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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The secretory activity of the hypothalamic-pituitary axis is influenced by suprahypothalamic regulatory mechanisms. To evaluate the effect of brain lesions on hormonal patterns, we investigated eight patients convalescing from hemispheric stroke and five sex- and age-matched healthy volunteers. Studies were conducted during two consecutive nights with continuous polygraphic recording and sequential blood sampling. Nocturnal plasma hormone measurements showed a normal rhythm of cortisol (a marker of ACTH), elevated prolactin concentrations (p less than 0.05) and low growth hormone values (p less than 0.05). The study suggests that major suprahypothalamic lesions influence hypothalamic function so as to facilitate prolactin secretion and inhibit growth hormone release. They have no effect on the more basic pattern of ACTH-cortisol secretion, however.
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PMID:Dissociated patterns of nocturnal prolactin, cortisol, and growth hormone secretion after stroke. 632 34

These studies were undertaken to clarify the role of the central and peripheral sympathetic nervous system and the renin-aldosterone system on the onset and maintenance of high blood pressure in essential hypertension (EH), and the following examinations were performed: 1) Urinary free norepinephrine and epinephrine excretion (UNEf and UEf), urinary conjugated norepinephrine and epinephrine excretion (UNEconj and UEconj), plasma norepinephrine and epinephrine concentration (PNE and PE), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured in 52 patients with EH, who were divided into two groups (borderline EH: b-EH, and sustained EH: s-EH), and fifteen normals (N). 2) Cardiac index (CI), total peripheral resistance index (TPRI), appearance time, mean transit time and stroke index (SI) were determined by the dye-dilution method in eight patients with b-EH, ten patients with s-EH and ten N. 3) Clonidine was administered orally in a single dose of 150 micrograms to seven patients with s-EH and three patients with b-EH, and PNE, PE and growth hormone (GH) were measured before and after the administration. 4) Isoproterenol was infused intravenously in a dose of 0.02 microgram/kg/min for 30 min to 18 patients with s-EH and six N, then plasma cyclic AMP (c-AMP) and PRA were determined before, during and after the infusion. 5) Methacholine was injected intramuscularly in a dose of 10 mg to seven N, and PNE, PE and PRA were measured before and after the injection. There were no significant differences of PNE, PE, UNEf and UEf among the three groups (b-EH, s-EH and N), but UNEconj in both b-EH and s-EH was higher than in N (b-EH: p less than 0.1, s-EH: p less than 0.05). PRA in s-EH was slightly lower not only in N but also in b-EH. PAC in b-EH and s-EH was slightly lower than in N. The difference of PAC between b-EH and s-EH was not found. CI and SI were higher than in N (p less than 0.05), but TPRI was normal. In s-EH, TPRI was slightly elevated as compared with b-EH (p less than 0.1). In s-EH, clonidine caused a significant lowering of both blood pressure and PNE with a simultaneously marked increment of GH; on the other hand, in b-EH blood pressure and PNE did not change significantly in spite of the distinct rise of GH. After the isoproterenol infusion, PRA and c-AMP increased, and there was a significant correlation between the initial level of PRA and the maximal increment of PRA after the infusion in both s-EH and N.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Studies on the role of the central and peripheral sympathetic nervous system and the renin-aldosterone system on the onset and maintenance of high blood pressure in essential hypertension]. 632 58

Two cases of pituitary apoplexy occurring in the course of long-term bromocriptine therapy for active acromegaly are described. Although bromocriptine was effective in lowering serum growth hormone levels and concomitant clinical improvement was achieved, both patients developed an acute episode suggesting pituitary apoplexy when the therapy was continued for 6 and 24 months, respectively. Surgery verified marked haemorrhage and necrosis of an eosinophilic pituitary adenoma in each case. Bromocriptine may have suppressed the growth of these pituitary adenomas resulting in necrosis of the tumour, followed by haemorrhage into the adenoma. Pituitary apoplexy has not been documented as a complication of bromocriptine therapy. This report points out a possible role of bromocriptine in the development of this catastrophe and that careful follow-up is required when long-term treatment with bromocriptine is attempted.
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PMID:Pituitary apoplexy in acromegaly during bromocriptine therapy. 729 48

