Pediatric liver transplantation experience and outcome in Chile.

INTRODUCTION: In 1994 our group began its experience with pediatric liver transplantation. The experience gained during this period is the largest in the country, positioning the Hospital Luis Calvo Mackenna and Clinica Las Condes as major referral centers in the public and private sectors. The aim of this study was to report our experience of our pediatric liver transplantation program during this period. METHODS: The liver transplantation database of Hospital Luis Calvo Mackenna and Clinica Las Condes between January 1994 and July 2011 was reviewed recording age, gender, indications for transplantation, surgical technique, complications, and survival. Survival rates were calculated using Kaplan-Meier analysis. RESULTS: During the period described 230 transplantations were performed in 189 pediatric patients. Fifty-five percent were male patients. The average age was 5 years. The main causes of transplantation were biliary atresia (50%), fulminant hepatic failure (25%), and other cholestatic diseases by 10%. Vascular and biliary complications were the leading cause of graft loss and retransplantation. The overall rate of retransplantation at 5 years was 20%. The technique of living donor was used in 28% of the cases. The 1-year patient actuarial survival rate was 80%, 73% at 5 years, and 68% at 10 years. In the last 3 years the survival rate at 1 year exceeds 90%. DISCUSSION: Our program includes more than 90% of the national liver experience. The incorporation of living donor is a milestone that has enabled us to save many patients who previously died while waiting for an organ. Its use in cases of full acute liver failure has allowed us to dramatically reduce mortality on the waiting list. Our results in the last 3 years reflect the experience that results in a significant decrease in mortality, comparing favorably to other series published in the international literature.

Bisphenol A alone or in combination with estradiol modulates cell cycle- and apoptosis-related proteins and genes in MCF7 cells.

OBJECTIVE: Bisphenol A (BPA) with its estrogenic properties is intensively studied since its presence in the environment and human body. Besides other adverse effects, the compound is suspected of contributing to hormone-related cancers. The present study was aimed to investigate short time (24 h) effects of BPA on the important genes/proteins involved in apoptosis and the cell cycle progression in the breast cancer cells MCF7. The experimental design covered cell treatment with a broad BPA concentration scale: 10-12M corresponding to ubiquitous exposure, 10-9M relevant to human levels, and 10-6M as experimentally usual. We further investigated the combined effects of low BPA dose (10-12M) with physiological concentration of estradiol (E2) (10-9M). METHODS: The expression of particular proteins and genes was studied by Western blotting and real time RT-PCR, respectively. RESULTS: Estrogenic effect of BPA was confirmed in the following checkpoints: mRNA expression of estrogen receptor α, expression of cyclin D1 and A2 proteins and CCNA2 gene, Bax and Bcl2 protein levels. For both cyclins protein levels, the maximum stimulation was present at 10-9M BPA and the effects resembled the "inverted U"-shape, a nonmonotonic dose-response curve reported for the action of xenoestrogens. The combined effect of low BPA dose with physiological E2 concentration differ from those of individual compounds, the character of stimulatory response is neither additive nor synergistic. CONCLUSIONS: The results obtained strongly support the evidence of BPA and BPA+E2 proliferation-promoting effects in human breast carcinoma cells, even after short time exposure, partially via reduced rate of apoptosis by the action of BPA+E2.

[Digestive disorders in Parkinson's disease: gastric atony, malabsorption and constipation]. / Trastornos digestivos en la enfermedad de Parkinson: atonía gástrica, malabsorción y estreñimiento.

INTRODUCTION: Constipation and gastric atony are two of the most important non-motor symptoms of the disease. The first is made significant by its high prevalence and precocity, since it may appear several years before the motor symptoms, and the second because of the repercussions it has on the absorption of oral medication used in this disease. DEVELOPMENT: Both the symptoms and their possible treatment are reviewed. CONCLUSIONS: In both cases treatment is based on hygienic-dietary measures that avoid substances that reduce peristalsis, prokinetic drugs like domperidone and, sometimes, infiltration of botulinum toxin, electrical stimulation or even surgical treatment.

Alcohol intake modifies leptin, adiponectin and resistin serum levels and their mRNA expressions in adipose tissue of rats.

