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

Ketanserin, a serotonin-2-receptor antagonist, was administered to 12 subjects with mild to moderate hypertension in a randomized, double-blind, placebo-controlled crossover trial. After 6 weeks of ketanserin (40 mg every 12 h), blood pressures measured 12 h after dosing were not significantly different from those obtained during the placebo period. However, 2 h after ketanserin administration, supine systolic and diastolic blood pressures declined 11 +/- 10 mm Hg (p less than 0.01) and 6 +/- 5 mm Hg (p less than 0.005) from predose values, whereas placebo caused no change in either systolic or diastolic blood pressure. At the time of peak antihypertensive activity, plasma renin activity, aldosterone, growth hormone, and prolactin levels were unchanged. Prolactin levels decreased slightly (4.1 +/- 3.0 vs. 3.7 +/- 2.9 ng/ml, p less than 0.05) during ketanserin therapy when measured 12 h after dosing. Other pituitary hormones, serum testosterone, plasma catecholamines, and plasma lipids showed no changes. Heart rate was also unchanged. Stroke volume, measured 2 h after dosing, increased (70 +/- 22 vs. 85 +/- 31 ml, p less than 0.05) with ketanserin therapy, but cardiac output did not change significantly. Ketanserin has a moderate antihypertensive effect and neutral metabolic-hormonal profile when used as monotherapy for the treatment of hypertension. However, further studies are needed to define the frequency of dosing that will provide 24-h antihypertensive activity.
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PMID:Antihypertensive therapy with ketanserin: metabolic and hemodynamic effects. 246 37

To investigate cardiovascular changes in experimental acromegaly, a growth hormone-secreting tumour (MtT-W-15) was implanted in adult female rats. Somatic and tumour growth occurred steadily during the 8 week study period, as did an increase in serum growth hormone titre. Weight of left ventricle and right ventricle increased directly with tumour growth, both on an absolute basis and when compared with normal rats of equal body weight. Atrial weight also increased substantially. Haematocrit declined sharply at first, and more slowly later with increasing tumour weight. Haemodynamic measurements were made on these animals at two stages of tumour growth using an anaesthetised open-chest preparation. Cardiac index (per g body wt), stroke index, stroke work, left ventricle +dP/dtmax, and dF/dtmax of aortic flow were greatly elevated in rats with the largest tumours (longer duration), and to a lesser extent in those with smaller tumours (shorter duration). Systemic peripheral resistance and heart rate were depressed. Ventricular weight increased non-linearly with increases in cardiac index. Cardiac output, stroke volume, stroke work and dF/dtmax normalised per g left ventricle weight were also elevated. Splenomegaly accompanied tumour growth; however, splenectomy of tumour-bearing animals failed to prevent development of anaemia and cardiomegaly. While a direct effect of elevated growth hormone provides the best explanation for development of cardiomegaly in this model, volume work overloading due to anaemia and water retention may be a contributory cause.
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PMID:Cardiomegaly and haemodynamics in rats with a transplantable growth hormone-secreting tumour. 315 90

Cardiovascular and Renal function were examined in two populations of long-term insulin-dependent diabetics, those with microalbuminuria, a sign of early, subclinical nephropathy and those with clinically manifest diabetic nephropathy. In addition, clinical variables of possible importance for the occurrence and prognosis of diabetic nephropathy were analyzed. Microalbuminuria - a mean of three over-night urinary albumin excretion rates greater than 20 micrograms/min - was found in 16% of Albustix-negative, normotensive, insulin-dependent diabetics. The microalbuminurics had higher supine blood pressures than normoalbuminurics. The albumin excretion rate in microalbuminurics correlated to blood pressure at rest but not to glycosylated haemoglobin. The cardiovascular responses to five different test manoeuvres revealed more evident signs of autonomic nerve dysfunction in microalbuminurics than in normoalbuminurics. The circulatory reactions during mental stress however, were almost identical in the two subgroups. Despite similar glomerular filtration rate and renal plasma flow the albumin excretion during mental stress increased in microalbuminurics, but remained unchanged in normoalbuminurics. It is postulated that a disturbance of glomerular basement membrane permeability is a pre-requisite for the elevated albumin excretion seen in microalbuminurics. Inability to regulate glomerular haemodynamics, due to autonomic nerve dysfunction, may also be a contributing factor. Such dysfunction perhaps even explains why microalbuminurics have higher blood pressures at rest compared with normoalbuminurics. In manifest diabetic nephropathy the rate of renal functional decline correlated to arterial blood pressure, while glycemic control showed no such relation. Patients with rapidly progressive nephropathy showed higher values of growth hormone than slow progressors. In patients with diabetic renal failure, cardiac catheterization revealed reduced stroke work and elevated left ventricular end-distolic pressure during exercise. Autonomic nerve dysfunction and arterial hypertension possibly contributed to the impaired cardiac performance. The existence of a specific diabetic cardiopathy must even be considered. There was a male predominance both in subclinical and manifest diabetic nephropathy. Age at onset of diabetes was lower in micro- as compared to normoalbuminurics. Duration of diabetes had no prognostic implication in subclinical or manifest nephropathy. The mortality rate was high in patients with manifest nephropathy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Studies of cardiovascular and renal function in subclinical and manifest diabetic nephropathy. 316 65

