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Transient nerve damage following intubation for trans-sphenoidal hypophysectomy.

PURPOSE: To describe a case of transient lingual and hypoglossal nerve damage following intubation for a trans-sphenoidal hypophysectomy. CLINICAL FEATURES: A 56-yr-old acromegalic man was scheduled for trans-sphenoidal hypophysectomy. He had been treated with octreotide six months previously which had reduced the swelling of the tongue to an acceptable degree to the patient. During the anesthetic procedure there were no problems. The intubation was performed without any difficulty, no force had been used to place the endotracheal tube, a throat pack was inserted and, before extubation, an oro-gastric tube was inserted. Three days after surgery the patient complained of numbness and swelling of the left side of the tongue, he had difficulty in moving the tongue, speaking difficulties and problems in swallowing food were noted. Also taste was lost on this side of the tongue. Left lingual and hypoglossal nerve damage was diagnosed, which was confirmed by the neurologist. After four months of intensive physiotherapy and speech therapy, the symptoms disappeared. CONCLUSION: This is a report of a very rare complication of lingual and hypoglossal nerve damage in an acromegalic patient. This incident suggests forceful laryngoscopy, hyperextension of the head and the throat pack (tightly packed in the oropharynx) can result in injury of the lingual and the hypoglossal nerves.

Acromegaly↗

Effects of testosterone, hypophysectomy and growth hormone treatment on clofibrate induction of peroxisomal beta-oxidation in female rat liver.

Induction of peroxisomal beta-oxidation by clofibrate under altered hormonal states was investigated in female rat liver. Treatment of rats with clofibric acid (CPIB) caused a significant increase in hepatic peroxisomal beta-oxidation, with female rats being less responsive than males (4.2- vs 12.2-fold increase). However, testosterone treatment following ovariectomy of female rats resulted in an enhanced response to CPIB, giving an induction (11.7-fold) comparable to that seen in male rats. Hypophysectomy of female rats also enhanced the induction (8.2-fold compared with 5.1-fold), suggesting a suppressive effect of a pituitary-dependent factor on CPIB induction of peroxisomal beta-oxidation. Continuous infusion of growth hormone to the hypophysectomized female rats suppressed the enhanced induction nearly to the initial level (6.1-fold). The stimulatory effects of testosterone and hypophysectomy on the enzyme induction were additive. These findings suggest the involvement of growth hormone, as well as male sex hormone, in regulating the responsiveness to CPIB induction of peroxisomal beta-oxidation in rat liver.

Animals↗

Effects of hypophysectomy and dexamethasone treatment on plasma beta-endorphin and pain threshold during pregnancy.

During pregnancy, rats and humans show an increase in pain threshold that is mediated by an endorphin system. In order to determine whether plasma beta-endorphin and/or other factors of pituitary origin are involved in pregnancy-induced analgesia in the rat, the effects of hypophysectomy (day 12 of pregnancy) or pharmacological suppression of pituitary function via dexamethasone administration (day 14-21 of pregnancy) were investigated. Hypophysectomy did not affect either the magnitude of the increase or the pattern of change in pain threshold despite the resulting decrease in stress-induced plasma beta-endorphin concentrations. However, the observed effect of the surgical and/or postsurgical procedure on pain threshold confounded unequivocal interpretation of these results. Pharmacological suppression of pituitary function with dexamethasone (2 micrograms/ml), a non-invasive procedure, also produced a significant decrease in resting plasma beta-endorphin levels. As was observed for surgical removal of the pituitary gland, this treatment did not produce a significant alteration in the magnitude of the increase in jump threshold. Furthermore, no correlation was found between plasma beta-endorphin concentrations and jump threshold values on day 21 of pregnancy. These results indicate that the pituitary gland does not play an essential role in the maintenance of opioid analgesia during pregnancy. It is suggested that pregnancy-induced analgesia depends on central rather than peripheral opioid systems.

Animals↗

Biosynthesis and transport of glycoproteins in the small intestinal epithelium of rats. I. Developmental change and effect of hypophysectomy.

