Dopamine blockade and natriuresis during water immersion in normal man

Natriuresis was studied during water immersion in eight normal subjects either in the absence or in the presence of dopamine blockade by domperidone. Creatinine clearance showed no significant changes; urine flow remained significantly above control values during water immersion, implying persistent suppression of antidiuretic hormone. The marked natriuresis seen during water immersion alone was significantly blunted (P less than 0.05) but not abolished during water immersion plus domperidone. Suppression of the renin-aldosterone system by water immersion alone was not significantly different from that obtained during water immersion plus dopamine blockade. On the contrary, plasma prolactin levels, previously suppressed during water immersion alone, were significantly stimulated during water immersion plus domperidone, thus indirectly suggesting a role of dopamine in mediating the blunted natriuresis seen during water immersion.     

Changes in the concentration of endogenous opiates in the blood and cerebrospinal fluid during acute painful stimuli and protective electroacupuncture analgesia

The concentrations of endogenous opiates (beta-endorphin, methionine-enkephalin, leucine-enkephalin) in the spinal fluid and arterial blood plasma has been studied in 16 dogs, using the model of acute pain stimulation under electroacupuncture analgesia (EAA). It has been shown that pain stimulation under EAA is accompanied by a significant increase in methionine-enkephalin++ and leucine-enkephalin concentrations (by 244 and 69.4%, respectively) in the spinal fluid. beta-endorphin level tends to increase. There is also a trend towards the reduction in beta-endorphin and methionine-enkephalin concentrations in the arterial blood plasma, which is indicative of effective antinociceptive stimulation of the endogenous opiate system. However, by the end of the first hour a decrease of methionine-enkephalin and leucine-enkephalin levels in the spinal fluid was paralleled by a trend towards beta-endorphin and methionine-enkephalin increase and a significant leucine-enkephalin increase in arterial blood plasma, which can account for the exhaustion of the opiate system.     

Plasma levels of corticotroph-type pro-opiomelanocortin derivatives such as beta-lipotropin, beta-endorphin(1-31), or adrenocorticotropic hormone are correlated with severity of postoperative pain

BACKGROUND: In the pituitary of lower species, pro-opiomelanocortin is expressed in corticotroph cells of the anterior and in melanotroph cells of the neurointermediate lobe; enzymatic processing in the corticotrophs results in the release of adrenocorticotropic hormone, beta-lipotropin, or beta-endorphin. In the melanotrophs, these fragments are further modified, eg, by N-terminal acetylation. In the human pituitary, these enzyme systems are located within the same cells in the anterior lobe. We studied the reactions of the pro-opiomelanocortin system under preoperative conditions as well as under postoperative pain. METHODS: In 17 patients undergoing hip or knee arthroplasty, we determined plasma concentrations of N-acetyl-beta-endorphin immunoreactive material, authentic beta-endorphin [beta-endorphin(1-31)], adrenocorticotropic hormone, beta-lipotropin immunoreactive material, and cortisol, as well as pain severity rated by the patients using a visual analogue scale before surgery, after surgery but still under spinal anesthesia, under postoperative pain, and 1 day after surgery. RESULTS: Only low levels of N-acetyl-beta-endorphin immunoreactive material were measured in 16 out of 17 patients. High concentrations (1st quartile/median/3rd quartile; pmol/L) of adrenocorticotropic hormone (22.5/55.8/124) and beta-lipotropin immunoreactive material (6.6/34.6/142) were observed under postoperative pain, accompanied by a small increase of beta-endorphin(1-31) concentrations (0.0/6.1/10.9). Preoperatively small but significantly elevated levels of corticotroph-type and melanotroph-type pro-opiomelanocortin derivatives were observed; in contrast, spinal anesthesia suppressed all pro-opiomelanocortin fragment release. Postoperative pain severity correlated with postoperative adrenocorticotropic hormone, beta-lipotropin immunoreactive material, and beta-endorphin(1-31) concentrations. CONCLUSIONS: We conclude that the melanotroph-type pro-opiomelanocortin system is not activated under postoperative pain; the increase of corticotroph-type pro-opiomelanocortin fragment levels is different in quantity and proportion under preoperative conditions or postoperative pain, respectively.     

