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Biomedical subjects

M J Tansey

Publications and source records attributed to M J Tansey.

14 recordsLinked to original sources
PubMed2001

Pituitary production of prolactin and prolactin-suppressing drugs.

Prolactin secretion from the anterior pituitary is mediated via dopaminergic pathways. Any process that alters dopamine production or transport in the central nervous system may lead to hyperprolactinemia. Most cases of hyperprolactinemia are due to prolactin secreting pituitary tumors or to medications which alter dopamine production. Prolactinomas cause amenorrhea, galactorrhea and infertility in women and impotence and neurological deficits in men. Dopamine receptor agonists are the mainstay of therapy for hyperprolactinemia as they rapidly lower serum prolactin and cause tumor shrinkage. In this paper we review the regulation of prolactin secretion, the clinical features and causes of hyperprolactinemia, and the use of dopamine agonists.

Dopamine Agonists↗
PubMed1993

Sumatriptan in the acute treatment of migraine.

Sumatriptan is a selective 5-HT1-like agonist, which is effective in the treatment of migraine and cluster headache. It has been rigorously assessed in clinical trials involving over 7000 patients who have treated over 35,000 migraine attacks. Both subcutaneous and oral sumatriptan provide a high level of efficacy with 86% of patients obtaining relief after a single 6 mg injection (at 2 h) and 75% after 100 mg oral sumatriptan (4 h), compared with up to 37% in the placebo-treated group (P < 0.001). The onset of effect is rapid, occurring 10 min after injection and 30 min after the tablet. Oral sumatriptan (100 mg) has been evaluated against ergotamine, 2 mg, plus caffeine, 200 mg (as Cafergot); and against aspirin, 900 mg, plus metoclopramide, 10 mg. Headache relief was superior in sumatriptan-treated patients; 66% obtaining relief at 2 h, compared with 48% on Cafergot (P < 0.001). The percentage of patients obtaining complete relief of headache (Grade 0, no pain) was significantly higher with sumatriptan (40%) than with Cafergot (14%) at 2 h. Associated symptoms such as nausea, vomiting and photophobia are effectively relieved by sumatriptan, whereas Cafergot provoked nausea and vomiting in a proportion of patients. Headache relief with sumatriptan was also superior to that seen with aspirin plus metoclopramide. Sumatriptan was as effective in the relief of accompanying nausea and vomiting as aspirin plus metoclopramide. The efficacy of sumatriptan is maintained after repeated long-term use; over a six-month period efficacy was comparable in the first and last attacks, regardless of how many attacks were treated.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1993

Long-term experience with sumatriptan in the treatment of migraine.

Sumatriptan, a specific 5-hydroxytryptamine agonist, is a novel acute treatment for migraine. The efficacy and safety profiles of sumatriptan have previously been demonstrated in several controlled short-term studies. However, because migraine is a recurrent disorder which may persist throughout adult life, sustained efficacy and tolerability are essential if sumatriptan is to be of value in clinical practice. These aspects were therefore evaluated in a programme of three 12-month studies. Sustained efficacy with long-term use of single 100-mg oral doses has been demonstrated in an open study in which 288 patients treated 8,094 migraine attacks. The long-term safety profile of oral and subcutaneous sumatriptan has been evaluated in a total of 849 patients who treated 24,907 migraine attacks in studies lasting up to 1 year. Sumatriptan was well tolerated. Adverse events did not differ qualitatively or quantitatively from those in short-term studies, irrespective of the frequency of attacks or the number of doses used. Migraine attacks were effectively treated with doses less than the recommended maximum and there was no evidence of any adverse effect on attack frequency. In long-term studies the high efficacy of sumatriptan is maintained, and the adverse event profile is unchanged and unaffected by attack frequency.

Administration, Oral↗
PubMed1986

Humoral and blood pressure effects of the angiotensin converting enzyme inhibitor ramipril in essential hypertension.

The humoral and antihypertensive activities of the angiotensin converting enzyme (ACE) inhibitor 2-[N-[(S)-1-ethoxycarbonyl-3-phenylpropyl]-L-alanyl]-(1S, 3S, 5S)-2-azabicyclo[3.3.0] octane-3-carboxylic acid (ramipril, Hoe 498) were investigated in 10 patients with essential hypertension (WHO stage I or II). After a 7-day placebo period, the patients were treated with 5 mg ramipril orally once daily for 14 days. Peak serum concentrations of the active metabolite M1 (dicarboxylic acid) of 5.4-62.0 ng/ml were observed 2-6 h after the first oral dose. The maximum ACE inhibition of 95% was reached 2-4 h after the first oral dose, inhibition exceeded 70% 24 h after dosing. The maximum drop in the systolic and diastolic blood pressure (random zero sphygmomanometer) was measured 4 h after ramipril (p less than 0.02, p less than 0.01), but blood pressure on days 7 and 14 of the treatment period was not different from pretreatment values. Automatically recorded blood pressure results showed a marked reduction of both systolic and diastolic blood pressure during treatment compared to placebo. No side effects occurred. From the present data it is concluded that ramipril is a potent ACE inhibitor in hypertensive patients and that further controlled studies are required for the evaluation of the antihypertensive effect of 5 mg ramipril in essential hypertension.