The biosynthesis and intracellular transport of glycoproteins in duodenal absorptive cells of intact rats at 6 and 24 days and hypophysectomized rats at 24 days of age were studied after 20 min intralumenal pulse-labeling of D-[3H]galactose, L-[3H]fucose, or D-[3H]mannose. Autoradiographic studies showed that the incorporation of sugars increased significantly in intact rats between 6 and 24 days. When rats were hypophysectomized at 6 days of age, the intestinal epithelium at 24 days incorporated D-[3H]galactose at a level significantly lower than that of intact rats at 24 days. Hypophysectomy also interfered with the developmental increase in D-[3H]mannose, but not in L-[3H]fucose, incorporation. Biochemical study indicated that the radioactivity in the lipid-free acid-precipitable glycoproteins in the intestine of 24-day-old intact rats at 20 min after D-[3H]galactose injection was 129% and 97% higher than that in 6-day-old rats and in 24-day-old hypophysectomized rats, respectively. The patterns of intracellular transport of newly synthesized galactosylated or fucosylated glycoproteins in all animal groups were similar; the labeled glycoproteins were initially present in the Golgi and were transported through the smooth endoplasmic reticulum to either the lateral membrane or the brush-border membrane within 60 min after the injection of labeled sugars. The proportion of labeled glycoproteins that migrated to the brush-border membrane, however, increased about twofold in the intact rats between 6 and 24 days of age at 60-240 min after D-[3H]galactose injection. Hypophysectomy interfered with developmental increase in the transport of glycoproteins from the apical cytoplasm to the brush-border membrane. It was concluded that the incorporation of monosaccharide precursors into glycoproteins and the proportion of newly synthesized galactosylated or fucosylated glycoproteins transported to the brush-border membrane increase during postnatal development. The developmental changes are regulated, at least partially, by the pituitary gland.

Animals↗

Hypophysectomy does not prevent development of striatal dopamine receptor supersensitivity induced by repeated neuroleptic treatment.

Hruska et al. (1980) reported that hypophysectomy prevented the onset of dopamine receptor supersensitivity. We have repeated this investigation administering haloperidol (0.75 mg/day) or sulpiride (2 X 15 mg/day) or saline for 17 days, followed by a 3 day drug washout period, to sham-operated or hypophysectomised rats. Haloperidol or sulpiride pretreatment caused an enhancement of apomorphine-induced stereotyped behaviour and increased the number of specific striatal [3H]spiperone binding sites (Bmax) in both hypophysectomised and sham-operated animals compared to their respective saline controls. We conclude that hypophysectomy does not prevent the onset of striatal dopamine receptor supersensitivity induced by repeated neuroleptic treatment in the rat.

Animals↗

Depletion of peripheral-type benzodiazepine receptors after hypophysectomy in rat adrenal gland and testis.

We examined the effect of hypophysectomy in rats on peripheral-type benzodiazepine receptors in the adrenal gland and testis. Following removal of the pituitary, binding sites for [3H]Ro5-4864, a ligand selective for peripheral-type benzodiazepine receptors, are depleted in these tissues in parallel with their atrophy. This reduction in receptor levels appears to be a primary effect of the hypophysectomy, since castration has no effect on benzodiazepine receptors in the adrenal gland, nor does adrenalectomy influence testicular levels of these receptors. Our results indicate that peripheral-type benzodiazepine receptors in these steroidogenic organs are localized to cells which are dependent on trophic maintenance by the pituitary.

Adrenal Glands↗

Sound stress activation of tryptophan hydroxylase blocked by hypophysectomy and intracranial RU 38486.

The rapidly reversible increase in cortical or midbrain tryptophan hydroxylase activity observed ex vivo after exposure of rats to 1-h sound stress was blocked by hypophysectomy, but not sham hypophysectomy, and restored by dexamethasone administration to the hypophysectomized animals (500 micrograms/day i.p. for 3 days). The response to sound stress was also lost with deafferentation of the hypothalamus. These results indicate that hypothalamic control of adrenal glucocorticoids is required for the serotonergic response to sound stress. The glucocorticoid antagonist, RU 38486, given intracerebroventricularly (200 micrograms/day for 4-5 days) or bilaterally, into the region of the central nucleus of the amygdala (100 micrograms 15 min before stress), blocked the sound stress-induced increase in tryptophan hydroxylase activity. In contrast, the antimineralocorticoid, RU 26752, was without effect. The block obtained with RU 38486 suggests that glucocorticoid is required by the neurons that relay the effects of sound stress to the rostrally projecting serotonergic neurons.