Pituitary adenomas associated with hyperprolactinemia: a clinical and immunohistochemical study of 97 patients operated on transsphenoidally

Immunohistochemical studies were performed on the tumors of 97 of 100 patients who had undergone an operation for a presumed prolactin-secreting pituitary adenoma; no tissue was available for study in the other 3 patients. Appropriate immunohistochemical studies were done to identify the presence of growth hormone, prolactin, adrenocorticotropic hormone, luteinizing hormone, follicle-stimulating hormone, and thyroid-stimulating hormone within the adenoma cells. The presence of a prolactin-producing pituitary adenoma was confirmed in 91 patients, 3 of whom had an adenoma that consisted of cells that contained prolactin and growth hormone. One other patient, not counted among the 91 with prolactinoma, had lactotrope and thyrotrope hyperplasia. Among the five patients whose adenoma did not contain prolactin cells, four had a null cell adenoma and one had a tumor consisting of follicle-stimulating hormone and luteinizing hormone immunoreactive cells. On the basis of preoperative serum prolactin values in these patients, we concluded that moderately increased values (30 to 200 ng/ml) of serum prolactin are not a reliable guide for determining whether a prolactin-producing pituitary adenoma is present, whereas levels exceeding 200 ng/ml are usually associated with a prolactin-secreting tumor.     

Differences between exclusive breastfeeders, formula-feeders, and controls: a study of stress, mood, and endocrine variables

The purpose of this study was to examine relationships among lactational status, naturalistic stress, mood, and levels of serum cortisol and prolactin and plasma adrenocorticotropic hormone (ACTH). Eighty-four exclusively breastfeeding, 99 exclusively formula-feeding, and 33 nonpostpartum healthy control women were studied. The postpartum mothers were studied cross-sectionally once between 4 and 6 weeks after the birth. Stress was measured using the Perceived Stress Scale, the Tennessee Postpartum Stress Scale, and the Inventory of Small Life Events. Mood was measured using the Profile of Mood States. Serum prolactin, plasma ACTH, and serum cortisol levels were measured by commercial ELISA (enzyme-linked immunosorbent assay) kits. Results indicate that breastfeeding mothers had more positive moods, reported more positive events, and perceived less stress than formula-feeders. Reports of stressful life events were generally equivalent in the two groups. Serum prolactin was inversely related to stress and mood in formula-feeders. When breast and formula-feeders were compared to controls, they had higher serum cortisol, lower stress, and lower anxiety. Breastfeeders had lower perceived stress than controls. Breastfeeders had lower depression and anger and more positive life events reported than formula-feeders. However, there were few correlations among stress, mood, and the hormones in postpartum mothers, and those only in formula-feeders, whereas strong relationships were found between serum ACTH and a number of stress and mood variables in controls. Postpartum mothers reported a range of stress and negative moods at 4 to 6 weeks, and in formula-feeders, serum prolactin was related to some of the stress and mood variables. Breastfeeding appears to be somewhat protective of negative moods and stress.     

Acute effects of cocaine on plasma adrenocorticotropic hormone, luteinizing hormone and prolactin levels in cocaine-dependent men.

Acute cocaine administration alters secretion of anterior pituitary hormones in experimental animals, and cocaine abuse may compromise neuroendocrine function in humans. The goal of this study was to examine cocaine's acute effects on neuroendocrine hormones in cocaine-dependent men. Plasma adrenocorticotropic hormone (ACTH), luteinizing hormone and prolactin levels were measured in 18 men before and after i.v. administration of cocaine (30 mg) or placebo. Each subject served as his own control during the i.v. placebo and cocaine administration conditions. Plasma cocaine levels peaked at 260 ng/ml within 5 min after the i.v. injection. Plasma ACTH levels increased significantly above base-line levels at 5, 15, 30 (P < .01) and 45 min (P < .05) after i.v. cocaine. Plasma luteinizing hormone levels increased significantly above base-line levels at 5 (P < .05) and at 15 min (P < .01) after i.v. cocaine. No changes in plasma ACTH or luteinizing hormone levels were found after i.v. placebo injection. Plasma prolactin levels decreased significantly at 30, 45, 60, 90 and 120 min (P < .01) after both i.v. cocaine and placebo administration. Cocaine-induced increases in plasma ACTH levels may be due to its effects on dopaminergic systems which modulate corticotropin-releasing factor release in brain.     