Adult↗
PubMed1985

The effect of the converting enzyme inhibitor HOE 498 on the renin angiotensin system of normal volunteers.

The converting enzyme inhibitor HOE 498 was evaluated in 12 normotensive male volunteers aged 21 to 26. The efficacy of single 5, 10 or 20 mg oral doses in blocking the pressor response to exogenous angiotensin I was tested in 3 of the subjects. All 3 doses of HOE 498 reduced the pressor response to exogenous angiotensin I to below 50% of control within 1,5 h following administration of the drug. Plasma renin and converting enzyme activity, blood angiotensin I, as well as plasma angiotensin II and aldosterone were measured serially before and up to 72 h following oral administration of a single dose of 2.5, 5, 10 or 20 mg of HOE 498 to groups of 5 volunteers each. As expected, blood angiotensin I levels and plasma renin activity rose while plasma converting enzyme activity, plasma angiotensin II and aldosterone concentration fell after administration of the drug. While the dose of 2.5 mg did not reduce plasma converting enzyme activity below 20% of control, the higher doses all resulted in plasma converting enzyme inhibition exceeding 90%. No side-effects were observed. It is concluded that in normal volunteers HOE 498 is an effective potent and long-acting converting enzyme inhibitor. Based on these preliminary findings it is expected that 5 mg HOE 948 will turn out to be adequate for therapeutic use.

Administration, Oral↗
PubMed1983

Relation between plasma free fatty acids and arrhythmias within the first twelve hours of acute myocardial infarction.

The relation between arrhythmias and plasma free fatty acid (FFA) levels measured every hour in the first 12 h after acute myocardial infarction was studied in thirty-five patients admitted 4.5 h (range 1-9 h) after the onset of symptoms. There was a significant relation between arrhythmias and high mean FFA levels in the first 12 h after acute myocardial infarction. A similar but weaker relation was observed for arrhythmias and high peak FFA levels but not high admission FFA levels. These results suggest that the arrhythmogenicity of FFA within the first 12 h of acute myocardial infarction may depend partly on FFA levels which remain consistently high. Because of the rapid and wide fluctuation of FFA levels during this time no single random value can be considered representative of the mean level, which may explain the conflicting results of previous studies.

Adult↗
PubMed1981

Plasma pancreatic polypeptide and gastrin in the assessment of autonomic activity in acute myocardial infarction.

Measurements of plasma pancreatic polypeptide and gastrin are reported for the first time in patients with acute myocardial infarction and compared with clinical signs of vagal or sympathetic overactivity. Pancreatic polypeptide concentrations were assessed as an index of vagal activity, but elevated values of pancreatic polypeptide found in 7 of the 13 patients on admission did not correlate with clinical evidence of vagal overactivity. The mean pancreatic polypeptide concentrations were not higher in patients with clinical vagal overactivity than in patients with clinical sympathetic overactivity during the 12 h after the onset of symptoms of acute myocardial infarction. Mean gastrin levels were significantly higher on admission and at 4, 5, 6 and 8 h after the onset of infarction in the patients with clinical features of sympathetic overactivity than in the patients with clinical vagal overactivity. Thus plasma gastrin warrants further assessment as an index of sympathetic overactivity in acute myocardial infarction.

Adrenergic beta-Antagonists↗
PubMed1979

The heart in diabetes mellitus. Part I. Biochemical basis for myocardial dysfunction.

The heart in acutely diabetic animals is subject to multiple inhibitions of glucose metabolism caused by enhanced metabolism of free fatty acids (FFA) and ketone bodies. Such metabolic changes may impair the reaction of the diabetic heart to oxygen lack. In chronically diabetic hearts the increased deposition of triglycerides in the heart and the formation of glycoproteins may underlie the newly recognized clinical entity of diabetic cardiomyopathy.

Alcoholism↗
PubMed1977

High mortality in obese women diabetics with acute myocardial infarction.

The factors associated with mortality in 89 diabetics and 793 non-diabetics with acute myocardial infarction who were initially admitted to a coronary care unit were analysed retrospectively. During their stay in hospital diabetics had twice the mortality of non-diabetics. The higher mortality among diabetics was largely accounted for by obese women, who had a hospital mortality of 43%. There was an increased incidence of congestive heart failure in such patients. A therapeutic trial should be performed in such patients to assess whether insulin has an effect on infarct size.

Acute Disease↗
PubMedDate not supplied

Plasma glucose on admission to hospital as a metabolic index of the severity of acute myocardial infarction.

A pilot study was carried out in 22 non-diabetic patients admitted to hospital within 12 hours of acute myocardial infarction to assess the plasma glucose level on admission as an index of infarct size, morbidity and prognosis. Blood free fatty acid, insulin and potassium concentrations were also measured. Mean enzymatically measured infarct size index was three times larger (p less than 0.005) and the incidence of large infarcts was significantly greater (p less than 0.05) in patients with high (greater than 7.5 mMol/L) than in patients with low (less than 7.5 mMol/L) admission glucose concentrations. Patients in the former group also had higher mean peak free fatty acid concentrations (p less than 0.05). Patients who died within six months of their first infarcts had higher initial glucose values than those who survived longer. Plasma glucose concentrations measured within 12 hours of the onset of symptoms of acute myocardial infarction can be used to differentiate those with large from those with small infarcts in non-diabetic patients.

Aged↗