Acoustic Stimulation↗

Effects of hypophysectomy on the testis of the European eel (Anguilla anguilla L.).

The pituitary control of testis activity in the freshwater silver European eel (Anguilla anguilla L.) was investigated by study of some variations of gonad structure and particularly changes in plasma levels of testosterone and 11-oxotestosterone (radioimmunoassay) following hypophysectomy. Germ cells comprised only spermatogonia, which were associated with Sertoli cells to form cysts. No mitotic activity of spermatogonia was observed. Gonadosomatic index (GSI) was low. Plasma levels of the main androgens (testosterone, 11-oxotestosterone) were under 1 ng ml-1. The male gonad appeared immature. After hypophysectomy, GSI decreased rapidly and cysts of germ cells were rapidly dissociated. Plasma level of testosterone decreased significantly, whereas that of 11-oxotestosterone increased significantly. These changes were not observed in sham-operated eels. Thus pituitary control appears essential for the maintenance of structural organization and secretory activity of the immature testis.

Anguilla↗

Effect of hypophysectomy, replacement therapy with ovine prolactin, and cortisol and triiodothyronine treatment on prolactin receptors of the tilapia (Oreochromis mossambicus).

The effects of hypophysectomy and subsequent replacement therapy with ovine prolactin (oPRL) on specific binding of 125I-oPRL to gill, kidney, and liver membranes of male tilapia were examined. The possible control of prolactin receptors by cortisol (F) and triiodothyronine (T3) was also studied using intact animals. In gill and kidney, hypophysectomy resulted in a significant decrease in specific binding that was partially restored (threefold increase) by three injections of oPRL, suggesting a role of the pituitary in the control of prolactin receptors. However, removal of the pituitary and replacement therapy with oPRL had no effect on binding by liver membranes. Cortisol and T3 treatment, alone or in combination, did not significantly affect prolactin binding by any of the tissues tested.

Animals↗

Growth hormone (GH)-dependent hepatic GH receptors in the Japanese eel, Anguilla japonica: effects of hypophysectomy and GH injection.

Control mechanisms of growth hormone (GH) receptors in the eel liver were examined by following the time course of changes in total (MgCl2-treated membranes) and free (untreated membranes) GH-binding sites after hypophysectomy and replacement therapy with homologous GH. Both total and free binding sites decreased significantly 1 week after hypophysectomy. Scatchard analysis indicated that the reduction in GH receptors was primarily due to a decrease in the number of binding sites, rather than to a change in binding affinity. When recombinant eel GH was injected intramuscularly into hypophysectomized eels (2 micrograms/g body wt), plasma GH concentration increased to a maximal value after 10 hr and decreased to the initial level by 72 hr. Free binding sites decreased to a minimal value 24 hr after the injection and returned to the initial level after 72 hr. The reduction in free binding sites seems to be due to occupation of GH receptors. Total binding sites increased gradually to almost twofold over those of the controls 5 days after the injection, the increase being due to an increase in the binding capacity. GH appears to be importantly involved in inducing and maintaining its own receptors in the eel liver.

Analysis of Variance↗

Inhibition by hypophysectomy of the hyperphagia and obesity following gold thioglucose.

The effect of hypophysectomy in mice previously treated with gold thioglucose (GTG) was studied with respect to changes in food intake and development of obesity. As expected, all mice treated with GTG alone exhibited lesions in the ventromedial hypothalamus (VMH), hyperphagia and obesity. Hypophysectomy of GTG treated mice prevented the appearance of hyperphagia and obesity. Daily administration of the adrenal corticoid, cortisone, completely restored the hyperphagia and obesity in GTG treated hypophysectomized mice. The amounts of cortisone used did not appreciably affect food intake or body weights of normal, hypophysectomized or GTG treated mice. These findings indicate that the hypothalamic hyperphagia and obesity which normally follows the administration of GTG is dependent on a functional pituitary gland. Furthermore, the specific ability of an adrenal corticoid to completely restore the hyperphagia and obesity of GTG treated hypophysectomized mice in the absence of other pituitary factors, suggests that the pituitary adrenal axis serves as an important link in the regulatory mechanism for control of feeding behavior in the mouse.

Adrenal Glands↗

Maternal estrogen and progesterone levels after hypophysectomy in early pregnancy and in term fetuses or newborn monkeys.