New pituitary peptide relationships

A glycoprotein molecule discovered in pituitary glands of experimental animals is thought to be the precursor molecule for the pituitary peptides ACTH and beta-lipotropin, molecules themselves known to contain the amino acid sequences of several smaller peptides subsequently isolated. Evidence now exists to suggest the enzymatic cleavage of ACTH to alpha-MSH and corticotropic-like intermediate lobe peptide (CLIP), pituitary peptides with effects upon the fetal pituitary gland. Beta-lipotropin is probable the prohormone for the peptides beta-MSH, gamma-lipotropin, methionine-enkephalin, and beta-endorphin. Beta-MSH may enchance the known physiologic effects of mammalian central nervous system transmitters, while the enkephalins and beta-endorphin have been shown to exhibit opioid analgesic properties as well as effects upon behavior, temperature regulation, and the release of growth hormone and prolactin. Homologies among their amino acid sequences and evidence for prohormone activity in ACTH, beta-lipotropin, and the putative ACTH-beta lipotropin precursor suggest the possibility of the presence of a previously unsuspected interrelationship in the synthesis and release of these various pituitary peptides.     

Plasma interleukin-1, tumour necrosis factor and hypothalamic-pituitary-adrenal axis responses during migraine attacks

To evaluate systemic cytokine and hypothalamic-pituitary-adrenal axis responses in migraine, we measured plasma levels of tumour necrosis factor, interleukin-1, adrenocorticotropic hormone, and cortisol, as well as body temperature during and between attacks in 20 migraine patients. We found no evidence of systemic rise of cytokines during migraine attacks. Plasma cortisol and adrenocorticotropic hormone responses were similar to those found to experimentally-induced pain in normal subjects, i.e. elevated cortisol and unchanged adrenocorticotropic hormone levels. Unexpectedly, body temperature tended to be lower during attacks.     

Neuroendocrine disorders in brain-dead donors at the time of multiorgan harvesting]

Changes in the level of antidiuretic hormone (ADH), adrenocorticotropic hormone (ACTH), somatotropic hormone (STH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), thyroid-stimulating hormone (TSH), prolactin (PL), thyroxin (T4), triiodothyronine (T3) and thyroxine-binding globulin (TBG) have been assessed before and during multiorgan excision in 22 donors with brain death. A progressing decrease in ADH blood supply and changes in ACTH, STH, FSH and PL content have been recorded. No regularities have been observed in LH level changes. TSH and thyroid hormone changes were in most cases characterized by a gradual decrease in their plasma levels. A drop in T3 concentration observed at the initial stage of the study was most pronounced with practically normal T4 and TBG values, that also decreased by the moment of heart excision. It has been concluded that brain death is accompanied by a considerable neuroendocrine disfunction and a marked syndrome of low T3 content.     

Stress hormone stability: processing of blood samples collected during parabolic flight. A pre-flight comparison of different protocols

OBJECTIVES: Compare different protocols for blood processing to be used during parabolic flights. DESIGN AND METHODS: Measurement of cortisol (COR), prolactin (PRL), adrenocorticotropic hormone (ACTH), epinephrine (EP) and norepinephrine (NOR) concentrations stored at different temperatures and intervals before analysis. RESULTS: COR, PRL and NOR showed no changes in concentration between analysis protocols. ACTH dropped by 60% when not analysed within 24 h. CONCLUSION: A standardised processing protocol that includes a 4-h delay following blood collection is suitable for the assessment of serum stress hormone concentrations.     

Plasma Methionine Enkephalin Levels — A Biological Marker for Migraine?

SYNOPSIS
Migraine patients, either during an attack or when pain-free, have significantly higher platelet-rich and platelet-poor plasma methionine-enkephalin levels than healthy race- and sex-matched and age-comparable controls. Although we did not observe differences in the platelet-rich samples between the patients subgroups, platelet-poor samples had higher peptide levels during a pain-free period than the values obtained for the patients during a migraine episode. Similarly, platelet-rich samples obtained from controls and patients during an attack had higher methionine-enkephalin levels than their corresponding platelet-poor plasma samples. These results provide new evidence supporting the involvement of the endogenous peptides in the etiology of migraine headache and suggest that plasma methionine-enkephalin levels could serve as a biological marker for this condition.     

