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Biomedical subjects

H Ibsen

Publications and source records attributed to H Ibsen.

At least 73 records · Page 4Linked to original sources
PubMed1992

[Treatment of hypertension in Norway. Indications, therapeutic intensity and economic aspects].

The Norwegian Society of Hypertension held its third scientific meeting in February 1991. One of the issues discussed was when to initiate drug treatment of uncomplicated essential hypertension and what level of blood pressure should be the goal of treatment. The American guidelines suggest that a blood pressure of 140/90 mm Hg or higher should be treated pharmacologically, whereas WHO suggests 160/95 mm Hg. The consensus at the meeting was that, in otherwise healthy subjects without end organ damage, a diastolic blood pressure of 100 mm Hg or more over three to six months should be treated with drugs, and that a safe goal would be around 135-140/85-90 mm Hg.

Drug Costs↗
PubMed1992

The influence of captopril on the epinephrine response to insulin-induced hypoglycemia in humans. The interaction between the renin-angiotensin system and the sympathetic nervous system.

The aim of this study was to assess whether an interaction exists between the renin-angiotensin system and the sympathetic nervous system at the level of the adrenal medulla during insulin-induced hypoglycemia in normal humans. Seventeen healthy volunteers were studied in a randomized, single-dose, double-blind, cross-over fashion using 25 mg captopril v placebo followed by an intravenous injection of 0.15 IU/kg insulin. Blood samples were obtained before and at 15 min intervals after insulin injection. Both plasma glucose level and heart rate were identical during captopril and placebo at rest and after insulin. Plasma renin activity increased after insulin and captopril. The increase in plasma epinephrine was lower after insulin and captopril compared to after insulin and placebo. Likewise the increase in plasma norepinephrine was blunted on insulin and captopril. Thus, when the generation of angiotensin II was blocked by captopril the insulin-induced rise in epinephrine and norepinephrine was blunted. This indicates that an interaction exists between the renin-angiotensin system and the sympathoadrenal system.

Adult↗
PubMed1990

The efficacy and tolerability of long-term felodipine treatment in hypertension. The Scandinavian Multicenter Group.

The antihypertensive effect of felodipine and hydrochlorothiazide, both given in addition to beta-blockers, were compared in this double-blind multicenter study in 103 patients. To all patients concluding the study (n = 92), felodipine was given openly, and the antihypertensive effect and tolerability was studied for 1 year. Patients with a diastolic blood pressure greater than or equal to 100 mmHg, despite beta-blocker treatment, were randomized to treatment with felodipine 5 mg twice daily (n = 51) or hydrochlorothiazide 25 mg (n = 52) once daily for 4 weeks. The dose was then doubled in all patients for a second 4-week period. During open follow-up, all patients were given felodipine 5-15 mg (starting dose 5 mg) twice daily in addition to the beta-blocker. Hydrochlorothiazide could also be added. Reductions in systolic and diastolic blood pressure were significantly greater with felodipine than with hydrochlorothiazide at both the low and high dose levels. There were significantly more responders (diastolic blood pressure less than or equal to 90 mmHg or fall of greater than or equal to 10 mmHg) in the felodipine group. Felodipine and hydrochlorothiazide were both well tolerated. Hydrochlorothiazide treatment was accompanied by a decrease in serum potassium and an increase in serum uric acid. One year of treatment felodipine therapy resulted in a blood pressure fall from baseline of 34/23 mmHg. The most commonly reported adverse event was ankle edema. No clinically important changes in blood tests were seen during felodipine treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1990

The effect of fosinopril sodium on cerebral blood flow in moderate essential hypertension.

The effect of the angiotensin converting enzyme (ACE) inhibitor fosinopril sodium on regional cerebral blood flow (rCBF) was investigated in 8 patients with moderate essential hypertension. A constant dose of chlorthalidone (25 mg/day) was given to stimulate the renin angiotensin system, and fosinopril sodium was given in incremental doses (10 to 40 mg/day) with the aim of obtaining a diastolic blood pressure at or below 90 mm Hg. Regional CBF was measured with xenon-133 inhalation tomography. Repetitive measurements were made at the start of treatment and again after 4 to 12 weeks treatment in the resting supine position, and during lower body negative pressure (LBNP) as a substitute for the upright position. Four hours after the first 10 mg dose of fosinopril the mean arterial pressure (MAP) had been reduced from 127 +/- 13 mm Hg to 105 +/- 9 mm Hg (P less than .01) without any significant change in mean CBF (55 +/- 9 mL/(100 g X min) at baseline versus 52 +/- 9 mL/(100 g X min) after fosinopril). After prolonged treatment with chlorthalidone and fosinopril, mean CBF was still unchanged from baseline levels, when measured 4 and 24 h after a single dose of fosinopril, despite a 10% reduction in MAP (P less than .01). LBNP did not lead to any significant change in rCBF. The regional distribution of CBF was normal in all patients throughout the study. We conclude that treatment with fosinopril sodium causes a moderate fall in blood pressure without any adverse effects on rCBF.

Adult↗
PubMed1989

Angiotensin converting enzyme inhibition and cerebral blood flow autoregulation in normotensive and hypertensive man.

