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185 patients with hyperprolactinaemia and prolactinoma were evaluated in a retrospective investigation. 128 patients were treated surgically whereby the prolactin serum level in 47% of the macroprolactinoma and 60% of the microprolactinoma patients was normalised (prolactin less than 25 ng/ml, no radiological evidence of tumor). Of those patients in whom the operation was less successful, a normal prolactin level could be achieved in 77% by additional therapy with dopamine agonists. Of 57 patients handled exclusively with drugs, the prolactin level was normalised by dopamine agonists in 78%. A small number of patients from both groups did not show a satisfactory fall in the prolactin level despite the use of markedly higher doses of dopamine agonists. During dopamine agonist therapy progressive tumor enlargement was detected radiologically in a previously operated patient.

Catecholamines have been suggested to be responsible for altered cellular immunity after stress. This study was performed to determine the effects of adrenaline and noradrenaline on lymphocyte subpopulations and NK cell functions. Subjects were given a subcutaneous injection of either NaCl, adrenaline (5 micrograms/kg), or noradrenaline (10 micrograms/kg). Catecholamine concentrations, subsets of peripheral blood lymphocytes, NK activity, and antibody-dependent cellular cytotoxicity (ADCC) were analyzed before (baseline) and 5, 15, 30, 60, and 120 min after injection. There were no differences between groups in the distribution of CD2+ and CD8+ lymphocytes over time. However, CD3+ and CD4+ T cells decreased significantly 5 to 60 min after injection of adrenaline. In contrast, NK cell numbers (CD16+, CD56+) increased significantly 5 min after injection of adrenaline and noradrenaline, reached the highest values 15 to 30 min postinjection, and subsequently declined to baseline values 60 (noradrenaline) and 120 (adrenaline) min, respectively, after injection. Similar alterations for NK activity and ADCC were observed after administration of both catecholamines. These data suggest that both sympathetic-adrenal hormones are similarly potent modulators of natural immunity and provide further evidence that catecholamines might be responsible for the observed alterations in immune functions after phases of acute stress.

Emotional stress is often followed by increased susceptibility to infections. One major role in the immediate immune response to infection is played by natural killer (NK) cells. This study was designed to establish whether acute psychological stress influences cellular immune functions and to elucidate the role of endocrine parameters as potent mediators of stress induced alterations of the immune system. Forty-five first-time tandem parachutists were examined continuously for their plasma concentrations of cortisol and catecholamines from 120 min before to 60 min after jumping. Lymphocyte subsets, NK activity, and ADCC were determined 2 hr before, immediately after, and 1 hr after jumping. There was a significant increase in sympathetic-adrenal hormones during (adrenaline, noradrenaline) and shortly after jumping (cortisol). Lymphocyte subsets and the functional capacity of NK cells revealed an increase immediately after jumping followed by a decrease significantly below starting values 1 hr later. These changes were significantly correlated to plasma concentrations of noradrenaline. Thus, quick mobilization of NK cells is suggested as one major mechanism for this effective adaptation of the immune system to stress situations.

The circadian and pulsatile TSH secretion profiles were investigated in 5 females at the time of menstruation and 21 healthy males by sampling blood every 10 min for 24 h. Computer-assisted analysis, i.e. the Cluster and Desade programs, revealed means of 9.9 +/- 1.7 (Cluster) and 11.4 +/- 3.9 (Desade) pulses/24 h. More than 50% of the TSH pulses were detected between 2000-0400 h. Male and female subjects showed no significant difference in the basal mean and pulsatile secretion of TSH or in the TSH response to TRH (200 micrograms). Repetition of the TSH secretion analysis in 4 healthy subjects after 1, 2, and 6 months (2 subjects) revealed a significantly better cross-correlation within than between individuals (P less than 0.0001). We modulate the circadian TSH secretion pattern by acute sleep withdrawal or prolonged sleep after a night of sleep withdrawal in six healthy male volunteers. Sleep withdrawal augmented the nightly TSH secretion (mean serum TSH, 2.1 +/- 1.3 mU/L; mean TSH in sleep, 1.3 +/- 0.5 mU/L; P less than 0.05), whereas sleep after sleep withdrawal almost completely suppressed the circadian variation (mean TSH, 1.1 +/- 0.7 mU/L; P less than 0.01). This modulation is due to a significant decrease in pulse amplitude, but not to an alteration in the frequency or temporal distribution of TSH pulses.