1. In autonomic failure, supine exercise lowers blood pressure and worsens postural hypotension. The somatostatin analogue, octreotide, reduces post-prandial and postural hypotension, but its effects on exercise-induced hypotension and on postural hypotension post-exercise are unknown. 2. Eighteen subjects with chronic sympathetic denervation were studied; 12 had pure autonomic failure and six had additional neurological features of the Shy-Drager syndrome. Haemodynamic, hormonal and biochemical changes were measured before, during and after incremental supine leg exercise on two occasions: on no treatment and after subcutaneous octreotide. Exercise was performed 120 min after octreotide in eight subjects and 60 min after octreotide in ten subjects. 3. Octreotide did not improve exercise-induced hypotension; the blood pressure fall was greater during exercise, but the blood pressure level was no different than without treatment. Heart rate, stroke distance, cardiac index and systemic vascular resistance were similar at rest and changed to the same degree with exercise on and off octreotide. After octreotide, resting levels of serum growth hormone, plasma noradrenaline, adrenaline and renin were unchanged, but glucose was higher and insulin was lower. There was no change in biochemical and hormone levels during exercise either off or on octreotide. 4. After octreotide, although the rate of blood pressure recovery was similar post-exercise, the levels of blood pressure were higher than in the non-treatment phase and postural hypotension was improved before and after exercise. 5. In conclusion, in primary autonomic failure, octreotide did not improve exercise-induced hypotension in the supine position, suggesting that octreotide-sensitive vasodilatory peptides do not contribute to the blood pressure fall.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of the somatostatin analogue, octreotide, on exercise-induced hypotension in human subjects with chronic sympathetic failure. 749 36

Ageing is followed by an involution of neuroendocrine functions, resulting in a decreased secretion of sex steroids and growth hormone. In addition, cortisol secretion may be inadequately elevated upon stress challenges, due to deficient braking functions by central glucocorticoid receptors. In combination, these endocrine perturbations will probably result in changes in psychological factors such as energy and well-being, altered body composition, and insulin resistance, as well as other risk factors for diseases characteristic of the ageing human, such as cardiovascular disease, non-insulin-dependent diabetes mellitus and stroke. This cluster of phenomena is frequently seen before the period of normal ageing, indicating premature ageing processes. The background factors in these conditions probably include psychosocial stressors, which are perceived differently depending on individual coping abilities. Socio-economic and other environmental factors, such as smoking and alcohol abuse, may well be responsible for the expression of this syndrome of premature ageing. Preventive and therapeutic trials with hormonal substitution therapy to treat these aberrations have been promising, and encourage further studies aimed at elucidating potential risks in relation to potential improvement of quality of life and, perhaps, longevity.
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PMID:Neuroendocrine ageing. 759 79

Pituitary adenomas are frequently encountered, benign intracranial tumours. Clinically classified according to their capacity to produce and secrete hormones, pituitary tumours are diagnosed from the clinical manifestations and biochemical findings of specific pituitary hormone overproduction or of impaired pituitary function due to pressure on normal pituitary cells, the pituitary stalk or the hypothalamus. Additionally, the tumour may result in neurological manifestations due to its effect as an intracranial space-occupying lesion. Pituitary adenomas may present acutely with pituitary apoplexy after intrapituitary haemorrhage or infarction. The subsequent hypofunction of the pituitary with concomitant neurological sequelae of an expanding intracranial mass are often associated with excruciating headache, diplopia and visual field defects. Gradually developing neurological deficits or secondary endocrine failure over several years may precede the recognition of non-secretory tumours (30-40% of pituitary adenomas) as well as some of the hormone-producing adenomas, especially when they expand beyond the confines of the sella turcica. Asymptomatic masses occur in the pituitary in 5-27% of unselected autopsy series. About 10-20% of pituitaries imaged as part of a brain study contain lesions 'consistent with a pituitary adenoma', with about half being pituitary adenomas ('incidentalomas'). Many advocate screening such cases for a wide spectrum of pituitary function abnormalities. Clinical judgement should be utilized to determine the extent of the work-up and the frequency of follow-up. Acromegaly, a clinical syndrome caused by excess growth hormone secretion, accounts for one-sixth of resected pituitary tumours. This disorder leads to chronic progressive disability and a shortened life span, with approximately 50% of untreated acromegalic patients experiencing premature death. The prevalence of acromegaly has been estimated to range from 50 to 70 per million, with the age of diagnosis usually between the third and fifth decades. Conditions associated with acromegaly include glucose intolerance, diabetes mellitus, lipid abnormalities, cholelithiasis, goitre, and hyperthyroidism, respiratory complications, hypertension, cardiovascular disease, and calcium metabolism abnormalities. An association between acromegaly and cancer, especially of the colon, is now recognized. Epidemiological series have indicated that cancer of the colon, breast and other types of malignancy are a cause of death with increased frequency in acromegalics compared with expected rates. Hypopituitary symptoms secondary to the mass effect of macroadenomas in acromegalic patients are common. Among premenopausal women, menstrual irregularities and galactorrhoea have been reported in 40-70%, while more than half of the men complain of impotence and decreased libido.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical features and differential diagnosis of pituitary tumours with emphasis on acromegaly. 762 86

