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PubMed2005

Castration of piglets: the analgesic effects of intratesticular and intrafunicular lidocaine injection.

OBJECTIVE: The aim of this study was to evaluate the analgesic effect of intratesticular and intrafunicular lidocaine for the surgical castration of piglets and to investigate the degree of nociception induced by lidocaine injection. STUDY DESIGN: Prospective controlled experimental study. ANIMALS: Forty-seven male Norwegian landrace piglets with normal testicular anatomy, aged 22 (+/-2.6 SD) days and weighing 7.4 +/- 1.4 kg. MATERIALS AND METHODS: Anaesthesia was induced and maintained using halothane delivered in oxygen. End-tidal halothane was stabilized at 1.3% for 20 minutes before mean arterial blood pressure (MAP) pulse rate and electroencephalography (EEG) monitoring began. After 5 minutes of data collection, scrotal skin was desensitized with lidocaine before either an intrafunicular (IF) (n = 15) or an intratesticular (IT) (n = 16) lidocaine injection was made. Pigs in the control group (n = 16) did not receive lidocaine. Ten minutes later, a scalpel and an emasculator were used to cut the funiculus spermaticus. The MAP, pulse rate and EEG were monitored continuously for 5 minutes after castration. RESULTS: During castration, MAP increased significantly, while pulse rate and EEG theta power fell significantly more in control, compared with the IT or IF groups. EEG alpha power fell more in the control group than in the IF group. No significant differences were found between the IF and IT groups. EEG, MAP and pulse rate responses to castration in the control group were significantly larger than the response to lidocaine injection. CONCLUSION/CLINICAL RELEVANCE: Injecting lidocaine into the funiculus spermaticus or into the testes is effective in reducing signs of nociception caused by castration. Lidocaine injection is less noxious than castration without local anaesthetic.

Anesthesia, General↗
PubMed1980

Effects of castration and testosterone substitution on body composition and muscle metabolism in rats.

Male weanling Wistar rats were castrated or sham-operated and followed for 12 weeks without substitution or with large (2 mg . 14 days-1) or small (0.2 mg . 14 days-1) intramuscular dose of testosterone enantate. Castration without substitution was associated with lower body weight and smaller fat cell sizes in different adipose tissue depots. The epididymal and caudal subcutaneous depots were the most sensitive to castration. The percentage of fast-twitch high-oxidative (type II A) muscle fibers decreased in the non-substituted castrated animals. There was a decrease in phosphorylase and lactate dehydrogenase activities in the white portion of the gastrocnemius muscle of the castrates. These changes were reversed by the large dose of testosterone. Removal of testosterone by castration thus seems to "feminize" male rats with respect to body composition and muscle metabolism.

Adipose Tissue↗
PubMed1984

Castration prolongs tolerance of young male rats to pulmonary O2 toxicity.

We tested the hypothesis that the normal loss of tolerance of neonatal rats to prolonged hyperoxic exposure at around 1 mo of age might be related to the marked increase in sex hormones occurring around this period. Male rats castrated at 20 days of age demonstrated significantly increased survival in greater than 95% O2 compared with sham-operated rats when exposed to high O2 at various ages greater than 45 days [castrated, 115 of 166 (69%) vs. sham, 59 of 156 (38%) (P less than 0.001)]. Testosterone replacement led to survival rates comparable with sham-operated rats [30 of 87 (34%)]. No such protective effect was observed in female rats [survival: ovariectomy, 16 of 33 (48%) vs. sham, 14 of 28 (50%)]. The improved survival in the older castrated males was not associated with an increase in lung antioxidant enzymes, which is normally seen in O2-tolerant neonatal rats. Castration did result in marked morphological lung changes, including significantly enlarged lung volumes (4.54 +/- 0.72 vs. 3.76 +/- 0.29 ml/100 g) and terminal air spaces [mean linear intercept (LM) = 51.6 +/- 5.0 vs. 46.3 +/- 4.1 micron (P less than 0.001)]. Testosterone replacement also prevented these morphological changes. The altered lung growth 1) may be related to the influence of other endocrine imbalances after castration and 2) may be an important factor in the relative O2 tolerance of the castrated male rats beyond the neonatal period.