The liver is central to the metabolic response to exercise but measurements of effects of reduced liver function on the physiological adaptation to exercise are scarce. We investigated metabolic, endocrine, pulmonary and haemodynamic responses to exercise in 15 healthy untrained controls (Co) and in 30 subjects with reduced liver function (i.e. liver cirrhosis, Ci). The following protocols were used: protocol 1 maximal oxygen uptake \(\dot V{\text{O}}_{{\text{2max}}}\) and anaerobic threshold (AT), protocol 2 stepwise increases in exercise intensity from 0 to 40% \(\dot V{\text{O}}_{{\text{2max}}}\) giving steady-stage conditions, protocol 3 1 h exercise at 20% \(\dot V{\text{O}}_{{\text{2max}}}\). Muscle glycogen content was determined in 15 Ci. Spirometry was essentially normal in Ci. Result: protocol 1 Ci had impaired \(\dot V{\text{O}}_{{\text{2max}}}\) and reduced AT (P < 0.05). Basal plasma concentrations of insulin, glucagon, growth hormone and adrenaline were increased in Ci (P < 0.05); cortisol was normal. During exercise, only glucagon remained different between groups. In protocol 2 Ci had decreased resting respiratory exchange ratio (RQ: p < 0.05) associated with increased plasma concentrations of free fatty acids and glycerol. They had disproportionately enhanced lipolysis and RQ. heart rate (+ 24%), ventilation (+ 28%), thermal effects of exercise (+ 31%) and intrapulmonary shunt volume (+ 76%), which accounted for 11.7 (SD 3.0) or 7.4 (SD 0.9%) of cardiac output during exercise in Ci and Co, respectively (P < 0.05 for all the differences reported). The metabolic effects of Ci were independent of the clinical and nutritional state of the patients. In protocol 3 muscle glycogen content was highly variable in Ci, but mean values were normal [16.9 (SD 8.9) μmol·g−1 wet mass]. Glycogen content positively correlated with resting and exercise-induced RQ, but negatively correlated with the exercise-induced alterations in plasma glucose concentration. From these results we concluded that with reduced liver function \(\dot V{\text{O}}_{{\text{2max}}}\), and AT are reduced, but metabolic, pulmonary and haemodynamic reponses per unit power output are enhanced. Muscle glycogen content would seem to contribute to the metabolic response, but its mobilization to be limited in individuals with reduced liver function.

Type A natriuretic peptide (CDD/ANP-99-126) in its circulating form was analyzed with respect to the localization of its bronchodilating effects in asthmatic subjects in vivo. The intravenous infusion of 5.7, 11.4, and 17.1 pmol kg-1 min-1 CDD/ANP-99-126 caused a significant bronchodilation of both central and peripheral airways. While the localization of the bronchodilating effects was similar to beta 2-agonists, an improvement in lung function parameters comparable to these substances was not observed. But other members of the natriuretic peptide family may reveal a stronger bronchodilating potency.

Emotional stress is often followed by increased susceptibility to infections. Natural killer (NK) cells play a major role in the immediate immune response controlling this susceptibility. In this study on 45 first-time parachutists, it is demonstrated that highly controlled psychological stress increased psychophysiological variables, enhanced the secretion of sympathetic-adrenal hormones and also led to a significant increase of NK cells and their cytotoxic activity followed by a decrease below starting values. This immunological alteration is correlated with the secretion of noradrenaline during the emotional strain. Quick mobilization of these cytotoxic effector cells is suggested as a major mechanism for the effective adaptation of the immune system to stress situations.

