic clamp (P less than 0.01). Omission of exogenous insulin during hyperglycemia did not modify the observed hormonal responses. Thus, the release of LH, FSH, TSH, and PRL in response to adequate acute stimuli at the pituitary level is not modulated by hyperglycemia in insulin-dependent diabetes, while arginine-induced GH release is suppressed. Since the effect of arginine on GH is most likely mediated by an action on the hypothalamus, the data suggest that elevated glucose concentrations may exert their modulatory influence on GH secretion at the hypothalamic rather than at the pituitary level.     

Progesterone induced modulations of serum hormonal profiles in adult male and female rats.

The impact of progesterone on serum hormonal profiles in the presence and absence of gonads was studied in adult male and female albino rats. Progesterone was administered intramuscularly for 30 days at a dose of 1 mg/100g body weight/day. Serum testosterone, estradiol and prolactin titres decreased in male and female rats with intact gonads given progesterone. While the levels of both luteinizing hormone (LH) and follicle stimulating hormone (FSH) decreased in male rats with intact gonads, only FSH decreased in female rats. The inhibitory effect of progesterone on serum estradiol, LH, FSH and prolactin persisted even after gonadectomy in male rats. This persistent inhibitory effect of progesterone was also seen on serum testosterone, FSH and prolactin levels of female rats. Ovariectomy modified progesterone action on LH, as is evident from the decreased levels of LH observed only in ovariectomized rats given progesterone. While progesterone had no effect on serum T3 and T4 in male rats, gonadectomy altered the levels of T3 and T4 in male and female rats. Progesterone increased the levels of T3 and decreased the levels of T4 in ovariectomized rats. Growth hormone (GH) and thyroid stimulating hormone (TSH) levels seem to be resistant to changes in progesterone titre, irrespective of the sex and gonadal status. The present data suggest the existence of a sex specific effect of progesterone on gonadotrophins. The data on T3, T4 and TSH reveals that progesterone has no effect on the pituitary thyroid axis in the presence of gonads.     

垂体激素水平对蛛网膜下腔出血患者临床诊断和预后的意义

目的观察蛛网膜下腔出血患者垂体激素水平的变化,探讨其对蛛网膜下腔出血临床诊断和预后的意义。方法采用血液生化自动分析仪测定58例蛛网膜下腔出血患者治疗前后和健康体检者血浆中皮质醇（COR）、促黄体生成素（LH）、生长激素（GRH）、促卵泡激素（FSH）、促甲状腺激素（TSH）、泌乳素（PRL）水平。结果蛛网膜下腔出血男性和女性患者治疗前后血浆COR、LH、GRH、FSH和PRL水平相比均具有统计学差异（P均〈0.05）,TSH水平无统计学差异（P均〉0.05）。以Hunt和Hess评级系统进行评级,Ⅲ~Ⅴ级蛛网膜下腔出血患者治疗前COR、LH、FSH和PRL水平与0~Ⅱ级患者相比升高,GRH水平下降（P均〈0.05）,TSH水平无统计学差异（P〉0.05）。结论蛛网膜下腔出血患者常伴随垂体激素分泌异常状态,检测其体内的COR、LH、GRH、FSH和PRL水平对蛛网膜下腔出血的临床诊断和预后判断具有重要意义。     

The localization of gonadotrophs in normal adult male and female rats

We investigated the localization of LH and FSH cells within the pituitary glands of normal adult rats. Groups of four female rats were decapitated at one of five different times during the estrous cycle. Four male rats were also decapitated. Paired horizontal flip-flopped serial paraplast sections from the dorsal, middle, and ventral portions of each pituitary gland were stained. For each pair, one section was stained with antirat LH-S4 and the other section with antirat FSH-S7, by the unlabeled antibody peroxidase-antiperoxidase method. All immunoreactive cells were counted, and the area of pars distalis in each section was determined. We studied the spatial distribution of gonadotrophs within the sections and determined if a polarization along the antero-posterior axis existed. In the "sex zone" of the pars distalis, the cross-sectional area of LH cells and the percentages of LH cells that also contained FSH and vice versa were determined and compared with those obtained from the entire pars distalis. Additional sections were stained for TSH, ACTH, GH, or PRL, and the distribution of stained cells was compared with that of those that stained for LH or LH/FSH, particularly in the sex zone and in the pars intermedia. The results indicate that 1) gonadotrophs are more evenly distributed dorsoventrally within the pars distalis of male rats than in that of female rats; 2) an antero-posterior polarity in gonadotropic distribution is more pronounced in male rats than in female rats; 3) gonadotrophs containing only LH are less numerous in male than female rats, and in the female tend to be centrally located within the pars distalis; 4) the sex zone contains PRL cells and gonadotrophs, and the percentages of gonadotrophs that contain LH or LH and FSH are not different from those of the entire pars distalis; 5) LH, and occasionally LH/FSH cells, are present between lobules of immunoreactive ACTH cells in the pars intermedia; and 6) LH cells in the pars intermedia are smaller than those in the sex zone or entire pars distalis.     

