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An injury to a side branch of the inferior vena cava (IVC) was incurred during laparoscopic right adrenalectomy. The hemorrhage was controlled with the aid of a laparoscopic balloon retractor, and laparotomy was avoided.
Surgical removal of phaeochromocytoma may be accompanied by acute cardiovascular changes. We report the haemodynamic changes in seven patients with retroperitoneal laparoscopic adrenalectomy for phaeochromocytoma. Transient hypertension (systolic pressure (SBP) > 160 mm Hg) was observed in all patients during manipulation of the tumour, in two patients during pneumoretroperitoneum insufflation, and in one patient during intubation. Small doses of nicardipine were sufficient to control these episodes of hypertension. Transient hypotension (SBP < 100 mm Hg) was observed in two patients during exsufflation and in one patient during repositioning to the lateral position. Our observations suggest that this approach provides relative haemodynamic stability, especially during pneumoretroperitoneum insufflation.
Restricting the food intake of laboratory mice and rats markedly reduces the incidence of spontaneous and experimentally induced cancers. Using the two-stage skin tumorigenesis model in CD-1 mice, we report now that food restriction suppresses 12-O-tetradecanoylphorbol-13-acetate (TPA) stimulation of epidermal [3H]thymidine incorporation as well as TPA promotion of skin papillomas, whereas adrenalectomy completely reverses the inhibition in [3H]thymidine incorporation and tumor development. These results suggest that the adrenal gland may play an important role in mediating the tumor inhibitory effect of food restriction.
Metastatic non-small-cell lung cancer is a common condition with a dismal prognosis. Although palliative chemotherapy improves survival and quality of life, nearly all patients die of progressive disease. Metastatic involvement of adrenal glands is not rare, but usually reflects widespread dissemination. Selected patients with single adrenal metastasis may be cured with surgery, although the level of evidence comes from single cases reports and short retrospective series. Here we report a patient with bilateral adrenal metastases from previously resected non-small-cell lung cancer, who remains free of disease four years after pre-operative chemotherapy and bilateral adrenalectomy.
The interrelationship between thyroid and adrenal hormones in the regulation of lipid accumulation of the liver during fasting was examined with the use of intact, sham operated and adrenalectomized (ADX) rats previously fed a high carbohydrate diet. Adrenalectomy depressed the lipid accumulation of the liver induced by fasting. This was restored by cortisone administration, but not by epinephrine injection. Lipid content of the liver during fasting tended to be decreased in rats made hyperthyroid by intraperitoneal injection of thyroxine compared to euthyroid-fasted rats. In rats made hypothyroid by oral administration of propylthiouracil, liver lipid content during fasting was significantly higher than that of euthyroid-fasted rats. These responses of liver lipid to thyroid activity were minimized in ADX rats. Cortisone tended to restore completely the liver response to thyroid activity. The maximal response of liver lipid to cortisone was obtained in hypothyroid-ADX rats. The injection of epinephrine alone did not cause any significant change in liver lipid content of ADX rats regardless of the thyroid status. These findings suggest that glucocorticoid must be present for thyroid function to exert its effect on the lipid accumulation of the liver induced by fasting.
The role of glucocorticoid (GC) in the diurnal variation of glycogenesis, glycogenolysis and hepatic glycogen levels was studied in starved-refed rats. Intact, adrenalectomized (ADX) and ADX-GC supplemented rats were either ad libitum fed a 65% glucose diet or starved for 48 hours and refed the glucose diet. At the end of the starvation period and at 4-hour intervals thereafter, rats from all six treatment groups were killed and hepatic glycogen levels, glycogen synthase and phosphorylase activity determined. Ad libitum-fed animals displayed the usual diurnal glycogen and enzyme activity rhythms. Adrenalectomy was without effect in the ad libitum-fed rats on glycogen level and glycogen synthase activity and, at most points, on phosphorylase activity. Starvation-refeeding profoundly affected both the synthesis and degradation of glycogen and these effects could, in part, be attributed to the presence or absence of the adrenals. The phosphorylase activity and the hepatic glycogen level appeared to be cued by GC, whereas GC was without effect on glycogen synthase. Starvation-refeeding stimulated glycogen synthase activity within the first 4 hours of refeeding in the intact rats and within the first 8 hours of refeeding in the ADX-GC rats. These results suggest that the glycogen response to starvation refeeding is, in part, mediated by the adrenal hormones.
Rats with obesity-producing, hypothalamic knife cuts (KC) were fed a purified high fat diet for 9 wk. KC rats consumed more energy (+70-100%) and retained energy with a much higher efficiency than control rats. Adrenalectomy of KC rats 1 wk (before gross obesity was evident) or 5 wk (when KC rats were 70% overweight) after KC surgery caused a reduction in energy intake to levels approximating those of control rats. Furthermore, energy retention in adrenalectomized KC rats was depressed more than could be explained on the basis of the reduction in energy intake. Two factors associated with the reduction in energy retention, urinary excretion of norepinephrine, an indicator of sympathetic nervous system activity, and GDP binding to brown adipose tissue mitochondria, an indicator of the thermogenic capacity of the tissue, were higher in vadrenalectomized KC rats than in pair-fed KC rats. Removal of the adrenals not only suppressed hyperphagia in KC rats fed a high fat diet, but also increased energy expenditure per kilocalorie consumed.