Pregnant rhesus monkeys (Macaca mulatta) were hypophysectomized at 8-10 weeks gestation to determine effects on plasma levels of estrone (E1), estradiol-17beta (E2), and progesterone (p). The first group of monkeys was subsequently fetectomized at 107-114 days. After hypophysectomy there was an initial decrease in maternal peripheral plasma E2 followed by a rise to preoperative levels within 4-5 weeks. Plasma levels of E1 and P were not markedly altered. After fetectomy, peripheral estrogen concentrations, especially E2, declined markedly. In the second experimental series, we have examined the effects of maternal hypophysectomy on levels of E1, E2 and P either (1) in both mother and newborn baby or (2) in mother, term fetus and umbilical vein. Groups of hypophysectomized and intact pregnant monkeys (3 each) were delivered by cesarean section at the expected time of parturition. Other hypophysectomized and intact monkeys (2 each) delivered normally. E2 levels were elevated significantly in plasma of hypophysectomized monkeys at the time of cesarean delivery and in newborn babies of hypophysectomized mothers shortly after parturition. Escept for these differences, the maternal hypophysis apparently is not a major factor in the control of E1, E2 and P concentrations in pregnant rhesus monkeys.

Animals↗

Effect of hypophysectomy on estrogen conjugation and on plasma and tissue concentrations of tritium after administration of 3H-estradiol-17beta.

Estradiol-17beta-6,7-3H was injected into ovariectomized (control) and ovariectomized, hypophysectomized (hypox) rats in order to study the binding of estradiol in the brain. Hypophysectomy resulted in a significant increase in the concentration of tritium in the hypothalamus, and preoptic area, as well as cortex, muscle, plasma and liver. However, since the liver was lighter in hypox rats, the total tritium content in the liver was unchanged from controls. Part of the weight reduction in the liver was due to a loss of stainable glycogen, which took place within 24 hours of hypox. The increase in circulating tritiated estradiol after hypox led us to investigate hepatic metabolism of estradiol. In vitro studies on liver slices from control and hypox rats demonstrated a significant reduction in the formation of conjugates of estrogen. Specifically, estradiol glucuronide and estrone sulfate formation were reduced in hypox rats and conversely the unmetabolized estradiol concentration was higher. Hypophysectomy for 24 hours results in a significant decrease in hepatic metabolism of estradiol-17beta.

Animals↗

Further observations of stage-specific effects seen after short-term hypophysectomy in the rat.

Although hypophysectomy has been a popular tool to study the effects of hormone deprivation as well as concomitant or subsequent hormone supplementation, there is relatively little morphological information available on the structural manifestation of pituitary removal on the testis. In the report, changes, in addition to those previously reported after short-term (6 days) hypophysectomy in the rat (Russell and Clermont, 1977), are described. Membrane-bound vacuoles (primarily) appeared within the basal region of the Sertoli cell at approximately the level of Sertoli-Sertoli junctions. In stages VIII through XI elongating spermatids were abnormal and manifested manchette indentation of the nucleus, a variety of other abnormal head shapes, acrosomal breaks and enlargement of the subacrosomal space. These defects were interpreted as the effect of declining hormonal levels in stage VII on spermatids that had survived the stage VII hormone sensitivity known to occur with severe hormone depletion. Abnormalities in the flagellum involving the mitochondrial sheath and fibrous sheath were detected. Preleptotene spermatocytes degenerated and could be identified in the process of doing so near the base of the seminiferous epithelium. The contact of preleptotene spermatocytes with the basal lamina was also significantly reduced. The results show that both Sertoli cell and germ cell abnormalities were present although germ cell abnormalities could be a secondary consequence of lack of appropriate stimulation of the Sertoli cell. Degeneration of basal compartment germ cells shows that germ cells other than those located in the adluminal compartment are vulnerable to hormonal withdrawal. The question of how hormone effects are mediated in the testis at midcycle to produce these effects is discussed.

Animals↗

Restoration of ability to reject xenografts and clear carbon after hypophysectomy of adult rats.