OBJECTIVE: Alcohol intake is known to interfere with endocrine system functions thus inducing hormonal and metabolic imbalance. The aim was to investigate the impact of chronic intake of mild alcohol concentration on serum leptin, adiponectin and resistin and their gene expression in epididymal adipose tissue (EAT) of rats. METHODS: The 28 days study was based on 3 experimental groups of adult male Wistar rats: 1/ ad libitum intake of 6 % ethanol solution and pelleted diet (A), 2/ pair fed animals (PF) fed pelleted diet in the same caloric amount as A rats on previous day (alcohol+diet), 3/ control rats (C) with unrestricted intake of water and pelleted diet. RT-PCR method was used for determination of adipokines gene expression in epididymal adipose tissue, serum levels were measured by ELISA kits. RESULTS: The animals of A group were characterized by reduced food and energy intake (-10 % vs C), lower body mass gain, reduced epididymal fat mass with smaller adipocytes. Alcohol consumption significantly increased glycemia, serum insulin was not affected. The raise of NEFA in A and PF rats gives the evidence of intensified lipolysis due to the deficiency of energy intake. Alcohol consumption significantly increased serum leptin and resistin, elevated adiponectin was present in A and PF rats. In parallel with increased serum levels the expression of adiponectin gene in epididymal adipose tissue was elevated in the same A and PF rats. Leptin and resistin mRNA levels were similar as in C regardless of alcohol intake or pair-fed feeding. Increased leptin and resistin levels positively correlated with glycemia and negatively with the size of adipocytes. Elevated serum leptin and resistin together with high adiponectin after chronic moderate alcohol intake could contribute to alteration of energy metabolism either individually or in reciprocal coordination. CONCLUSIONS: 28 days consumption of 6 % ethanol solution changed the nutritional status of rats and induced significant elevation of serum leptin and resistin, while elevated gene expression in epididymal adipose tissue was proved for adiponectin only. Elevated serum adipokines could contribute to increased glycemia and altered glucose homeostasis.

Rats with monosodium glutamate-induced obesity and insulin resistance exhibit low expression of Galpha(i2) G-protein.

In order to test the potential role of inhibitory G-proteins in mechanisms of insulin resistance in adipose tissue of obese animals we determined the content of Galpha(i1) and Galpha(i2) proteins and an extent of protein tyrosine phosphorylation in epididymal fat tissue cell membranes using immunoblot. Monosodium glutamate-induced obese rats displayed adipose tissue hypertrophy, elevated levels of insulin, leptin and slightly elevated serum glucose. We found significantly decreased protein content of Galpha(i2) in adipose tissue plasma membranes of obese rats. This was in accordance with lower protein tyrosine phosphorylation noticed in adipose tissue cell homogenate of glutamate-treated animals. Our results confirm the role of Galpha(i2) in development of insulin resistance by crosstalk between the reduced level of inhibitory G-protein and insulin receptor mediated most likely by activation of phosphotyrosine protein dephosphorylation.

Living donor liver transplantation in pediatric patients with acute liver failure: safe and effective alternative.

UNLABELLED: Living donor liver transplantation (LDLT) for patients with acute liver failure (ALF) is still controversial. To be considered a feasible alternative, this therapeutic option should offer similar results to transplants performed with cadaveric grafts, without significant risks for donors. The aim of this study was to compare the outcomes of pediatric patients with ALF who were transplanted with either cadaveric or living donor grafts. PATIENTS AND METHODS: Between March 1994 and February 2007, 149 patients under 18 years were transplanted, including 43 (28.8%) with ALF. We reviewed the demography, etiology, surgical technique, complications, and long-term results in this group. Patient actuarial survival was determined by Kaplan-Meier analysis. RESULTS: The median age of the recipients was 4.8 years (range 1.2 to 18) including 26 boys and 17 girls. Sixteen (37.2%) underwent LDLT. Three patients in the living donor group needed a second graft (18.7%) versus 7 (26%) among the cadaveric group. No mortality or serious morbidity was observed in living donors. Fifteen patients died. Septic and neurologic complications, and primary graft non-function were the most frequent causes of death. All patients died during the first year after liver transplant. Actuarial 1- and 5-year survivals were 65% without a significant difference between the groups. CONCLUSION: Considering that patients with ALF have no chance of survival without transplantation and that cadaveric grafts remain a limited resource, especially in our country, these results showed that LDLT was a valid option for these patients, as well as a secure procedure for the donors.

Hormone response to stress in rat strains of different susceptibility to immunologic challenge.