To determine if diet-induced obesity is associated with depressed serotonergic activity (as is genetic obesity), we examined hypothalamic biogenic amines in 11-wk-old genetically lean (Fa/Fa) male Zucker rats raised in small (3 pups/dam) or control (8-9 pups/dam) litters. Five-week-old rats were adrenalectomized or sham-operated and, 1 wk later, fed either 11% of energy as fat (low fat) or 68% of energy as fat (high fat) diets for 5 wk. Tissue punches from the ventromedial nucleus (VMN), the paraventricular nucleus and the preoptic area were assayed via HPLC. Rats fed high vs. low fat had a greater percentage of body fat and brown fat mitochondrial GDP binding, whereas serotonergic turnover was lower. Small litter vs. control litter animals had lower VMN and preoptic concentrations of 3,4-dihydroxyphenylacetic acid, a major metabolite of dopamine. Although adrenalectomy resulted in smaller, leaner rats, it did not differentially affect the rats that became fatter. Because VMN and preoptic dopaminergic activities were depressed in small litter vs. control litter rats but the percentage of body fat was unchanged, this decreased dopamine metabolism is probably not causal to the obesity development. However, the same cannot be said for the attenuated serotonergic activity, although such activity may not be directly related to the degree of obesity.
The effects of adrenalectomy (Ax) on urethan-induced lung tumors were determined in strains of mice that vary in their respective tumor susceptibilities: A/J (sensitive), BALB/cByJ (intermediate), and C57BL/6J (B6, resistant). Ax increased tumor number in both A/J (by 25%) and B6 mice (by 400%), but not in BALB/cByJ mice. The relative proportions of adenomas exhibiting the alveolar or papillary histological growth patterns were unchanged. Implantation of corticosterone-containing pellets into adrenalectomized B6 mice restored tumor multiplicity to that of sham-operated mice and into adrenalectomized A/J mice reduced multiplicity below that of sham-operated mice. Corticosterone, therefore, regulates neoplastic development of mouse lung epithelial cells.
A growing number of studies have implicated the hypothalamic-pituitary-adrenal (HPA) axis in acute and chronic alcoholization and in ethanol withdrawal. In order to study the ethanol/HPA axis interaction during alcohol withdrawal, we performed experiments using adrenalectomized (ADX) male rats alcoholized by a chronic pulmonary alcoholization procedure. Eight hours after the 3 weeks of the alcoholization procedure, the rats were evaluated for a tremor activity. In order to reduce the great variability of the withdrawal tremors, we estimated the supersensitivity of the withdrawn rats to the tremorogenic compound harmine. We also studied the effect of a hydrocortisone treatment given in the drinking bottle during the alcoholization procedure on the harmine-induced tremors of ADX and sham rats. Alcohol withdrawal resulted in increased tremor response to 10 mg/kg harmine, and a protective effect of adrenalectomy on this effect was observed. Hydrocortisone administration to ADX or sham rats did not affect the tremor profile of the alcohol withdrawn rats.
Hyperprolactinemia (HP) induced in female rats by dopaminergic receptor blockers enhanced ovarian estradiol (E2) release in response to human chorionic gonadotropin (hCG) or human follicle-stimulating hormone (hFSH) in vitro. Uterine weight and ovarian aromatase activity were also increased. In contrast, ovarian androgen (A) release in response to hCG was reduced. Injections of ovine prolactin (oPrl) also enhanced E2 response to hCG in vitro. The increased E2 response was not due to a direct effect of Prl on ovarian aromatase activity since administration of oPrl to hypophysectomized rats failed to enhance the formation of E2 from testosterone (T) in vitro, and inhibited the increase in the enzyme activity induced by FSH. Adrenalectomy (ADRX) of intact rats, which did not affect mean serum gonadotropin levels, blunted the effect of HP on the E2 response to hCG. The suppression was partially reversed by corticosterone (B). Serum progesterone (P) and T were similar in controls and HP-ovariectomized (OVX) rats with intact adrenals. Likewise, serum androstenedione (delta 4) and dehydroepiandrosterone (DHA) were not altered in intact, HP rats as compared with controls. Thus, an increase in adrenal secretion of these steroids does not appear to mediate the effect of Prl on ovarian E2 response to gonadotropins. Ovaries of HP rats showed more large follicles than controls. In contrast, ovaries of HP-ADRX rats had a decreased number of large follicles. It is suggested that: a) in intact prepubertal rats Prl increases the E2 response of the ovary to gonadotropins by facilitating follicular development rather than by a direct action on aromatase activity, and b) when follicular development is stimulated by FSH, an inhibitory effect of Prl on aromatase activity becomes apparent. The effect of Prl on the E2 response of the ovary to gonadotropins is not mediated by the adrenal cortex. Rather, it appears that while Prl facilitates the development of large, E2-producing follicles by promoting the growth of small- and medium-sized follicles, an adrenal component influences follicular growth at a step subsequent to Prl.
