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Biomedical subjects

M Stimpel

Publications and source records attributed to M Stimpel.

At least 19 recordsLinked to original sources
PubMed1992

[How reliable is oscillometric blood pressure determination at the finger using the Omron device?].

The precision of oscillometric blood-pressure measurements on the finger with the model HEM-812F, manufactured by Omron, was compared to the standard method. The digital measurements from 180 inpatients (115.0 +/- 1.2 mmHg systolic, 68.8 +/- 0.8 mmHg diastolic) were significantly lower than oscillometric measurements from the upper arm using a Bosomat (121.3 +/- 1.4 mmHg systolic, 74.2 +/- 0.9 mmHg diastolic). Correlation coefficients were r = 0.713 for systolic and r = 0.683 for diastolic values, with significant variance of individual values. In direct comparison of the two methods immediately after ergometry the differences were even greater (57 mmHg systolic, 32 mmHg diastolic). Significantly lower digital pressures at the finger were noted in comparison with direct blood-pressure measurements after punction of the femoral artery. Because of significant differences of blood-pressure measurements compared to the Riva-Rocci method, the digital measurement with the HEM-812F device (Omron) can not be generally recommended.

Blood Pressure Determination↗
PubMed1992

[Does the captopril test improve the diagnosis of primary hyperaldosteronism?].

Plasma concentrations of renin and aldosterone were measured before and 60 min after taking 25 mg captopril in 242 patients with arterial hypertension (124 men, 118 women, aged 51.9 +/- 12.7 years; unilateral aldosterone-producing adrenal adenoma in 8, idiopathic hyperaldosteronism in 16 and essential hypertension in 189). Basal plasma aldosterone levels were twice as high in those with adenoma or hyperaldosteronism (216.9 +/- 99.1 pg/ml and 256 +/- 123 pg/ml, respectively) as in those with essential hypertension (117.7 +/- 115 pg/ml). Basal renin levels in adenoma and idiopathic hyperaldosteronism (1 +/- 0.8 microU/ml and 2.6 +/- 1.9 microU/ml, respectively) were decreased compared with those in essential hypertension (13.1 +/- 14.2 microU/ml). The basal aldosterone/renin ratio was higher in adenoma (436 +/- 370 pg/microU) and idiopathic hyperaldosteronism (615 +/- 950 pg/microU) than in essential hypertension (52.9 +/- 151.3 pg/microU). The sensitivity of this ratio in combination with the aldosterone concentration was 100% for recognizing an adrenal adenoma, its specificity 92.7%. The mean plasma aldosterone level after captopril administration did not change in adenoma patients, but fell to 162 +/- 85 pg/ml (P less than 0.001) in those with idiopathic hyperaldosteronism. These data indicate that the captopril test contributes to distinguishing primary from idiopathic hyperaldosteronism.

Adenoma↗
PubMed1989

[Atrial natriuretic peptide and its significance for arterial hypertension].

Atrial natriuretic peptide is a recently discovered cardiac hormone with natriuretic, vasodilatory and hypotensive activities. The role of this hormone in the pathophysiology of hypertension is of particular interest. In contrast to an earlier concept, a deficiency of the atrial peptide could not be found in animal models of hypertension or in patients. ANP plasma levels were elevated in SHR with accelerated hypertension, in salt-sensitive Dahl rats, in rats with DOCA-salt-hypertension and in animals with renovascular hypertension. Elevated ANP levels under these conditions can be explained by an expansion of the intravascular volume or by an elevated atrial wall stretch induced by the hypertension itself. In patients with primary hypertension, plasma levels of the peptide are raised in some patients and are normal in others. Plasma ANP levels correlate with age, blood pressure and signs of left ventricular hypertrophy. A negative correlation is described between ANP and renin. Measurement of plasma ANP levels does not allow a differentiation between primary and secondary forms of hypertension. Elevated ANP levels are also found in primary hyperaldosteronism and in renal failure. Stimulation of ANP secretion by physical exercise and dietary salt loading is maintained in hypertension. Infusion of 1-28-hANP leads to a reduction in systemic arterial pressure in normotensives and hypertensives. The natriuresis induced by exogenous ANP is more pronounced in hypertensives. Stimulation of endogenous ANP secretion does not prevent the rise in blood pressure possibly due to a reduction in ANP receptors in target tissues.

Acromegaly↗
PubMed1989

Therapeutic value of calcium antagonists in autonomous hyperaldosteronism.