Animals↗
PubMed2006

Docetaxel followed by castration improves outcomes in LNCaP prostate cancer-bearing severe combined immunodeficient mice.

PURPOSE: Androgen ablation is the standard initial treatment for advanced prostate cancer; however, tumors eventually develop androgen independence and become incurable. Chemotherapy is commonly used after hormone treatment fails but has not shown significant survival benefit. Studies suggest that androgen ablation can select for a population of hormone-independent cells that are also relatively chemotherapy resistant. Thus, it may be therapeutically advantageous to target prostate cancer with chemotherapy before hormone ablation. This study was undertaken to determine the relative efficacy of such an approach in a preclinical model of prostate cancer. EXPERIMENTAL DESIGN: Severe combined immunodeficient mice bearing human LNCaP prostate tumors were treated with docetaxel and/or surgical castration applied singly, concurrently, or in different sequences. Treatment efficacy was determined by tumor volume and growth delay measurements. The extent of apoptosis in tumors in response to treatments was assessed via terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) assays. In addition, Western blots were done to study the relative expression of Bcl-2 and Bax in the tumors. RESULTS: Docetaxel followed by castration showed the most potent antitumor effects. In contrast, with the exception of castration alone, castration followed by docetaxel produced the least antitumor activity. TUNEL assays confirmed that the density of apoptotic tumor cells was significantly greater for docetaxel followed by castration than for any other treatment. In tumors of mice treated with single modality therapies, Bax to Bcl-2 ratios decreased significantly after castration, whereas this ratio remained high after docetaxel treatment. CONCLUSION: A treatment sequence of docetaxel followed by hormone ablation may be more effective in treating prostate cancer than concurrent docetaxel/hormone therapy or hormone ablation followed by docetaxel.

Animals↗
PubMed1975

Effect of castration upon hypothalamic luteinizing hormone releasing factor (LH-RF).

The effect of castration upon hypothalamic LH-RF synthesis and content was determined in mature male rats. In each single experiment 20 hypothalami from both normal and 60-day-castrated rats were bisected into symmetrical portions. For the determination of LH-RF synthesis 20 hypothalamic halves were incubated for 120 min. After incubation the tissue was homogenized in medium containing 1 N acetic acid, and centrifuged; 1.0 ml of the supernatant was used to test LH-RF activity. In the other 20 halves, hypothalamic LH-RF content was determined: the samples were homogenized without incubation in 1 N acetic acid, centrifuged, and LH-RF activity was tested in 1.0 ml of the supernatant. LH-RF activity was determined in vivo in ovariectomized rats pre-treated with estrogen-progesterone by measuring, by radioimmunoassay, the LH modifications in serum after the i.v. administration of the extracts. Hypothalamic LH-RF content was significantly higher in control than in castrated rats (p is less than 0.001). After incubation there were no changes in the LH-releasing potency of control hypothalami compared with non-incubated tissue, whereas a significant increase (616%) was found after the incubation of hypothalami from castrated rats. On the other hand, after incubation LH-RF activity was higher (p is less than 0.02) in castrated than in control hypothalami. These results suggest that castration stimulates the release and synthesis of hypothalamic LH-RF in male rats.

Animals↗
PubMed1984

Effects of castration and ethanol on amygdaloid substance P immunoreactivity.

These studies were designed to determine the effects of castration and ethanol (ETOH) on the relative content of substance P (SP) immunoreactivity in the hypothalamus and the central and medial amygdaloid nuclei (CM-AM). Differences visualized immunocytochemically between saline-treated intact and castrated rats indicated that a visible decrease in the number and intensity of immunostained fibers within the CM-AM occurred following castration. Conversely, the number of labeled fibers and the intensity of the reaction product was greater in castrated rats treated with ETOH as compared to the castrated rats receiving only saline. In ETOH-treated intact animals, the number of SP-containing fibers of the CM-AM was slightly greater than the saline-treated intact controls. Similar results were seen for specific regions of the hypothalamus although they were less pronounced than that visualized in the CM-AM. These data indicate that both castration and administration of ETOH affects hypothalamic and amygdaloid content of SP, and also suggests that ETOH may diminish the release of SP. Possible interactions between SP and luteinizing hormone-releasing hormone are discussed.