Nitric oxide (NO), previously identified with endothelium derived relaxing factor (EDRF), is thought to play a role in central neurotransmission: it is characterized by high lipid solubility and short half life, and NO-synthase, the enzyme which generates NO from L-arginine, has been found in the central nervous system (CNS), both in neuronal and glial cells. NO is believed to be involved in many neural events, such as neurotoxicity from N-methyl-D-aspartate (NMDA) receptor overstimulation, brain damage from vascular stroke, fever, nociception, memory and appetite control. Recent evidence implicates NO as a modulator of endocrine secretions, with inhibition of insulin, growth hormone (GH) and oxytocin release and stimulation of vasopressin (AVP), adrenocorticotropin (ACTH) and corticotropin releasing hormone (CRH) release. NO and prostaglandins could mediate neuroendocrine activities of cytokines such as interleukin-1 (IL-1) and interleukin-2 (IL-2), particularly in the CNS.
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PMID:Nitric oxide: a gas as a modulator of neuroendocrine secretions. 818 Dec 9

The purpose of this study was to determine the prevalence of low serum insulin-like growth factor-I (IGF-I) and testosterone in men with poststroke hemiplegia. Serum concentrations of IGF-I, total testosterone, and free testosterone were compared in healthy young men, healthy old men, and old men with poststroke hemiplegia. A low IGF-I level, below the lower 2.5 percentile of the healthy young men, occurred in 85% of the healthy old men, and in 88% of the poststroke hemiplegic patients. When a low IGF-I was defined as a value below the lower 2.5 percentile of the healthy old men, the prevalence in the hemiplegic men was 5%. For total testosterone, a value below the lower 2.5 percentile in the healthy young men occurred in 78% of the healthy old men and in 79% of the stroke survivors. Low total testosterone, defined as a value below the lower 2.5 percentile of the healthy old men, occurred in 17% of the hemiplegic men. The results with free testosterone were similar. Compared with healthy young men, most healthy old men have low serum IGF-I and testosterone levels. Old hemiplegic men resemble healthy old men in their IGF-I levels, but they have more cases of severe hypogonadism (total tostosterone < 193ng/dL). Because correction of IGF-I and testosterone deficiencies in younger adults improves muscle strength, work capacity, and quality of life, treatment with human growth hormone and testosterone may be a useful adjunct to physical measures in the rehabilitation of selected hemiplegic stroke survivors.
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PMID:Hyposomatomedinemia and hypogonadism in hemiplegic men who live in nursing homes. 818 56

The effects of growth hormone (GH) plus insulin-like growth factor-1 (IGF-1) were tested in an experimental model of cardiac failure treated with chronic angiotensin-converting enzyme (ACE) inhibition. Myocardial infarction was induced in rats by left coronary artery ligation. Two weeks after ligation, the animals received either captopril (2 g/L in drinking water) or water for 3 months. The rats were then given either GH (2 mg/kg/day) plus IGF-1 (2 mg/kg/day) or vehicle for 14 days. Captopril treatment decreased mean arterial pressure (MAP), left ventricular end-diastolic pressure (LVEDP) and systemic vascular resistance (SVR) (p < 0.05), and increased cardiac index (CI) and stroke volume index (SVI) (p < 0.05). GH/IGF-1 or captopril+GH/IGF-1 treatment decreased MAP, LVEDP, and SVR (p < 0.05), and increased left ventricular maximum dP/dt, CI, and SVI (p < 0.05). The increases in CI and SVI were significantly greater in the captopril+GH/IGF-1-treated animals than in those treated with captopril alone (p < 0.05). The beneficial effect of captopril in reducing cardiac hypertrophy was preserved in the captopril+GH/IGF-1 group. The results indicate that GH/IGF-1 and captopril can improve cardiac performance in congestive heart failure by independent and complementary mechanisms.
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PMID:Beneficial effects of growth hormone and insulin-like growth factor-1 in experimental heart failure in rats treated with chronic ACE inhibition. 858 84

Pituitary apoplexy as a complication of cerebral angiography has been described in only a few case reports. Some studies have reported the clinical resolution of active acromegaly after pituitary apoplexy. We present a patient with active acromegaly due to a growth hormone (GH)-secreting pituitary macroadenoma, who developed anterior and posterior pituitary insufficiency following cerebral angiography. Furthermore, a significant reduction in tumour size was accompanied by normalization of mean 24 h in GH insulin-like growth factor I (IGF-I) and IGF binding protein 3 levels.
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PMID:Pituitary insufficiency and regression of acromegaly caused by pituitary apoplexy following cerebral angiography. 876 45


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