Effects of gonadectomy and chlorpromazine treatment on prolactin, LH, and FSH secretion in young and old rats of both sexes

Old male rats, and female rats in the states of senile persistent estrus (PE) and senile repetitive pseudopregnancy (RPD) were compared with young controls in the change of serum prolactin (PRL), LH, and FSH concentrations after gonadectomy and chlorpromazine (CPZ) treatment. Old male rats (18–21-month old) and PE (12–15-month old and 18–19-month old) and RPD (18–23-month old) female rats showed higher serum PRL levels. In both young and old male rats, orchidectomy did not cause any significant changes in serum PRL levels. The effect of ovariectomy on serum PRL levels was smaller in old female rats. CPZ treatment increased serum PRL levels in young controls of both sexes, 12-month old males and 12–15-month old PE rats. The sexual difference in PRL secretion in response to CPZ was observed at these ages. In 18–21-month old males and 18–23-month old females, CPZ did not significantly increase serum PRL levels. These results suggest that the higher serum PRL levels in intact old male and female rats may be partly due to the lowered activity of the hypothalamic dopaminergic inhibition. The changes in serum LH levels in response to ovariectomy were smaller in old female rats than in young controls, whereas male rats did not show any age-related changes in response to orchidectomy on serum LH levels. There was no appreciable age-difference in the increase in serum FSH levels after gonadectomy in either sex.     

Evidence for a thyrotropin inhibitory effect of histamine in man.

Because of certain side effects of cimetidine therapy which may be hormonally mediated (e.g. gynecomastia), there has been recent interest in the possible endocrine effects of this H2 histamine receptor-blocking agent used in the treatment of peptic ulcer disease. Accordingly, the effect of chronic cimetidine therapy on anterior pituitary function was examined in 12 adult men with mild peptic ulcer disease. TRH and insulin-hypolycemic stimulation tests were performed by standard methods. Serum for TSH and PRL RIA was obtained after TRH; serum for GH, cortisol, and PRL RIA was obtained after insulin-induced hypoglycemia. In addition, serum for LH, FSH, testosterone, and PRL was obtained every 4 h for 24 h. After these baseline studies, 300 mg cimetidine were administered orally 4 times a day for 4--8 weeks and the studies were repeated as before. Chronic treatment with cimetidine caused a significant increase in the peak TSH response to TRH at 30 min (mean peak TSH value before cimetidine, 7.0 microU/ml; after cimetidine, 10.2 microU/ml; P less than 0.05) as well as a significant increase in the TSH area under the curve. There was no statistically significant effect of cimetidine on basal TSH or basal or stimulated PRL secretion. Cimetidine had no effect on the GH, PRL, or cortisol response to insulin-induced hypolycemia or the 24-h secretion of LH, FSH, testosterone, or PRL.     

Increased sensitivity to the negative feedback effects of testosterone induced by hyperprolactinemia in the adult male rat

High plasma levels of PRL induced by transplants of two donor pituitaries under the kidney capsule of adult male rats resulted in a prolonged suppression of plasma levels of LH and FSH although testosterone levels were maintained within normal limits. Castration of rats with pituitary transplants resulted in a normal though delayed rise in serum levels of both LH and FSH to levels equivalent to those in normal castrated controls. This increase in gonadotropin levels occurred in spite of maintenance of elevated PRL levels. Two experiments were carried out in which testosterone was restored after castration by Silastic testosterone-containing implants of various lengths (Exp 1:60, 30, and 10 mm; Exp 2: 30, 20, 10, 5, and 2 mm). In both experiments 60- and 30-mm testosterone implants prevented the postcastration rise in LH and FSH in both control and hyperprolactinemic rats. However, although the shorter testosterone implants delayed this rise in control rats, levels of LH and FSH increased by 4 days and were not significantly different from castrated rats without testosterone implants by 15 days after castration. In contrast, this rise in gonadotropins was abolished or considerably delayed by the shorter implants in hyperprolactinemic rats, demonstrating an increase in sensitivity of the hypothalamic pituitary axis to the negative feedback effects of testosterone in these animals. These results suggest that 1) to maintain suppression of gonadotropin secretion in hyperprolactinemia high levels of PRL alone are insufficient and gonadal steroids are required, and 2) high levels of PRL appear to sensitize the hypothalamic-pituitary axis to the negative feedback effects of gonadal steroids.     

The effect of neoplasia-induced hypercalcemia on the neuroendocrine axis of the Fischer rat

The effects of neoplasia-induced hypercalcemia on the hypothalamic-pituitary axis of the Fischer rat were determined by measuring the responses of TSH to TRH, PRL to TRH and haloperidol, and LH to LHRH in 3 groups of 8 rats prior to and at 4 and 8 days after transplantation of a Leydig cell tumor. The mean serum calcium was 8.2 ± 0.2 mg/dl in 8 Fischer rats pretransplantation; had risen at 4 days posttransplantation to 9.8 ± 0.2 mg/dl; and at 8 days was 11.2 ± 0.1 mg/dl. TSH response to TRH was greater in the pretransplant rats than in the groups studied at 4 and 8 days posttransplant. Basal PRL levels and PRL responses to TRH and haloperidol were less in the groups studied at 4 and 8 days posttransplant. Basal LH values were similar in all 3 groups, but the LH response to LHRH was less for the posttransplant groups. The TSH response to TRH, PRL responses to TRH and haloperidol, and LH responses to LHRH were less in the 8 days posttransplants than in the groups studied at 4 days posttransplantation. There were significant negative correlations between TSH (r = ?0.79) and PRL (r = ?0.80) responses to TRH, PRL responses (r = ?0.94) to haloperidol and LH responses (r = ?0.91) to LHRH and the serum calcium. The results indicate that increasing levels of serum calcium following Leydig cell tumor transplantation are associated with suppression of adenohypophysial release of TSH, PRL, and LH; the degree of suppression is related to the magnitude of hypercalcemia achieved in this model.