Changes in blood composition, renal function, aldosterone and antidiuretic hormone (ADH) concentrations were investigated in 10 untrained male subjects when swimming (60 min at a heart rate of about 155 beats.min-1, water temperature 28 degrees C) and during the subsequent 3 h in a sitting position. Many specific effects of either exercise or immersion were abolished or attenuated; no significant changes in plasma aldosterone, [ADH], [K+], [Cl-], or of urinary volume, glomerular filtration rate, free water or osmolar clearance were observed. The urine was diluted resulting in lowered [Na+]. In blood some quantities which are only slightly influenced by immersion increased during swimming ([Na+], [Lac-], [H+], osmolality, [creatinine]). Exercise induced plasma volume loss, calculated from increasing [Hb], was small (110 ml), probably because interstitial fluid enters the vascular space during the initial phase of immersion. One might anticipate that the training effects on fluid and electrolyte metabolism and circulation are different when swimming and when performing endurance sports on land.

Publisher Summary This chapter describes the application of the CBA (cytochemical bioassay) segment assay and CBA section assay for the determination of human thyroid-stimulating hormone (TSH) in health and disease. TSH is a glycoprotein hormone, produced by, and released from, the anterior pituitary gland. Classic bioassays were not sensitive enough to determine TSH levels in plasma of normal euthyroid or of hyperthyroid patients. The TRH test is one of the most important tests for the study of pituitary–thyroid function. The chapter presents a study in which CBA technique is used to investigate patients with euthyroid goiter and a negative TRH test. By the use of CBA, it is determined that the circulating basal levels of biologically active TSH are low and the pituitary gland in these patients is unresponsive to TRH. The chapter also discusses that the lysosomal response in thyroid follicle cells not only occurs after stimulation by TSH, but also after activation by other thyroid stimulators.

Publisher Summary This chapter describes the episodic hormone secretion in the regulation and pathophysiology of the reproductive system in man. The reproductive system has been extensively analyzed with respect to episodic hormone secretion, its underlying mechanisms of regulation, and pathophysiology. Infusions of testosterone and dihydrotestosterone at twice the daily production rate of testosterone in normal men significantly reduce LH pulse frequency and mean LH concentrations. As this approach may seem pharmacologic instead of physiologic, the use of anti-estrogens and anti-androgens may be preferred. Dopamine infusion reduces the mean LH level but does not influence LH pulse frequency. When gonadotropins are substituted, a continuous or a slow release from a depot of injection is sufficiently effective to normalize spermatogenesis in the same percentage of patients as with pulsatile LHRH infusion.

Idiopathic delayed male puberty is defined as a delay of puberty beyond the age of 16, with prepubertal testosterone levels, normal gonadotropin responses to GnRH (excluding pituitary failure), and normal androgen responses to a single hCG injection (excluding testicular Leydig cell dysfunction), in absence of serious disease. Ten boys with this condition were evaluated as to their spontaneous LH, FSH, and PRL secretory patterns during a 24-h sampling period (20-min intervals). After this all patients were treated with pulsatile infusions of GnRH (25 ng/kg . pulse every 90 min for 10 days. Two groups could be distinguished by means of their pretreatment LH secretory pattern. Five patients had nighttime pulsatile elevation of LH levels, as usually occurs in early puberty. The other five patients did not have such a pattern (prepubertal type). The GnRH treatment resulted in increased LH and testosterone levels in both groups. All patients with pretreatment nighttime pulsatile LH secretion had steady pubertal development during the post-GnRH treatment observation period, whereas the other patients did not. In conclusion, among a number of tests, including chronic pulsatile GnRH treatment for 10 days, only the nocturnal LH secretory pattern differentiated delayed puberty from permanent hypothalamic hypogonadism in boys.