The chronic effect of the calcium antagonist nitrendipine was investigated on blood pressure (BP), plasma aldosterone concentration (PAC), plasma renin activity (PRA), and serum potassium in six patients with primary aldosteronism, either due to an (unilateral) aldosterone-producing adenoma (APA; n = 3; age, 44 +/- 4 years; PAC, 312 +/- 96 pg/ml; PRA, less than 0.1 ng/l.h; serum potassium, 2.8 +/- 0.3 mmol/l) or to bilateral idiopathic hyperaldosteronism (IHA; n = 3; age, 49 +/- 1 years; PAC, 212 +/- 32 pg/ml; PRA, 0.1 +/- 0.1 ng/l.h; serum potassium, 3.3 +/- 0.2 mmol/l). After withdrawal of antihypertensive medications at least 3 weeks prior to the study, nitrendipine was given orally in a daily dosage of 40 to 60 mg. BP, PAC, PRA, and serum potassium were determined before (see data above) and after 4 weeks of nitrendipine therapy. After 4 weeks, BP was significantly reduced (178 +/- 10 to 165 +/- 6 mmHg systolic, 109 +/- 7 to 101 +/- 6 mmHg diastolic) in three patients with APA and in two with IHA. No significant changes of PAC, PRA, and serum potassium were observed in these patients. However, one patient with clinical characteristics of IHA and a long-term history of diuretic therapy showed a complete normalization of BP, PAC, PRA, and serum potassium, suggesting that the etiology of autonomous hyperaldosteronism in this patient might differ from typical primary aldosteronism. From these findings we conclude that calcium antagonists may be helpful in lowering BP in those patients with primary aldosteronism who develop intolerable side effects under treatment with spironolactone or trilostane.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1989

Impact of acute and chronic sodium loading on atrial natriuretic peptide and renin in man.

The relationship between the renin-angiotensin system and the atrial natriuretic peptide and its contributions to the control of sodium balance is not clarified. We therefore studied plasma renin concentration (PRC) and plasma levels of atrial natriuretic peptide (ANP) in normal subjects during acute and chronic salt loading. Acute intravascular volume expansion by iv infusion of 2000 ml of normal saline resulted in sharp rise in plasma ANP from 122 +/- 24 to 405 +/- 141 pg/ml (p less than 0.05). This increase was only transient with plasma ANP returning to control levels after 240 min. In contrast, reduction in plasma renin concentration was less pronounced, however it was persistent for up to 240 min paralleled by a reduction in plasma protein. Reciprocal changes in ANP plasma levels and PRC were observed during dietary modification in sodium intake. At the end of low sodium diet over 4 days, supine plasma ANP averaged 49 +/- 7 pg/ml and levels increased to 128 +/- 38 pg/ml after 6 days of high sodium intake in 11 healthy subjects (p less than 0.05). In contrast, PRC values averaged 69.8 +/- 19.8 microU/ml and 14.4 +/- 6.5 microU/ml during low and high sodium diet respectively (p less than 0.01). The inverse relation between PRC and ANP was seen after prolonged dietary sodium loading over 15 days in 8 additional subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Natriuretic action of ANP is blunted by ACE inhibition in humans.

We investigated the impact of angiotensin I-converting enzyme (ACE) inhibition by enalapril (3 X 2.5 mg p.o.) on the renal action of acute intravenous (i.v.) infusion of atrial natriuretic peptide (1-28-hANP 0.1 micrograms/kg/min for 30 min) in 10 normal subjects. During the control infusion of ANP, urinary sodium excretion rose from 4.5 +/- 0.8 to 11.2 +/- 2.2 mEq/min and urine volume from 32 +/- 14 to 115 +/- 34 ml/30 min. This increment in urinary volume and sodium output during ANP infusion was almost completely reduced by ACE inhibition. ANP plasma levels before and during the infusion and stimulation of urinary cGMP excretion were unaltered by ACE inhibition. However, enalapril treatment reduced systolic blood pressure (SBP) from 112 +/- 3 to 106 +/- 3 mm Hg and diastolic blood pressure (DBP) from 71 +/- 2 to 66 +/- 3 mm Hg. The small rise in glomerular filtration rate (GFR) during the control infusion of ANP was not observed after pretreatment with enalapril. The study demonstrates the importance of the renin-angiotensin system for the natriuretic and diuretic action of ANP in normal humans.

Adult↗
PubMed1988

[Diagnostic significance of the clonidine suppression test in suspected pheochromocytoma].

A clonidine suppression test and the measurement of the catecholamine (noradrenaline and adrenaline) concentration in 24-hour urine were undertaken on 13 patients with benign phaeochromocytoma (PCC), 30 patients with benign hypertension (BHT) and ten healthy, normotensive volunteers. In 11 patients with PCC (85%) the clonidine suppression test gave true-positive results (no significant suppression of initially raised plasma-catecholamine concentration after oral intake of 300 micrograms clonidine). Continuous fall in plasma-catecholamine level after clonidine occurred in two patients with PCC and only moderately elevated initial levels (false-negative results, 15%), as well as in all patients with BHT and all normal controls (true-positive, 100% each). A false-negative result for catecholamine concentration in 24-hour urine was obtained in only one patient (8%). In all others there were either true-positive results (urine concentration greater than 200 micrograms/24 h in 12 patients with PCC, 92%) or true-negative results (urine concentration less than 150 micrograms/24 h in all patients with BHT, 100% each). Compared with direct catecholamine measurement in 24-hour urine, the clonidine suppression test did not fulfil the criteria for further investigations in those patients who had moderately raised plasma-catecholamine levels.

Adrenal Cortex Function Tests↗
PubMed1988

Relationship between plasma atrial natriuretic peptide and left atrial and left ventricular involvement in essential hypertension.