Adrenalectomy (ADX) in rats has been shown to induce apoptosis of hippocampal granule cells. We tested whether neurotrophins are able to protect hippocampal neurons in this neurodegeneration model. Acid fucshsin stain was used to identify pyknotic cells in ADX rats treated for 4 days with NT-3, NT-4-5 or cytochrome-C, as a control protein. Cytochrome-C injections slightly decreased cell death on the ipsilateral side. NT-3 did not further promote this effect. Significantly less cell death was observed bilaterally in hippocampus treated with NT-4/5. TUNEL end labeling also confirmed the results. Our results demonstrated that NT-4/5, but not NT-3, promotes hippocampal neuron survival in adrenalectomized rats. They further show that injections of a control solution can induce a local protective effect.
The neuroendocrine and the immune systems are interconnected. Monoclonal antibodies against major histocompatibility complex (MHC) class I, class II, CD4, CD8, pan T cells, and macrophages were used for immunostaining brains from adrenalectomized (ADX) and shamoperated rats to investigate the potential involvement of the immune/inflammatory mechanisms in the neurodegeneration of hippocampus after ADX. Our results demonstrate upregulation of MHC class II, CD4 antigens and activated microglial marker-ED1 expression selectively in the hippocampus after ADX. The absence of CD5 reactivity precludes that these activated cells were T lymphocytes. The activated microglial cells may either be instrumental in the hippocampal neuronal loss or activated secondarily to the neuronal degeneration after long-term adrenalectomy.
The effect of long-term adrenalectomy on NMDA receptors in the rat hippocampus was studied. Hippocampal sections of control and adrenalectomized rats were incubated with [3H]MK-801, a radiolabeled non-competitive inhibitor of the NMDA receptor. Analysis by in vitro autoradiography showed a significant decrease in [3H]MK-801 binding in the dentate gyrus, CA1 and CA4 areas, as well as the temporal cortex. Results of this study suggest that glucocorticoids are vital for the regulation of the NMDA receptors.
The expression of glucocorticoid receptor (GR) in rat adrenocorticotropin (ACTH)-containing neurons in rat brain was immunohistochemically investigated. ACTH-containing cell bodies were found mainly in the arcuate nucleus. Most of these neurons exhibited GR immunoreactivities in their nuclei. ACTH-containing nerve fibers were distributed in the bed nucleus of the stria terminalis, periventricular nucleus, retrochiasmatic nucleus, parvocellular part of paraventricular nucleus and dorsomedial hypothalamic nucleus. After adrenalectomy there was a marked decrease of ACTH immunoreactivity, as well as GR immunoreactivity, in neurons of the arcuate nucleus, but ACTH immunoreactivity in the fibers was not affected. These results indicate that glucocorticoids up-regulate ACTH and GR production in hypothalamic arcuate neurons, but that glucocorticoid-induced changes could be delayed in the fibers derived from these neurons.
Using a new assay for inactive renin in rat plasma, inactive renin was unchanged 24 h after bilateral adrenalectomy but increased about threefold, from 0.43 Goldblatt units (GU)/l (range 0.27-0.62 GU/l; n = 14) to 1.24 GU/l (0.74-1.94 GU/l; n = 14) after 48 h. The increase was abolished by substitution with the mineralocorticoid deoxycorticosterone acetate. The results are in accordance with the high plasma concentration of inactive renin, previously reported in humans with adrenal insufficiency, and do not support activation of inactive renin in the circulation.
The influences of combined adrenalectomy and castration and of a replacement therapy with estradiol and glucocorticoids were examined in the rat pancreas. At the light microscope level, the surgical treatment changed the overall shape of the acini and caused widening of intralobular and interlobular spaces as well as partial depletion of zymogen granules. A significant reduction of the acinar lumen size was observed in castrated-adrenalectomized (CasX-AdreX) animals. This could be reversed by a replacement therapy with glucocorticoids. Moreover, triamcinolone even caused a significant lumen enlargement as compared to sham-operated animals. Such an enlargement was not observed with dexamethasone. Both these glucocorticoids caused an increase in zymogen granule content of the acinar cell. At the ultrastructural level, hitherto undescribed type of precipitates was observed in the acinar lumen of CasX-AdreX rats. Precipitates that exhibited a laminated aspect were identified as luminal laminated bodies. The latter could have some interest from the etiological point of view of certain pancreatic diseases, such as cystic fibrosis and pancreatitis. Replacement therapy with estradiol did not affect the frequency of these precipitates, but glucocorticoid had a significantly inhibitory effect. From our observation, it is clear that some steroid exert a profound influence on the acinar cell and that a replacement therapy with glucocorticoids or estradiol do not totally restore the normal aspect of the pancreas acinar tissue. It suggests that some unknown factors from adrenals or testis are still required in addition to glucocorticoids and estrogens for the maintenance of the structural integrity of the gland.
To our knowledge, laparoscopic right adrenalectomy has not been previously reported after orthotopic liver transplantation. The aim of this report is to demonstrate the feasibility of the laparoscopic approach in this technically challenging situation, and to outline some considerations unique to this clinical setting.