The acute effect on the lower limit of cerebral blood flow (CBF) autoregulation of an angiotensin converting enzyme (ACE) inhibitor, captopril, was studied in normotensive volunteers and in hypertensive patients. Baseline CBF was measured using xenon-133 inhalation tomography, and changes in CBF were measured using the arterio-venous oxygen difference method. Cerebral blood flow autoregulation was studied in two separate normotensive groups, one group of 12 volunteers serving as a control, and one group of 12 volunteers studied after the administration of captopril 50 mg. In a group of seven hypertensive patients CBF autoregulation was studied before and 1 h after the administration of captopril 25 mg. In the normotensive volunteers the median lower limit of CBF autoregulation was 83 and 74 mmHg in the untreated and the captopril-treated group, respectively, with no significant difference between the two groups. In five of the hypertensive patients the lower limit of CBF autoregulation was lowered by captopril, in median by 22 mmHg. However, in two patients it was increased, by 3 and 13 mmHg, respectively. It is proposed that the shift in the lower limit of CBF autoregulation seen in some of our cases, and which has previously been documented in experimental studies, may be dependent on the activity of the sympathetic nervous system.

Adult↗
PubMed1988

Lithium clearance and renal tubular sodium handling during acute and long-term nifedipine treatment in essential hypertension.

1. In two separate studies the lithium clearance method was used to evaluate the influence of acute and long-term nifedipine treatment on renal tubular sodium reabsorption. 2. In the acute study, after a 4 week placebo period two doses of 20 mg of nifedipine decreased supine blood pressure from 155/101 (20.6/13.5) +/- 11/4 (1.5/0.5) to 139/88 (18.5/11.7) +/- 16/9 (2.1/1.2) mmHg (kPa) (means +/- SD; P less than 0.01). Lithium clearance, glomerular filtration rate and sodium clearance did not change. Therefore the calculated values of absolute proximal and absolute distal sodium reabsorption rates were also unchanged, as were potassium clearance, urine flow and body weight. 3. In the long-term study, lithium clearance, glomerular filtration rate, sodium clearance, potassium clearance, urine flow and body fluid volumes were measured after a 4 weeks placebo period and after 6 and 12 weeks of nifedipine treatment. As compared with placebo, mean supine blood pressure decreased significantly. The glomerular filtration rate did not change but lithium clearance fell by 30%. Consequently, the absolute and the fractional proximal sodium reabsorption increased significantly. The fractional distal sodium reabsorption did not change. Sodium clearance, fractional sodium excretion, potassium clearance, plasma volume and extracellular fluid volume were also unchanged. 4. In conclusion, we found no changes of renal tubular sodium reabsorption during acute nifedipine treatment, whereas long-term nifedipine treatment caused a redistribution of tubular sodium reabsorption without a change in overall sodium excretion or body fluid compartments.

Absorption↗
PubMed1988

Hypokalemia and ventricular arrhythmias in acute myocardial infarction.

In the present study, 408 patients with acute myocardial infarction were included. The serum concentration of potassium was assessed on admission. Episodes of ventricular fibrillation and/or ventricular tachycardia within the following 6 hours were registered. A significant positive correlation between hypokalemia and the incidence of malignant ventricular arrhythmias was demonstrated. Ongoing treatment with diuretics at the time of admission did not appear to be of any significance for the development of ventricular fibrillation or ventricular tachycardia. Out of 100 hypokalemic patients, only 33 were treated with diuretics. The main reason for hypokalemia in the early phase of an acute myocardial infarction is most likely an activation of the sympathetic nervous system leading to an influx of potassium from the extracellular to the intracellular body fluid compartment.

Diuretics↗
PubMed1986

Effects of combined therapy with amiloride and hydrochlorothiazide on plasma and total body potassium, blood pressure, and the renin-angiotensin-aldosterone system in hypertensive patients.

After a run-in period of 8 weeks on a regimen of hydrochlorothiazide (HCT, median dosage 75 mg/day), patients with essential hypertension were randomly allocated to continued hydrochlorothiazide therapy (Group I) or additional treatment with amiloride (Group II, median dosage 15 mg/day, or 5 mg per 25 mg hydrochlorothiazide) for the following 12 weeks. Thereafter all the patients were changed to treatment with a fixed combination tablet containing 5 mg amiloride and 50 mg hydrochlorothiazide (Moduretic), keeping the thiazide dosage unchanged for an additional 12 weeks. In Group I patients there was no change in plasma potassium, total body potassium content or the renin-angiotensin-aldosterone system during the 12 weeks on HCT. When the treatment was changed to Moduretic, significant increases were found of 10% in plasma potassium and 3% in total body potassium content. No important stimulation of the renin-angiotensin-aldosterone system was found. In Group II patients addition of an average of 15 mg amiloride to the hydrochlorothiazide treatment led to significant increases in plasma potassium and total body potassium content of approximately 15% and 4%, respectively. There was also a significant increase in the plasma concentrations of renin, angiotensin II and aldosterone. Reducing the average dose of amiloride to 7.5 mg/day by use of Moduretic did not lead to decrease in plasma potassium or total body potassium content. Plasma concentrations of renin, angiotensin II, and aldosterone were decreased, but the individual changes varied markedly and no significant overall change was found.

Adult↗