[Ovarian tissue cryopreservation--an opportunity to preserve fertility in women with cancer]. / Kryokonzervace ovariální tkáne--sance na záchranu fertility zen s nádorovým onemocnením.

Chemoterapy is one of the basic modalities of oncological therapy and usually leads to permanent consequences. Infertility is one of the most common consequences resulting from irreversible gonadal damage. The potentially effective method of reproductive function protection in women undergoing chemotherapy is ovarian tissue cryopreservation. This paper summarizes the medical and scientific knowledge in this interesting multidisciplinary medical field an also presents authors own experience with this novel and interesting method of ovarian tissue protection.

Plasma catecholamines and renin activity in wrestlers following vigorous swimming.

Cardiovascular and neuroendocrine responses to exercise in a physically fit and an untrained group of young healthy subjects were compared to study the significance of physical fitness for performance in a discipline for which the athletes were not trained. Ten wrestlers of national rank prepared for an international competition (age 18 years) and 9 untrained healthy males (age 21 years). Exercise consisted of 27-min swimming, freestyle, in water of 29 degrees C, with last 3 min increased to maximal effort. The blood pressure, heart rate and sublingual temperature were measured and blood samples were withdrawn before exercise, immediately after and after a 30 min period of rest. Catecholamines were analyzed by radioenzymatic method and plasma renin activity (PRA) using commercial kits. Systolic blood pressure and heart rate after swimming were increased comparably in the two groups, diastolic pressure was unchanged in the controls and decreased in the wrestlers. Plasma cortisol remained unchanged. Plasma glucose tended to increase in the controls and so decrease in wrestlers, with a significant difference between them after swimming (p < 0.05). However, plasma adrenaline was concomitantly increased in both groups (p < 0.01). Noradrenaline and PRA were increased after swimming in both the control and trained group. The increments of noradrenaline and PRA in wrestlers were significantly reduced compared to the control group (p < 0.01, p < 0.05, respectively). Higher physical fitness in athletes significantly reduced plasma noradrenaline and angiotensin responses to maximal exercise demanding special skill in work performance which had not been included in their training program. Training of wrestlers did not cause an exaggerated plasma adrenaline response to exercise.

Neuroendocrine response during stress with relation to gender differences.

Neuroendocrine activation belongs to the main characteristics of the stress response. This response is not uniform but depends on the stress stimulus involved and on many other factors including the gender of the individual. In rats, corticosterone and ACTH levels as well as functional activity of the hypothalamo-pituitary-adrenocortical axis are higher in females compared to males under both basal and stress conditions. Marked sex differences were observed in stress-induced changes posterior pituitary hormone release. In male rats, release of vasopressin is not stimulated during stress conditions without an osmotic component while in female rats a rise in plasma vasopressin levels was observed even after short immobilization. Oxytocin release is enhanced in response to the majority of stress stimuli and it was found to be greater in females than in males. Mentioned gender differences are attributed to the effect of sex steroids, particularly those of estrogens. Not enough information is available on gender differences in the neuroendocrine response during stress in humans. We observed a greater neuroendocrine activation in women than in men in response to heat exposure in sauna with pronounced differences in ACTH and prolactin release and partly also after a cold-pressor test. Understanding of gender differences in neuroendocrine response during stress might contribute to the explanation of the development of some emotional and other disorders with higher incidence in women.

[Immunoendocrine interactions and autoimmune diseases]. / Imunoendokrinné vzt'ahy a autoimunitné ochorenia.

Communications between the immune and endocrine systems are bidirectional. A number of reports have demonstrated that many hormones have profound effects on the immune system. Cytokines produced by cells of the immune system cause changes in the neuroendocrine function. It is shown in various animal models with experimentally induced and spontaneously occurring autoimmune diseases that alterations of the immunoendocrine interactions are involved in the breakdown of self tolerance. This review discusses the role of disturbances along the hypothalamo-pituitary-adrenal and lactotrophic axes in the development of autoimmune diseases. This finding of the defective immuno-endocrine communications may lead to more specific therapy of autoimmune diseases in man. (Fig. 1, Ref. 51.).

[Glutamate neurotransmission, stress and hormone secretion]. / Glutamátová neurotransmisia, stres a sekrécia hormónov.

Glutamate neurotransmission has been investigated in relation to several physiological processes (learning, memory) as well as to neurodegenerative and other disorders. Little attention has been paid to its involvement in neuroendocrine response during stress. Penetration of excitatory amino acids from blood to the brain is limited by the blood-brain barrier. As a consequence, several toxic effects but also bioavailability for therapeutic purposes are reduced. A free access to circulating glutamate is possible only in brain structures lacking the blood-brain barrier or under conditions of its increased permeability. Excitatory amino acids were shown to stimulate the pituitary hormone release, though the mechanism of their action is still not fully understood. Stress exposure in experimental animals induced specific changes in mRNA levels coding the glutamate receptor subunits in the hippocampus and hypothalamus. The results obtained with the use of glutamate receptor antagonists indicate that a number of specific receptor subtypes contribute to the stimulation of ACTH release during stress. The authors provided also data on the role of NMDA receptors in the control of catecholamine release, particularly in stress-induced secretion of epinephrine. These results were the first piece of evidence on the involvement of endogenous excitatory amino acids in neuroendocrine activation during stress. Neurotoxic effects of glutamate in animals are well described, especially after its administration in the neonatal period. In men, glutamate toxicity and its use as a food additive are a continuous subject of discussions. The authors found an increase in plasma cortisol and norepinephrine, but not epinephrine and prolactin, in response to the administration of a high dose of glutamate. It cannot be excluded that these effects might be induced even by lower doses in situations with increased vulnerability to glutamate action (age, individual variability). (Tab. 1, Fig. 6, Ref. 44.).