Amygdala↗
PubMed1985

Chronic morphine treatment induces hypersensitivity to testosterone-negative feedback in castrated male rats.

Studies were undertaken to determine the effects of chronic stimulation of opiate receptors on the negative feedback effects of testosterone (T) on luteinizing hormone (LH) secretion in the male rat. In an initial study, castrated male rats received replacement levels of T (2 ng/ml) or chronic morphine (M) treatment for 7 days. When initiated at the time of castration, both T and M treatments prevented the castration-induced hypersecretion of LH. However, when the treatments commenced 2 weeks after castration, only T restored LH secretion to the low levels seen in intact rats. In a second study, rats castrated 2 weeks previously were exposed to chronic M or placebo (control) treatment in the presence of various dosages of T. In rats receiving T alone, LH secretion was unaffected at T levels up to 600 pg/ml serum, but thereafter there was a dose-dependent suppression of LH release by T. Serum T levels which reduced LH secretion by 50% were estimated to be 966 pg/ml. In contrast, in castrated rats receiving both M and T treatment, a 50% reduction in LH secretion was estimated to be at 300 pg T/ml serum and maximal inhibition of LH secretion was achieved at serum T levels of greater than 600 pg/ml. Neither T alone nor M plus T treatment altered the responsiveness of the anterior pituitary to LHRH in vitro. These findings indicate that M may enhance the sensitivity of the hypothalamus to T feedback by approximately 3-fold and raise the possibility of the existence of an opioid-sensitive neural component which may modulate the negative feedback effects of T on LH secretion.

Animals↗
PubMed1993

Castration effects on the gonadotrope cell populations of the fetal sheep pituitary in late gestation.

This immunocytochemical study focused on the role of fetal gonads in the regulation of gonadotrope cell populations in the fetal sheep pituitary in late gestation. Male and female sheep fetuses were castrated at 112-115 days of gestation and maintained in utero until 139-140 days gestation when their pituitaries were collected. Intact twins served as controls. The percentages of the different gonadotrope cell populations (i.e. the number of gonadotrope cells vs. the total number of the pituitary cell counted) and the mean cell area were determined. Castration did not affect the LH cell percentage in either sex but resulted in a decrease in the individual LH cell areas of both males and females (46.4 +/- 0.6 vs. 51.6 +/- 0.4 microns 2, p < 0.01, in males and 43.0 +/- 0.5 vs. 50.0 +/- 1.1 microns 2, p < 0.01, in females). By contrast, the FSH cell percentage was increased about twofold in castrated fetuses when compared to intact animals (3.5 +/- 0.3 vs. 1.6 +/- 0.3, p < 0.01, in males and 2.3 +/- 0.1 vs. 1.1 +/- 0.3, p < 0.02, in females). Moreover, castrated males had higher FSH cell percentages than castrated females (p < 0.02). The individual FSH cell area was smaller in castrated fetuses than that in controls (44.7 +/- 1.4 vs. 51.2 +/- 1.4 microns 2, p < 0.05, in males and 42.1 +/- 0.8 vs. 51.6 +/- 0.8 microns 2, p < 0.01, in females).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effects of castration and sex steroids on sexually dimorphic development of the mouse submandibular gland.

The aims of this study were to characterize sexual dimorphism in the submandibular glands of young adult mice and to determine how sex differences arise during postnatal development. In the mouse submandibular glands, prominent sexual dimorphism was observed at 30 days of age, when the male gland was superior in both the relative occupied area (ROA) and the mitotic rate of the granular convoluted tubules (GCT) to those of the female. By neonatal castration, this sexual dimorphism was abolished, and the intraglandular structures of castrated males were similar to those of normal females. In castrated mice of both sexes, daily treatment with testosterone and 5 alpha-dihydrotestosterone for 10 days from 20 days induced only the ROA of the GCT to increase to the normal male levels but not those of the other three regions of the glands, the acini, intercalated ducts and excretory striated ducts. Testosterone responsiveness of the glands, considering both the glandular weight gain and the mitotic rate of the GCT, was significantly higher in castrated males than in castrated females. On the other hand, 17 beta-estradiol had no effect on the glands of castrated mice. Therefore, the present study suggests that the testicular hormones are responsible for the masculine development of GCT of the glands, but not the ovarian hormones, and that there is a sex difference in the responsiveness of the glands to testosterone, which is more effective in males than in females.