OBJECTIVE: The aim of this study was to compare the changes in plasma levels of hormones involved in modulation of the immune system function after exposure to stress in two rat strains with different susceptibility to immunoantigens. METHODS: Adult rat males of Lewis (LEW) and Fischer 344 (FIS) strains were exposed to restrain stress for 2 hours and blood samples were collected during stress exposure. Other groups of animals were exposed to restrain stress for 2 hours and sacrificed 3 hours later for blood and organ collection. Corticosterone, testosterone, dehydroepiandrosterone, 17beta-estradiol and progesterone were estimated by radioimmunoassay, epinephrine and norepinephrine levels were determined by radioenzymatic method. RESULTS: The levels of plasma corticosterone and catecholamines were significantly higher during stress exposure in FIS as compared to LEW rats. Greater decrease of testosterone levels and higher levels of estradiol were noted after exposure to stress in LEW rats. Higher values of progesterone plasma levels were noted in FIS rats after stress. CONCLUSIONS: These results demonstrated the differences in the response of catecholamines, adrenal and gonadal steroids after exposure to stress in LEW and FIS rats with lower levels of hormones with anti-inflammatory action in LEW rats.

Long-time alcohol intake modifies resistin secretion and expression of resistin gene in adipose tissue.

Elevated serum resistin is implicated in insulin resistance associated with obesity and type 2 diabetes mellitus. Alcohol consumption interferes with the nutritional status, metabolic and hormonal activity of the drinker. Impact of ethanol intake on resistin level and resistin metabolic effects is unknown. Effect of long-time (28 days) ad libitum moderate alcohol (6% ethanol solution) intake on serum resistin and resistin mRNA level in adipose tissue of rats (A) was compared to control (C) and pair-fed (PF) animals. PF rats were fed the same caloric amount as A rats on previous day. Alcohol consumption resulted in reduction of food and energy intake, decreased body mass gain, epididymal fat pads mass and smaller adipocytes (vs. C rats). Alcohol intake significantly increased serum resistin and glucose, insulinemia remained unchanged. Systemic insulin resistance was not proved by HOMA, QUICKI and McAuley indexes, but impaired insulin effect on glucose transport in isolated adipocytes was present. Elevated serum resistin was positively correlated with glycemia (r = 0.88, p < 0.01) and negatively with fat cell size (r = -0.73, p < 0.05). High resistin level as the consequence of long-time alcohol intake could contribute to smaller adipocytes, higher glycemia, attenuation of insulin-stimulated glucose transport in adipocytes. Diminished resistin gene expression in adipose tissue of A and PF rats was present.

Calambres musculares y mialgias secundarias a zolmitriptán / Muscle cramps and myalgia related to zolmitriptan

No disponible

Paraparesia espástica por estenosis de canal dorsal por enfermedad de Paget / Spastic paraparesis due to stenosis of dorsal caused by Paget’s disease

No disponible

[Levels of hormones in plasma and in synovial fluid of knee joint of patients with rheumatoid arthritis]. / Hladiny hormónov v plazme a v synovialnej tekutine kolenného klbu pri reumatoidnej artritíde.

BACKGROUND: Dysfunction of endocrine system is very likely one of the important risk factors involved in the pathogenesis of rheumatoid arthritis. The aim of the present study was to investigate the levels of selected hormones in plasma and in synovial fluid of knee joint of patients with rheumatoid arthritis or with osteoarthritis, which could affect the inflammatory processes. METHODS AND RESULTS: Thirty nine patients with rheumatoid arthritis (22 females and 17 males) and 12 patients with osteoarthritis (6 females and 6 males) were investigated. Concentrations of the following hormones were determined in plasma and synovial fluids: cortisol, 17-beta-estradiol, progesterone, dehydroepiandrosterone, aldosterone, testosterone, prolactin, insulin and C-peptide by using radioimmunoassay kits. Increased levels of 17-beta-estradiol and insulin were found in patients with rheumatoid arthritis as compared to those with osteoarthritis. The plasma concentrations of other hormones under study were not significantly different in these groups of patients. Higher levels of 17-beta estradiol, progesterone and aldosterone were noted in inflammatory knee exudate of patients with rheumatoid arthritis. The levels of other hormones in exudates of patients with rheumatoid arthritis and those with osteoarthritis were not significantly different. The ratio of 17-beta estradiol / cortisol, 17-beta estradiol / testosterone and 17-beta estradiol / dehydroepiandrosterone showed increased proportions of estrogens over androgens or glucocorticoids in exudate from patients with rheumatoid arthritis. CONCLUSIONS: These results demonstrated that steroid and peptide hormones are transferred to synovial fluid of knee. The presence of insulin, C-peptide and aldosterone was described for the first time in synovial fluid. In patients with rheumatoid arthritis a predomination of the levels of proinflammatory estrogens over androgens was found in knee exudate. Also the levels of aldosterone and progesterone were elevated in inflammation knee exudate. This suggests that these hormones present in synovial fluid may affect the local rheumatoid inflammatory processes.