Postoperative persistence of elevated growth hormone (GH) levels in patients with acromegaly usually suggests residual adenoma tissue secreting GH and is an indication for further treatment. In rare cases, spontaneous normalization of serum GH levels in patients with acromegaly has been reported to occur as a consequence of intratumoral hemorrhage (pituitary apoplexy). We report two patients in whom persisting acromegaly was documented 1 and 2 weeks, respectively, after transsphenoidal operation and who experienced spontaneous normalization of GH levels. In one patient, this favorable outcome was found 1.5 years after the operation and followed a pregnancy. The other patient, whose GH values normalized 3 months after operation, had received preoperative treatment with a new, long-acting somatostatin analog.
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PMID:Spontaneous postoperative normalization of growth hormone levels in two patients with acromegaly not cured by transsphenoidal surgery. 320 Mar 94

A 34-year-old man with acromegaly was observed, and the clinical course and various endocrinological deficiencies occurring before, during and after the development of pituitary apoplexy were evaluated. Following the attack, the patient experienced acute reductions in growth hormone (GH) and other pituitary hormones, adrenohypophyseal insufficiency and transient diabetes insipidus which appeared subsequent to glucocorticoid therapy. The level of growth hormone in serum and cerebrospinal fluid (CSF) was measured synchronously, and the respective regressions of GH levels in serum and CSF were observed. The results demonstrated the utility of measuring hormonal levels in CSF in the clinical evaluation of pituitary apoplexy in a patient with a functioning pituitary tumor.
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PMID:Spontaneous remission of acromegaly after pituitary apoplexy following head trauma. 320 21

We report a case of acromegaly followed by pituitary apoplexy in which hormonal changes during the course of an acute episode were investigated. Serum growth hormone level increased markedly during the acute phase, and, subsequently, decreased rapidly. Finally, serum growth hormone level remained low and did not respond to stimulation. In contrast, the serum cortisol level remarkably decreased during the most serious stage and returned to the previous level after pituitary apoplexy. The low level of cortisol during the acute phase is compatible with the patient's manifestation of adrenal insufficiency, and hydrocortisone sodium succinate administration improved the critical state of the patient dramatically.
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PMID:Transient elevation of serum growth hormone level during pituitary apoplexy in acromegaly. 351 99

Ten consecutive patients with subarachnoid hemorrhage (SAH) of unknown cause were examined for sellar abnormalities and pituitary dysfunction. The diagnosis of SAH rested on a typical history and the demonstration of blood in the cerebrospinal fluid (computed tomography (CT), lumbar puncture). Initial CT and four-vessel angiography were performed in all patients, and five had repeat angiography. Endocrinological assessment was done after the initial angiography, and abnormal findings from this first study were reassessed 3 months later. The follow-up study included a high resolution CT scan of the sellar region. One patient had panhypopituitarism. Insufficient growth hormone secretion alone or combined with a low plasma concentration of estradiol or testosterone was found in another seven patients. The sella was ballooned or enlarged in three patients, and four patients had at follow-up a partly empty sella. A spontaneous development of a partly empty sella from an adenoma with suprasellar extension was observed in the patient with panhypopituitarism. This patient had experienced pituitary apoplexy with resulting SAH. Based on sellar enlargement, an empty sella, and pituitary dysfunction, this pathogenesis was suggested in another three patients. Our findings suggest that hemorrhagic necrosis in a pituitary adenoma may be an important cause of SAH with normal angiography.
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PMID:Subarachnoid hemorrhage with normal cerebral angiography: a prospective study on sellar abnormalities and pituitary function. 380 31

The authors report a case of pituitary apoplexy that developed in a patient shortly after bromocriptine therapy was started for a growth hormone-secreting pituitary adenoma. The tumor was associated with visual impairment and ocular palsies, and was treated by transsphenoidal decompression. Although spontaneous tumor necrosis cannot be excluded, a causal role of bromocriptine treatment is suggested.
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PMID:Pituitary apoplexy in an acromegalic patient during bromocriptine therapy. Case report. 402 Apr 51

A 42-year-old man with diabetes mellitus and probably acromegaly had a pituitary apoplexy with left-sided oculomotor palsy. There was an immediate fall in blood glucose concentration. Pituitary insufficiency promptly developed. Blood glucose levels remained normal for the next two years. During the first year after the pituitary apoplexy, severe proliferative retinopathy developed in the left eye, which became almost blind. Only mild retinopathy was present on the right side. Plasma concentrations of growth hormone remained low after the apoplexy, and the acromegalic features subsided. The explanation of these findings may be that the proliferative retinal angiopathy was caused by compression of the cavernous sinus at the time of the apoplexy. This would lead to impaired venous drainage, thus resembling occlusion of the central retinal vein, which may cause retinopathy similar to that seen in diabetes mellitus.
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PMID:Pituitary apoplexy, the Houssay phenomenon, and accelerated proliferative retinopathy. 403 88

An 11 year old, tall boy presented with symptoms typical of pituitary apoplexy. A large necrotic and haemorrhagic tumour was removed, which was shown to be an adenoma secreting growth hormone and prolactin. Subsequent treatment comprised cranial irradiation and hormone replacement. Eighteen months after operation growth was static and plasma growth hormone and prolactin concentrations were undetectable. Treatment of pituitary apoplexy should comprise excision of the tumour and postoperative irradiation; such treatment after early recognition of the condition offers the best chance of preserving normal pituitary function in children with gigantism.
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PMID:Spontaneous endocrine cure of gigantism due to pituitary apoplexy. 631 18


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