Animals↗
PubMed1979

Administration of gonadal steroids to the castrated male rat prevents a decrease in the release of gonadotropin-releasing hormone from the incubated hypothalamus.

The influence of testosterone on gonadotropin-releasing hormone (GnRH) secretion was assessed indirectly by altering the serum testosterone concentration of male rats and measuring GnRH release from their incubated hypothalami 1 wk later.GnRH release from hypothalami of castrated rats was 13.4+/-1.2 (SE) pg/h, compared to 35.3+/-3.8 pg/h from hypothalami of intact rats (P < 0.001). GnRH release from the hypothalami of castrated rats treated with testosterone propionate, 100 or 500 mug daily, was 25.0+/-3.4 pg/h and 27.9+/-3.6 pg/h, which is significantly greater (P < 0.05 and P < 0.01, respectively) than that from hypothalami of castrated rats treated only with sesame oil.A similar decrease in GnRH release from hypothalami of hypophysectomized rats and prevention of this decrease by treating the hypophysectomized rats with testosterone propionate is evidence that the observed effects of testosterone are not mediated via luteinizing hormone and(or) follicle-stimulating hormone secretion. Treatment of castrated rats with either dihydrotestosterone propionate or estradiol benzoate also prevented the decrease in GnRH release from the hypothalami of castrated rats. We conclude that testosterone, dihydrotestosterone, and estradiol all prevent the decrease in GnRH release from hypothalami of castrated rats treated with these steroids. The possibility exists that these steroids may also maintain GnRH secretion in vivo.

Animals↗
PubMed1991

Castration.

Castration is not a metaphor within the array of psychoanalytic theories, but a pathological belief operative in the unconscious, which originated during the period of childhood sexuality. Of the two major anxieties, separation and castration, castration anxiety is the most overlooked in clinical discourse and theoretical awareness. Castration conflicts have a developmental history and are composed of phases as much as separation-individuation is. These extend from the preoedipal to the oedipal years and beyond and, as separation conflicts, persist throughout life. Clinical material is demonstrated from across the diagnostic spectrum and all developmental levels. Phylogenetic studies are corroborative. As loss of love is a wider derivative of separation anxiety, castration anxiety radiates out to wider fears of invasion and injury to the body. The transference neurosis is more attuned to encompass separation than castration conflicts. This stratum of psychopathology makes reconstruction and the recovery of historical data indispensable.

Adult↗
PubMed1977

Differential response of luteinizing hormone-releasing hormone in the basal hypothalamus and the preoptic area following anterior hypothalamic deafferentation and/or castration in male rats.

Serum LH, FSH and LHRH concentrations and the LHRH content in the medial basal hypothalamus (MBH) and the preoptic area (POA) were measured by radioimmunoassay in male rats 33 days after anterior hypothalamic deafferentation (AHD) and/or castration. In castrate rats following AHD, there was a significant decrease in serum LH, FSH, and LHRH concentrations, whereas, in intact rats, serum LH was elevated in AHD over the sham AHD rats. Castration and AHD each caused a significant fall in the LHRH levels in the MBH; the decline was more pronounced in rats undergoing both castration and AHD. In contrast, deafferentation in intact and castrate rats resulted in the accumulation of LHRH activity in the POA. These studies support the suggestion that a) a substantial amount of LHRH normally found in the MBH of intact and castrate male rats originates in the rostral regions and, b) the LHRH-containing neural elements within the MBH have the competence to respond to a loss in the circulating testicular steroids.

Animals↗
PubMed1983

Retarded development of castration cells after adrenalectomy or sham adrenalectomy.