Peptide hormones and histamine in plasma and synovial fluid of patients with rheumatoid arthritis and osteoarthrosis.

OBJECTIVES: Hormones other than adrenal and gonadal steroids may play also a significant role in the pathogenesis of rheumatoid arthritis. The aim of this study was to investigate the levels of selected peptide hormones and histamine in synovial fluid of knee joints and in plasma of patients with rheumatoid arthritis and with osteoarthrosis. METHODS: The concentrations of insulin, C-peptide, prolactin, growth hormone, free triiodothyronine (FT3), thyrotropin (TSH), and histamine were determined in synovial fluid and plasma of 27 patients with rheumatoid arthritis (RA) and in 12 patients with osteoarthrosis (OA). RESULTS: The presence of peptide hormones in synovial fluid was demonstrated. The levels of TSH and growth hormone were lower in synovial fluid than in plasma in both groups, while those of prolactin were comparable in synovial fluid and in plasma. The levels of C-peptide (p < 0.05), insulin and FT3 were higher in synovial fluid than in plasma of OA patients, but lower in synovial fluid of RA patients as compared to their levels in plasma. Significant positive correlations between the levels in plasma and synovial fluid were observed in prolactin (p < 0.001, r = 0.741) and TSH (p < 0.05, r = 0.88) only. After age adjustment, no significant differences in synovial fluid and in plasma levels of all hormones were found between OA and RA patients. The levels of histamine in plasma were similar in RA and OA patients, in synovial fluid of both groups histamine was found in almost undetectable amounts. CONCLUSIONS: The selected peptide hormones, e.g. insulin, C-peptide, prolactin, growth hormone, FT3 and TSH, are present in synovial fluid of RA and OA patients, some of them in the concentrations comparable to these in plasma. The role of the locally present hormones in pathogenesis of RA has to be investigated in further studies and analyses.

Hormone concentrations in synovial fluid of patients with rheumatoid arthritis.

OBJECTIVE: Alterations in local concentrations of hormones, affecting directly synovial cells, could be involved in the modulation of the rheumatic inflammatory processes. The aim of present study was to investigate the levels of selected hormones (steroids, peptide and thyroid hormones) in synovial fluid of knee joint of patients with rheumatoid arthritis (RA) and control individuals with non-rheumatic exudate (with osteoarthrosis, OA). METHODS: Thirty-eight patients, 22 female and 16 males, with rheumatoid arthritis (RA) and 12 subjects with osteoarthrosis (OA, control group, 6 females and 6 males) participated in the study. Concentrations of cortisol (CS), 17-beta-estradiol (ES), dehydroepiandrosterone (DHEA), progesterone (PRG), aldosterone ALD), prolactin (PRL), insulin (INS), and C-peptide were determined by radioimmunoassay in synovial fluid. Insulin binding to isolated cell membrane of cells from synovial sediment was estimated by using radioiodine labeled insulin. In a group of patients (10 with RA and 4 with OS), the levels of free threeiodothyronine (FT3), TSH and growth hormone (GH) were also determined in synovial fluid. RESULTS: Increased levels of ES in synovial fluid of RA patients were observed, and higher differences were noted in men. TE concentrations were moderately elevated in synovial fluid of RA patients, however the ratio of ES/TE was significantly higher in male RA compared to OA patients. Higher levels of PRG, ALD and growth hormone were noted in synovial fluid of RA patients. Besides the steroid hormones the presence of insulin and C-peptide was noted in synovial fluid and the correlation between the levels of these two peptides was highly significant. The concentrations of INS and C-peptide in synovial fluid of patients from RA and OA group were not significantly different, however, highly significant increase of insulin binding to isolated membrane of synovial cells was found. Concentrations of cortisol, dehydroepiandosterone, prolactin, TSH and FT3 in synovial fluid were not significantly different in RA and OA groups. CONCLUSIONS: Besides the steroids also insulin, c-peptide, GH and FT3 were found in synovial fluid. The elevated ALD and GH levels in synovial fluid of RA patients and the presence of INS in synovial fluid with increase of INS binding to plasma membranes of cells from synovial fluid of RA patients suggest that besides the gonadal steroids also these hormones may affect the local inflammatory processes.