Central stimulation of hormone release and the proliferative response of lymphocytes in humans.

The central nervous system (CNS) may communicate with the immune system by direct innervation of lymphoid organs and/or by neurotransmitters and changes in neuroendocrine functioning and hormone release. The consequences of selective transient changes in circulating hormones on immune functioning in humans have not yet been studied. To address this problem, the authors evaluated the lymphoproliferative responses to optimal and suboptimal concentrations of phytohemagglutinin (PHA) and pokeweek mitogen (PWM) under selective enhancement of circulating growth hormone, prolactin, or norepinephrine. The authors failed to demonstrate any effect of elevated growth hormone levels after clonidine challenge on the lymphoproliferative response to mitogens. Similarly, the results did not show any effect of elevated prolactin concentrations induced by domperidone administration on the immune test. Exposure of volunteers to cold resulted in elevation of plasma norepinephrine levels without changes in growth hormone, epinephrine, or cortisol secretion. Cold exposure induced elevation of plasma norepinephrine and reduction of the lymphoproliferative response to the suboptimal dosage of PHA. The reduction was significant 180 and 240 min after exposure. These results are indicative of a relationship between norepinephrine and immunity.

Low ambient temperature and neuroendocrine response to hypoglycemia in men.

Nutritional factors, such as an excess or a deficiency of glucose, play an important role in neuroendocrine regulations. Hormonal and metabolic responses to hypoglycemia were examined in healthy non-obese volunteers under conditions of low ambient temperature. Hypoglycemia was induced by intravenous injection of insulin in two randomized trials performed at room temperature and at 4 degrees C. At room temperature, the typical neuroendocrine response to hypoglycemia was established. The increases of ACTH, beta-endorphin, growth hormone and cortisol in response to insulin hypoglycemia failed to be modified by low ambient temperature. Acute cold exposure significantly reduced epinephrine and totally inhibited prolactin response to insulin-induced hypoglycemia. In spite of significant changes in epinephrine response to hypoglycemia at low ambient temperature, no striking differences in plasma glucose levels compared to those measured at room temperature were observed. However, under conditions of low temperature the reestablishment of normoglycemia was delayed. No changes in free fatty acids were found under our experimental conditions. The presented data show that low ambient temperature exerts selective effects on some neuroendocrine and metabolic parameters.

Studies on the physiological role of ANF in ACTH regulation.

To investigate the impact of changes in the level of the endogenous atrial natriuretic factor (ANF) on pituitary-adrenocortical activity, the secretion of corticotropin (ACTH) and corticosterone was studied under the conditions of enhanced and decreased circulating ANF levels in rats. Volume expansion (intravenous infusion of 5 ml of saline within 2 min) induced significant elevation in ANF levels 5 min after the infusion, whereas ACTH levels remained unchanged during the first 20 min and were elevated only at 40 min, i.e. at the time when ANF levels were again normal. Water deprivation for 48 h resulted in decreased ANF levels and increased corticosterone concentrations. ANF concentrations in peripheral blood obtained under thiopental anesthesia were lower than those in blood sampled in the same rats in conscious state. However, such changes were not observed in water deprived animals. In addition, ANF was found to be present in the hypophysial portal blood of anesthetized rats. In conscious sheep, portal ANF levels were significantly higher than those in peripheral blood. Our results support the suggestion of an inhibitory role of ANF in the control of ACTH release and indicate that this role of ANF is physiologically relevant.

Relationship between endocrine, immune, and clinical variables in patients with systemic lupus erythematosus.

OBJECTIVE: To assess the frequency of increased plasma prolactin (PRL) in patients with systemic lupus erythematosus (SLE) and to evaluate its relationship to other hormonal and immune variables. METHODS: Thirty-five patients with SLE with various levels of disease activity were studied. Plasma PRL, cortisol, growth hormone (GH) were determined by radioimmunoassay and interleukin 6 (IL-6) by ELISA: SLE activity was evaluated using the European Consensus Lupus Activity Measurement (ECLAM). RESULTS: Increased plasma PRL concentration (> 20 ng/ml) was recorded in 11 patients (31%). No correlation was found between plasma PRL and GH, IL-6, cortisol, or C-reactive protein, nor was any significant correlation observed between plasma PRL and the ECLAM score. Patients with hyperprolactinemia were, however, found to have been treated with higher doses of prednisone therapy than patients with normal plasma PRL. Further analysis of the relationship of plasma PRL and therapy showed that patients with SLE selected by the attending physician for prednisone therapy in doses > or = 10 mg/day were more frequently hyperprolactinemic. CONCLUSION: Our findings that patients with SLE with a more active form of the disease and who are less responsive to therapy had increased plasma PRL levels more frequently may be indicative of a potential relationship of hyperprolactinemia to severity of disease.