Immunologic hormone detection in hypophyseal adenomas: correlation of serum hormone findings with immunocytochemical hormone levels in tumor tissue

Forty-four out of 82 patients with neurosurgically removed pituitary adenomas showed preoperatively elevated plasma hormone levels of prolactin (PRL; 22 patients), of human growth hormone (hGH; 15 patients), and of adrenocorticotropic hormone (ACTH; 7 patients). Immunocytochemical detection of the hypersecreted hormone in paraffin sections of tumour tissue, was possible in all 7 patients (100%) with Cushing's disease, in 20 patients (90%) with hyperprolactinaemia, and in 10 patients (66%) with acromegaly. In a further 3 cases beta-TSH, in one case beta-LH, and in 8 cases alpha-HCG were demonstrated in sections of tumour tissue. No clinical evidence of endocrine disturbance was found in any of these latter cases. More than one anterior pituitary hormone was detected in sections of tumour tissue in 7 cases. An overall qualitative correlation of 85% was found between the elevated plasma hormone level and immunocytochemical hormone detection in tumour tissue sections. Since there is no correlation between conventional histological staining modalities (acidophilic, basophilic, chromophobic) on the one hand, and the level of plasma hormones or immunological hormone detection in tumour tissue on the other hand, modern histological diagnosis of a pituitary adenoma should include assessment of the functional state as found by immunocytochemical hormone determination.     

The value of plasma prolactin levels in the prediction of the responsiveness of growth hormone secretion to bromocriptine and TRH in acromegaly

Abstract. The mechanism of the inhibition of growth hormone secretion in response to bromocriptine and the ability of thyrotropin releasing hormone to stimulate growth secretion in acromegaly is unknown. In the present study the relationship between the plasma prolactin concentration of untreated acromegalic patients and the reaction of growth hormone to thyrotropin releasing hormone and bromocriptine was investigated.
Plasma prolactin levels were elevated in thirty-three (42%) of seventy-nine untreated acromegalic patients. Seventeen patients had mildly elevated prolactin levels, but in sixteen the plasma prolactin concentration was higher than 30 ng/ml. Bromocriptine (2.5 mg) inhibited growth hormone secretion by more than 50% in 22% of the normoprolactinaemic, in 53% of the mild hyperprolactinaemic and in 88% of the patients with a prolactin level above 30 ng/ml ( P <0.01 v. normoprolactinaemic; P <0.01 v. mildly elevated prolactin levels). An increase of growth hormone secretion by more than 100% of the basal value in response to thyrotropin releasing hormone was observed in 44% of the normoprolactinaemic, in 59% of the mildly hyperprolactinaemic and in 75% of the clearly hyperprolactinaemic patients; ( P <0.01 v. normo-and mildly hyperprolactinaemic patients).
Conclusion: An increased plasma prolactin concentration in patients with acromegaly is accompanied in most patients by a higher sensitivity of growth hormone secretion to bromocriptine.     

Effects of hypnotic analgesia and hypnotizability on experimental ischemic pain

Mechanisms of hypnotic analgesia are still poorly understood and conflicting data are reported regarding the underlying neurochemical correlates. The present study was designed to investigate the effects of hypnotically induced analgesia and hypnotizability on experimental ischemic pain, taking into account pain and distress tolerance as well as the neurochemical correlates. 11 high hypnotizable Ss and 10 low hypnotizable Ss, as determined by scores on the Stanford Hypnotic Susceptibility Scale, Form C (Weitzenhoffer & E. R. Hilgard, 1962), were administered an ischemic pain test in both waking and hypnotic conditions. The following variables were measured: (a) pain and distress tolerance, (b) anxiety levels, and (c) plasma concentrations of beta-endorphin and adrenocorticotropic hormone (ACTH). Results confirmed significant increases of pain and distress tolerance during hypnosis as compared to the waking state, with positive correlations between pain and distress relief and hypnotizability. Moreover, a hypnotically induced dissociation between the sensory-discriminative and the affective-motivational dimensions of pain experience was found, but only in high hypnotizable Ss. Hypnotic analgesia was unrelated to anxiety reduction and was not mediated either by endorphins or by ACTH.     

Thyroid Hormone Inhibition of the Prolactin Response to Thyrotropin-Releasing Hormone