Earlier work suggested that a new pituitary function might account for the decline of minimal O2 consumption with age by decreasing peripheral tissue responsiveness to thyroxine and triiodothyronine. It was of interest to see if removal of the pituitary from adult rats could restore juvenile competence in other systems of the body by reversing the postulated age-associated end-organ hypothyroidism. Four and 64 week old intact rats reject xenografts in 6 and 13.8 days, respectively. After hypophysectomy and thyroxine replacement, 64 week old rats reject xenografts in 6.5 days. Four and 64 week old intact rats have a Vmax of colloidal carbon clearance of 18.9 and 2.5 mg/kg fat free body weight, respectively. After hypophysectomy and thyroxine replacement 60 week old rats have a Vmax of 15.5 mg. Corticosterone was the only other hormone given to the hypophysectomized rats and at the various doses tested it did not appear to affect the rates of the two functions studied.

Age Factors↗

The anti-aging action of hypophysectomy in hypothalamic obese rats: effects on collagen aging, age-associated proteinuria development and renal histopathology.

Hypophysectomy in young male Wistar rats aged 70 days, like food restriction begun at the same age, retarded the life-long rate of collagen aging in tail tendon fibres and inhibited the development of age-associated proteinuria and renal histopathology. Hypothalamic lesions which increased the food intake of hypophysectomized rats from 7 g to 15 g/day and produced obesity did not alter the rate of either collagen aging or proteinuria development, nor reduce life expectancy, but increased the incidence of abnormal glomeruli. In the intact rats elevation of food intake from 7 g to 15 g/day increased the rate of proteinuria development, but did not affect the rate of collagen aging. Hypophysectomy was found to have a greater anti-collagen aging effect than food restriction, when food intakes were the same in both groups. These studies suggest a pituitary-hormonal effect on collagen aging and a food-pituitary-hormone-mediated effect on the development of age-associated proteinuria.

Adrenal Cortex Hormones↗

Differential effects of hypophysectomy upon analgesia induced by two glucoprivic stressors and morphine.

Pain threshold elevations induced in rats following acute exposure to stressful cold-water swims and to inescapable foot shocks are significantly attenuated by hypophysectomy. The present study investigated the effects of hypophysectomy upon the dose-dependent and time-dependent analgesia induced by morphine and by the glucoprivic agents, 2-deoxy-D-glucose (2-DG) and insulin. Two reflex pain tests, the tail-pinch and the flinch-jump were employed. In normal rats, insulin induced prolonged (180 min) analgesia at doses of 16 U/kg on the tail-pinch test and 256 U/kg on the flinch-jump test. However, the same agents induced small and brief pain threshold elevations in hypophysectomized animals. By contrast, though 2-DG increased both measures in both groups, its effects were more marked in hypophysectomized rats. Hypophysectomized rats also exhibited a potentiated analgesic effect on both tests following high doses of morphine. On the other hand, low doses of morphine transiently increased tail-pinch thresholds in normal, but not hypophysectomized subjects. These data provide further evidence of multiple pain-inhibitory mechanisms in which the pituitary plays a complex, but integral part.

Analgesia↗

Effect of hypophysectomy and growth hormone on immune development in the domestic fowl.

The effect of hypophysectomy and recombinant growth hormone (rcGH) treatment on the growth and development of the immune system was investigated in young chickens. Flow cytometric analysis of cell surface markers revealed no changes in the proportion of thymocytes expressing CT-1a, CD4, and/or CD8 among any of the treatment groups. In contrast, the proportion of both single positive CD4 and CD8 peripheral blood lymphocytes (PBL) was altered in hypox birds treated with rcGH compared to the vehicle-treated group. Specifically, rcGH treatment produced a decrease in the proportion of CD8+ cells and an increase in the percentage of CD4+ PBL. There was little change in the labeling intensity of PBL or thymocytes associated with any treatment; however, double positive (CD4+CD8+) thymocytes from hypophysectomized chicks that were not given rcGH had increased fluorescence relative to rcGH supplemented hypox chicks. As expected, hypophysectomy reduced body, skeletal, and thymic growth. Treatment of hypox chicks with rcGH enhanced body weight while thymic weights were somewhat increased. Skeletal growth was not significantly altered by rcGH. Bursal growth appeared refractory to either treatment. These studies support the conclusion that growth hormone influences thymic growth and the maturation of thymus-derived lymphocytes. These results also demonstrate a biological activity for chicken growth hormone derived through recombinant technology.

Animals↗