Low levels of dehydroepiandrosterone sulphate in plasma, and reduced sympathoadrenal response to hypoglycaemia in premenopausal women with rheumatoid arthritis.

OBJECTIVES: To evaluate the function of the hypothalamic-pituitary-adrenal axis and sympathoadrenal system in premenopausal women with rheumatoid arthritis (RA). METHODS: Insulin-induced hypoglycaemia (0.1 IU/kg) was produced in 15 glucocorticoid-naive patients with long term RA with low disease activity and in 14 healthy women matched for age and body mass index. Concentrations of glucose, adrenocorticotropic hormone (ACTH), cortisol, Delta4-androstenedione (ASD), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulphate (DHEAS), 17alpha-hydroxyprogesterone (17OHP), epinephrine (EPI), norepinephrine (NE), interleukin 6 (IL6), and tumour necrosis factor alpha (TNFalpha) were analysed in plasma. RESULTS: Patients had comparable responses of glucose, cortisol, ACTH, ASD, and 17OHP to hypoglycaemia, without any signs of hypothalamic insufficiency. Patients had lower basal DHEAS than controls (3.03 (0.37) micromol/l v 5.1 (0.9) micromol/l, respectively; p<0.05); borderline lower basal DHEA levels (p = 0.067); while the response of DHEA to hypoglycaemia was comparable to that of controls. Patients with RA had lower EPI (p = 0.005) and NE (p<0.001) responses to hypoglycaemia. TNFalpha and IL6 were higher (p<0.05) in patients with RA (TNFalpha 8 (2.8) pg/ml in RA v 1.1 (0.5) pg/ml in controls and IL6 15.1 (6.7) pg/ml v 1.4 (0.7) pg/ml). CONCLUSIONS: Lower basal DHEAS levels, without concomitant differences or changes in DHEA, ASD, 17OHP, and cortisol responses to hypoglycaemia in patients with RA, indicate an isolated decrease in adrenal androgen production. Significantly lower responses of EPI and NE to hypoglycaemia may suggest sympathoadrenal hyporeactivity in patients with RA.

Does orthostatic stress influence the neuroendocrine response to subsequent hypoglycemia in humans?

Neuroendocrine response to stress stimuli is influenced by previous stimuli of different nature. The aim of the study was to test whether antecedent orthostatic stress may affect the neuroendocrine response to subsequent hypoglycemia. A group of 12 (6 men, 6 women) nonobese, healthy volunteers aged 19 to 27 y (mean 24 +/- 0.8) participated in the study in two sessions: controlled insulin-induced hypoglycemia to 2.7 mmol/L for 15 min either with or without antecedent orthostatic stress (30 min of 60 degrees head-up tilt before insulin administration). Orthostatic stress caused a significant decrease in plasma volume (-9.6%; P < 0.001) and a significant increase in plasma renin activity, aldosterone, norepinephrine (P < 0.01), and adrenocorticotropic hormone (ACTH) concentrations (P < 0.05) in all subjects. Growth hormone response to hypoglycemia was diminished in women (P < 0.01). The epinephrine response to hypoglycemia was diminished in women in comparison to men (P < 0.001), but was unaffected by antecedent orthostatic stress. Hypoglycemia failed to induce the ACTH release after its elevation during orthostatic stress. ACTH response to moderate hypoglycemia without previous orthostatic stress was evident only in men in comparison to women (P < 0.05). We conclude that the epinephrine, growth hormone, and ACTH responses to hypoglycemia were diminished in women. Except ACTH, the neuroendocrine response to mild hypoglycemia was not affected by previous orthostatic stress in healthy subjects. In the case of ACTH, the first stress stimulus is consequential for the subsequent response of this hormone, probably due to short-loop negative feedback effects.

Hypothalamic-pituitary-adrenal axis function in ankylosing spondylitis.