The influence of serum triiodothyronine (T(3)) and thyroxine (T(4)) concentrations on the release of prolactin in man was studied by determining the prolactin response to synthetic thyrotropin-releasing hormone (TRH) in hypothyroid and hyperthyroid patients before and after correction of their serum thyroid hormone abnormalities. The maximum increment in serum prolactin above the basal level (maximum Delta prolactin) was used as the index of response to TRH.In 12 patients with primary hypothyroidism, the maximum Delta prolactin in response to TRH fell from 100.5+/-29.1 ng/ml (mean +/-SEM) before treatment to 36.1+/-6.0 ng/ml (P < 0.01) during the 4th wk of treatment with 30 mug T(3) + 120 mug T(4) daily. The mean serum T(3) level increased from 57+/-8 to 138+/-10 ng/100 ml, and the mean serum T(4) level increased from 3.0+/-0.4 to 7.2+/-0.4 mug/100 ml during this treatment. In eight normal subjects the maximum Deltaprolactin in response to TRH was not significantly different during the 4th wk of treatment with 30 mug T(3) + 120 mug T(4) daily from the response before treatment. In 10 patients with hyperthyroidism, the maximum Deltaprolactin in response to TRH increased from 14.2+/-2.9 ng/ml before treatment to 46.9+/-6.7 ng/ml (P < 0.001) during antithyroid treatment. The mean serum T(3) level fell from 313+/-47 to 90+/-8 ng/100 ml, and the mean serum T(4) level fell from 20.8+/-2.5 to 6.8+/-0.6 mug/100 ml during this treatment.These results show that changes from normal serum levels of T(3) and T(4) are associated with changes in prolactin responses to TRH; subnormal serum levels of T(3) and T(4) increase TRH-induced prolactin release, whereas substantially higher than normal serum levels of T(3) and T(4) inhibit this release.     

Dopamine during α- or β-Adrenergic Blockade in Man: HORMONAL, METABOLIC, AND CARDIOVASCULAR EFFECTS

We studied the contribution of alpha- and beta-adrenergic receptor activation to the cardiovascular, metabolic, and hormonal effects of dopamine. At a concentration of 1.5 mug/kg.min, the infusion of dopamine in 12 normal volunteers was associated with a transient but significant rise in pulse rate, which was prevented by propranolol. Venous plasma glucose did not change throughout the experiments, and a mild increase in plasma free fatty acid levels observed during the administration of dopamine alone was antagonized by propranolol. In contrast, neither the beta-adrenergic blocker, propranolol, nor the alpha-adrenergic blocker, phentolamine, was effective in inhibiting the dopamine-induced rise in plasma glucagon (from 82+/-9 to 128+/-14 pg/ml; P < 0.005) and serum insulin (from 7.5+/-1 to 13+/-1.5 muU/ml; P < 0.005) or its suppression of plasma prolactin (from 8.5+/-1 to 5.2+/-0.8 ng/ml; P < 0.001). Although serum growth hormone levels did not change during the infusion of dopamine alone, an obvious rise occurred in three subjects during the combined infusion of propranolol and dopamine.Whereas some metabolic and cardiovascular effects of dopamine are mediated through adrenergic mechanisms, these observations indicate that this is not the case for the effects of this catecholamine on glucagon, insulin, and prolactin secretion, and thus provide further support for the theory of a specific dopaminergic sensitivity of these hormonal systems in man.     

Ovarian steroid hormone modulation of the acute effects of cocaine on luteinizing hormone and prolactin levels in ovariectomized rhesus monkeys

Cocaine stimulates significant increases in luteinizing hormone (LH) and decreases prolactin levels in gonadally intact rhesus monkeys, but cocaine did not alter plasma levels of these anterior pituitary hormones in ovariectomized females. These findings suggested that ovarian steroid hormones may contribute to the endocrine effects of acute cocaine administration. To test this hypothesis, the acute effects of cocaine and placebo-cocaine on plasma LH and prolactin levels were examined in five ovariectomized rhesus females during three chronic hormone replacement conditions: 1) estradiol (E2beta) treatment (0.0015-0.006 mg/kg/day i.m.), 2) progesterone treatment (0.32 mg/kg/day i.m.), and 3) combinations of progesterone (0.32 mg/kg/day i.m.) and E2beta (0.002 and 0.004 mg/kg/day i.m.). Cocaine (0.8 mg/kg i.v.) did not alter prolactin or LH in ovariectomized monkeys without ovarian steroid replacement. During chronic estradiol treatment, cocaine produced an estradiol dose-dependent decrease in prolactin. Cocaine also decreased prolactin during treatment with progesterone alone and progesterone + E2beta (0.004 mg/kg/day i.m.). Cocaine stimulated a significant increase in LH during treatment with progesterone alone, but not during treatment with progesterone + E2beta, or three of four estradiol treatment doses. Cocaine pharmacokinetics did not differ as a function of hormone replacement conditions. Together, these data suggest that both E2beta and progesterone modulate cocaine's effects on prolactin, whereas E2beta alone and in combination with progesterone, do not facilitate LH release in response to cocaine in ovariectomized rhesus females.     