Castration produces hypertrophy of gonadotropes, stimulates a shift in storage patterns to cells that store LH and FSH together, and results in a significant rise in serum LH and FSH within 12 h. Adrenalectomy retards and attenuates this postcastration rise for 24 h (1, 2). In this study, we examined the effect of adrenalectomy on castration cell morphological development. The increased percentages of LH and FSH cells that are seen normally 24 h after castration were not seen if adrenalectomy or sham adrenalectomy was performed simultaneously. In fact, the percentages of LH cells were below control values. The expansion in the average area of LH and FSH cells was also retarded after simultaneous castration and adrenalectomy or sham adrenalectomy. The corticotrope population responded as expected to adrenalectomy and the surgical stress of castration, with an increase in the percentage and area of stained cells as well as partial degranulation. The serial sections showed no ACTH staining in gonadotropes after any of the surgical treatments. The gonadotropic storage patterns were altered, however. In castrated rats exposed to simultaneous adrenalectomy or sham adrenalectomy, the percentage of LH/FSH cells was reduced from 70% of gonadotropes in intact rats to 30%. Over 60% of the serially sectioned gonadotropes stored only one hormone, and these monohormonal cells tended to occur in clusters. Our experiments thus show that the gonadotropin storage pattern can be shifted with experimental manipulation. This may also reflect shifts in the site of hormone storage within a given cell. We suggest that adrenalectomy or sham adrenalectomy retards the postcastration rise in gonadotropins by preventing the immediate expansion of the granulated cell population and causing an apparent loss in the numbers of certain types of gonadotropes.

Adrenalectomy↗
PubMed1986

Alpha and luteinizing hormone beta messenger ribonucleic acid (RNA) of male and female rats after castration: quantitation using an optimized RNA dot blot hybridization assay.

In this study we examined the changes in alpha and LH beta mRNAs in anterior pituitaries of male and female rats after castration. mRNA concentrations were measured by an optimized RNA dot blot hybridization assay. Rat alpha and LH beta cDNAs were nick-translated to specific activities of 2-5 X 10(8) cpm/micrograms and were used as hybridization probes. The total RNA per assay, RNA per dot, and saturating amounts of probe were optimized. The intra- and interassay coefficients of variation were 5% and 28%, respectively. Both alpha and LH beta mRNA concentrations increased after castration, but marked differences were observed in the kinetics of responses in male and female rats. In males, alpha and LH beta mRNAs were increased by 24 h postcastration (by 25% and 38%, respectively), and 4- to 5-fold increases over intact controls were evident by 18 days. Alpha mRNA rose rapidly and had doubled by 2 days, whereas LH beta mRNA concentrations showed a similar increase by 6-7 days postcastration. The slower rise in LH beta mRNA was associated with a transient decline in serum and pituitary LH concentrations between 2 and 6 days after castration. In female rats, alpha mRNA increased more slowly. Alpha concentrations had doubled by 10 days, while a similar increase in LH beta mRNA occurred 7 days after castration. Thereafter, both subunit mRNAs continued to rise, and by day 20 alpha mRNA was increased 5-fold and LH beta mRNA 16-fold over values in intact females. Serum and pituitary LH concentrations rose gradually, and both were increased by 7-10 days after castration. The increase in serum and pituitary LH followed a time course similar to that of the progressive rise in LH beta mRNA concentrations. These data show that an increase in steady state LH subunit mRNA concentrations is one of the mechanisms involved in increased gonadotropin biosynthesis and secretion after castration. The kinetics of LH subunit mRNA and LH secretory responses are different in male and female rats and suggest that the concentration of LH beta mRNA may be a limiting factor in LH secretion.

Animals↗
PubMed1976

Prolactin binding sites in the male rat liver following castration.

Specific binding sites for prolactin (PRL) have been detected in membrane preparations from the liver of the male rat following castration. The magnitude of the increased binding following castration varied with the age of the animals and with the time after castration. The effect of castration did not appear to be PRL mediated, since increases or decreases of serum PRL levels after pharmacological agents had no effect on PRL binding. The pituitary, however, seems to have a critical role in mediating the increase in PRL binding. Adrenalectomy did not influence the extent of binding of PRL after castration. Testosterone administration, however, completely prevented the increased PRL binding which followed castration. These studies suggest that testosterone has a modulating effect on hepatic PRL binding sites. The maintenance of such binding activity requires not only PRL, but also a functioning pituitary.