OBJECTIVE: To assess basal function and responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis in patients with ankylosing spondylitis during dynamic testing. METHODS: Insulin induced hypoglycaemia (IIH) (Actrapid HM 0.1 IU/kg, as intravenous bolus) was induced in 17 patients and 11 healthy controls matched for age, sex, and body mass index. Concentrations of glucose, adrenocorticotrophic hormone (ACTH), cortisol, insulin, dehydroepiandrosterone sulphate (DHEAS), 17alpha-hydroxyprogesterone, interleukin 6 (IL-6), and tumour necrosis factor alpha (TNFalpha) were determined in plasma. RESULTS: Comparable basal cortisol levels were found in the two groups, with a trend to be lower in ankylosing spondylitis. In the ankylosing spondylitis group, there were higher concentrations of IL-6 (mean (SEM): 16.6 (2.8) pg/ml v 1.41 (0.66) pg/ml in controls; p<0.001) and TNFalpha (8.5 (1.74) pg/ml v 4.08 (0.42) pg/ml in controls; p<0.01). Glucose, insulin, ACTH, DHEAS, and 17alpha-hydroxyprogesterone did not differ significantly from control. The IIH test was carried out successfully in 11 of the 17 patients with ankylosing spondylitis, and the ACTH and cortisol responses were comparable with control. General linear modelling showed a different course of glycaemia (p = 0.041) in the ankylosing spondylitis patients who met the criteria for a successful IIH test compared with the controls. CONCLUSIONS: The results suggest there is no difference in basal HPA axis activity and completely preserved responsiveness of the HPA axis in patients with ankylosing spondylitis. The interpretation of the different course of glycaemia during IIH in ankylosing spondylitis requires further investigation.

Effect of space flight and head-down bedrest on neuroendocrine response to metabolic stress in physically trained subjects.

The aim of this study was to evaluate the association of plasma epinephrine (EPI) and norepinephrine (NE) responses to insulin induced hypoglycemia (ITT) 3 weeks before the space flight (SF), on the 5th day of SF, on the 2nd and 16th days after the landing in the first Slovak astronaut, and before and on the 5th day of prolonged subsequent head-down (-6 degrees) bed rest (BR) in 15 military aircraft pilots. Blood samples during the test were collected via cannula inserted into cubital vein, centrifuged in the special appliance Plasma-03, frozen in Kryogem-03, and at the end of the 8-day space flight transferred to Earth in special container for hormonal analysis. Insulin hypoglycemia was induced by i.v. administration of 0.1 IU/kg BW insulin (Actrapid HM) in bolus. Insulin administration led to a comparable hypoglycemia in pre-flight, in-flight conditions and before and after bed rest. ITT led to a pronounced increase in EPI levels and moderate increase in NE in pre-flight studies. However, an evidently reduced EPI response was found after insulin administration during SF and during BR. Thus, during the real microgravity in SF and simulated microgravity in BR, insulin-induced hypoglycemia activates the adrenomedullary system to less extent than at conditions of the Earth gravitation. Post-flight changes in EPI and NE levels did not significantly differ from those of pre-flight since SF was relatively short (8 days) and the readaptation to Earth gravitation was fast. It seems, that an increased blood flow in brain might be responsible for the reduced EPI response to insulin. Responses to ITT in physically fit subjects indicate the stimulus specificity of deconditioning effect of 5 days bed rest on stress response. Thus, the data indicate that catecholamine responses to ITT are reduced after exposure to real as well as simulated microgravity.

The response of endocrine system to stress loads during space flight in human subject.

The responses of endocrine system to the exposure to stress-work load and hormonal changes during oral glucose tolerance tests were studied in the Slovak astronaut before (three weeks before flight), during (on the 4th and the 6th days of space flight), and after space flight (1-3 days and 15-17 days after space flight) on board of space station MIR. Blood samples during the tests were collected via cannula inserted into cubital vein, centrifuged in the special appliance Plasma-03, frozen in Kryogem-03, and at the end of the 8-day space flight transferred to Earth in special container for hormonal analysis. Preflight workload produced an increase of plasma norepinephrine and a moderate elevation of epinephrine levels. Plasma levels of insulin, growth hormone, prolactin and cortisol were not markedly changed immediately or 10 min after the end of work load. The higher increases of plasma growth hormone, prolactin and catecholamine levels were noted after workload during space flight as compared to preflight response. The higher plasma glucose and insulin levels were noted during the oral glucose tolerance test in space flight and also in the post flight period. Plasma epinephrine levels were slightly decreasing during glucose tolerance test; however, plasma norepinephrine levels were not changed. The similar patterns of catecholamine levels during glucose tolerance test were found when compared the preflight, in-flight and post flight values. These data demonstrate the changes of the dynamic responses of endocrine system to stress-work and metabolic loads during space flight in human subject.