A neuroendocrinological study in female migraineurs: prolactin and thyroid stimulating hormone responses

To evaluate the change of the neurotransmitter function in migraine, a neuroendocrinological study was performed in eleven female migraineurs and nine female controls. Thyrotropin releasing hormone, luteinizing hormone releasing hormone, and insulin were simultaneously loaded (the Triple test). Before and after loading, serum glucose, prolactin (PRL), thyroid stimulating hormone (TSH), luteinizing hormone, follicle stimulating hormone, adrenocorticotropic hormone, cortisol, human growth hormone and beta-endorphin were measured. The Triple test produced an increase of PRL in both migraine and control groups, but in migraineurs the increase was significantly larger than in controls. TSH also increased in response to the test, but the TSH response in patients was less than in controls, although not significantly so. The responses of other substances showed no significant differences between the two groups. Although dopaminergic hypofunction in migraine has been proposed by some authors, the present findings rather suggest a serotonergic hyperfunction.     

Influence of phlebotomy treatment on abnormal hypothalamic-pituitary function in genetic hemochromatosis

To test the hypothesis that deficiencies in hypothalamic-pituitary function in genetic hemochromatosis result from cellular injury by iron deposits, we conducted provocative tests in 11 men with genetic hemochromatosis before and after iron depletion by serial phlebotomy and in 10 control subjects. We gave combination intravenous injections of insulin (0.15 U/kg), luteinizing hormone releasing hormone (LHRH, 100 micrograms), and thyrotropin releasing hormone (400 micrograms) and then measured plasma glucose, growth hormone, corticosteroids, follicle-stimulating hormone, luteinizing hormone, prolactin, and thyroid-stimulating hormone at 30-minute intervals for 90 minutes. Phlebotomy caused a substantial decrease in median values for serum ferritin, deferoxamine-chelatable iron, and hepatic iron concentration. Before phlebotomy, stimulation by hypoglycemia and thyrotropin releasing hormone caused significantly less secretion of growth hormone (P = 0.004) and prolactin (P = 0.03) in patients than in control subjects. No significant improvement was noted, however, in growth hormone or prolactin secretion after phlebotomy. Of the 11 patients, 7 had secondary hypogonadism, and phlebotomy did not improve the serum testosterone, follicle-stimulating hormone, luteinizing hormone, or responses to LHRH in any case. Chlorpromazine injections failed to elevate serum prolactin in all patients, and administration of levodopa caused a partial reduction in serum prolactin; thus, the hypothalamus may be an important locus of endocrine malfunction in these patients. We conclude that abnormal hypothalamic-pituitary function in genetic hemochromatosis is not substantially improved by iron-depletion therapy.     

高压氧治疗对亚急性期创伤性脑损伤患者腺垂体功能的影响

目的 观察高压氧（HBO）治疗对亚急性期创伤性脑损伤（TBI）患者腺垂体功能的影响。 方法 采用随机数字表法将66例亚急性期TBI腺垂体功能低下患者分为对照组及HBO组,每组33例。2组患者均给予常规治疗（包括脱水降颅压、抗感染、预防癫痫、预防褥疮、营养神经、补液及康复治疗等）,HBO组在此基础上辅以HBO干预,HBO治疗压力为0.2 MPa(2.0 ATA),每日治疗1次,每周治疗6次,共治疗20次。于治疗前、治疗20次后采用化学发光免疫分析法检测患者血清中促肾上腺皮质激素（ACTH）、生长激素（GH）、促甲状腺激素（TSH）、催乳素（PRL）、黄体生成素（LH）、卵泡刺激素（FSH）、皮质醇（COR）、胰岛素样生长因子-1（IGF-1)、游离四碘甲状腺原氨酸（FT4）、睾酮（TES）及雌二醇（E2）水平,对ACTH、GH、TSH、PRL、LH、FSH赋值并计算垂体总体激素评分。 结果 治疗20次后发现HBO组PRL、LH、TES的对数值及垂体总体激素评分［分别为（1.3±0.2）μg/L、（1.0±0.4）mU/L、（2.5±0.2）ng/dl和（22.0±2.6）分］均显著高于对照组水平［分别为（1.1±0.2）μg/L、（0.8±0.3）mU/L、（2.4±0.3）ng/dl和（20.5±2.3）分］,组间差异均具有统计学意义(P＜0.05)。 结论 在常规干预基础上辅以HBO治疗能进一步提高亚急性期TBI患者多种激素水平,促进垂体功能恢复。