Adrenal Glands↗
PubMed1991

Effect of aging, castration, and testosterone administration on ribonuclease and ribonuclease-inhibitor activities in the prostate of rats.

Free ribonuclease (RNase)-inhibitor activities in both ventral and dorsal prostates had their highest peaks in 4-week-old rats and smallest peaks in around 7-week-old animals. Total RNase activity in the ventral prostate decreased overall with age, while that in the dorsal prostate increased. No significant amount of free RNase activity was found in either prostate. Weight, protein content, and free RNase-inhibitor activity in both prostates decreased after castration and increased after administration of testosterone to castrated rats. Total RNase activity in the ventral prostate was increased by castration and decreased by testosterone administration. In the dorsal prostate, total RNase activity had two peaks, 7 d after castration and 2 d after testosterone administration. A large amount of free RNase activity was found in the ventral prostate 7 d after castration and this activity was decreased by testosterone administration. In the dorsal prostate, free RNase activity was not detected after castration and testosterone administration. These results suggest that changes in the level of RNase-inhibitor in both prostates are involved in the regulation of their RNA content through the control of free RNase activity.

Aging↗
PubMed1983

[Effects of castration on the gonadotropin level in prepubertal males--a study on pubertal development].

The effects of prepubertal castration on circulating levels of LH and FSH were examined longitudinally in 3 male pseudohermaphrodites (1 yr., 6 yrs., 9 yrs.) and one Lt. monorchid (7 yrs.), and gonadotropin levels of prepubertal anorchism (9 yrs.) were also studied longitudinally. After castration, plasma LH and FSH concentration in the patient 1 yr. of age elevated significantly and progressively, but in two other patients 6 and 7 yrs. of age, a significant elevation of plasma LH and FSH was not observed from 90 to 450 days after the castration. Plasma LH and FSH concentration of one patient 9 yrs. of age, castrated at 1 yr., showed prepubertal values from 9 to 11 yrs. of age, and the abrupt elevation of LH and FSH occurred at 11-2/12 yrs. of age. From these observations we concluded that although castration in early childhood resulted in an immediate elevation of gonadotropin levels, a significant elevation of gonadotropin did not occur in midchildhood castration. These findings have also confirmed the evidence that the hypothalamic-pituitary-gonadal negative feedback mechanism is operative in early childhood, and supported the action of a CNS inhibitory mechanism which restrains the gonadotropin synthesis and secretion and inhibits puberty during the interval of mid-childhood.

Castration↗
PubMed1976

Effect of unilateral and bilateral castration and cryptorchidism on serum gonadotrophins in the rat.

The effects of unilateral and bilateral cryptorchidism and castration on serum concentrations of testosterone, FSH and LH in adult male rats were examined. The results provide no evidence for compensatory growth or development of the remaining scrotal testes up to 32 days after unilateral castration, although the scrotal testis of unilaterally cryptorchid rats showed enlargement when compared with those of control rats (P less than 0 - 05) at 32 days. Unilateral treatments had few significant effects on serum hormones, but testosterone was increased on day 4 (P less than 0 - 05) in unilaterally cryptorchid rats and on day 32 (P less than 0 - 05) in unilaterally castrated rats, compared with controls, and FSH levels were higher in unilaterally castrated rats on day 16 (P less than 0 - 05). Bilateral cryptorchidism caused an increase in serum FSH within 4 days (P less than 0 - 05) and in serum LH by 8 days (P less than 0-05) after surgery, with both hormones reaching levels double those found in control rats (P less than 0 - 01) by day 16, while testosterone levels were maintained at or above control values. Bilateral castration resulted in a marked decrease in testosterone levels (P less than 0 - 01) and a sharp increase in serum gonadotrophins. FSH had nearly doubled (P less than 0 - 01) and LH had increased fourfold (P less than 0 - 01) 4 days after castration, their levels reaching 773% (LH) and 287% (FSH) of control values by 32 days (P less than 0 - 01). The observations support the hypothesis of a separate, testosterone-independent feedback system of the testis on the hypophysis.

Animals↗