In order to investigate the role of cardiac hypertrophy in atrial natriuretic peptide (ANP) secretion in patients with essential hypertension, plasma levels of ANP were measured after overnight rest in 36 patients with untreated hypertension and in 31 normotensive controls. In the hypertensive subjects, plasma levels were correlated with left ventricular (LV) and left atrial abnormalities detected by chest X-ray, electrocardiogram (ECG) and M-mode echocardiography. Plasma ANP levels in patients with hypertension averaged 146 +/- 27 pg/ml compared to 46 +/- 7 pg/ml in the normotensive subjects (P less than 0.001). In patients with hypertension a significant correlation was found between ANP and supine systolic blood pressure (r = 0.54, P less than 0.001) and between ANP and diastolic blood pressure (r = 0.38, P less than 0.05). Furthermore, plasma ANP levels were correlated with total heart volume (r = 0.68, P less than 0.01), LV mass (r = 0.525, P less than 0.001), LV posterior wall thickness (r = 0.39, P less than 0.05), Sokolow-Lyon index (r = 0.721, P less than 0.001) and end-diastolic diameter of the left atrium (r = 0.334, P less than 0.05). The results suggest a contribution of LV and left atrial abnormalities to ANP secretion in essential hypertension.

Adult↗
PubMed1988

Are calcium antagonists helpful in the management of primary aldosteronism?

The chronic effect of the calcium antagonist nitrendipine, a 1,4-dihydropyridine derivative, on blood pressure (BP), plasma aldosterone concentration (PAC), plasma renin activity (PRA), and serum potassium was investigated in six patients with primary aldosteronism, either due to an (unilateral) aldosterone-producing adenoma (APA) (n = 3; age 44 +/- 4 years; PAC: 312 +/- 96 pg/ml; PRA: less than 0.1 ng/L/h; serum potassium: 2.8 +/- 0.3 mmol/L) or to bilateral idiopathic hyperaldosteronism (IHA): (n = 3; age 49 +/- 1 years; PAC: 212 +/- 32 pg/ml; PRA: 0.1 +/- 0.1 ng/L/h; serum potassium: 3.3 +/- 0.2 mmol/L). After withdrawal of antihypertensive medications 2 weeks prior to the study, nitrendipine was given orally in a daily dosage of 40-60 mg. BP, PAC, PRA, and serum potassium were determined before and after 4 weeks of nitrendipine therapy. After 4 weeks, blood pressure was significantly reduced (178 +/- 10 to 165 +/- 6 mm Hg systolic, 109 +/- 7 to 101 +/- 6 mm Hg diastolic) in three patients with APA and in two with IHA. No significant changes of PAC, PRA, and serum potassium were observed in these patients. However, one patient with clinical characteristics of IHA and a long-term history of diuretic therapy showed a complete normalization of BP, PAC, PRA, and serum potassium, suggesting that the etiology of autonomous hyperaldosteronism in this patient might differ from typical primary aldosteronism. From these findings, we follow that calcium antagonists do not normalize BP, PAC, PRA, and serum potassium in patients with APA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Plasma levels of atrial natriuretic peptide (ANP) in patients with paroxysmal supraventricular tachycardia and concomitant polyuria (urina spastica)].

A concomitant diuresis and natriuresis has been reported to occur in 30-50% of patients with paroxysmal supraventricular tachycardia. While the increase of the diuresis may be secondary to an inhibition of vasopressin, the etiology of the natriuresis is presently not well understood. To determine the role of atrial natriuretic peptide (ANP) in the pathogenesis of tachycardia-induced polyuria, we measured ANP levels in two female patients (aged 59 and 68 years) with recurrent episodes of paroxysmal supraventricular tachycardia during such attacks, as well as after conversion to a normal sinus rhythm. In both patients, episodes of supraventricular tachycardia were associated with both a large increase in ANP plasma levels (560 resp. 1.208 pg/ml; normal range: 50 +/- 10 pg/ml) and polyuria. Despite elevated ANP plasma levels, no diuretic and natriuretic response to tachycardia could be observed during episodes of shorter duration, some of which occurred in the older patient studied. After restoration of a normal sinus rhythm, ANP plasma levels decreased to baseline levels (107 resp. 32 pg/ml). The results of this study show that the secretion of ANP is increased during episodes of paroxysmal supraventricular tachycardia, suggesting that ANP might contribute to the pathogenesis of natriuresis and diuresis frequently associated with supraventricular tachycardia.

Aged↗
PubMed1988

[Atrial natriuretic peptide (ANP) in essential hypertension: a humoral marker for salt sensitivity and hypertensive heart disease at a clinically asymptomatic stage?].

Out of 32 patients (f = 10, m = 22; mean age: 46 +/- 3 years) with untreated essential (primary) hypertension (WHO-classification I-III) and without clinical signs of congestive heart failure or chronic renal failure, 19 showed plasma-ANP base levels above the normal range (greater than 100 pg/ml; normal range: 50 +/- 10 pg/ml). While high sodium loading caused an increase of plasma ANP levels and a concomitant decrease of plasma renin and aldosterone concentrations, low sodium loading caused the opposite pattern of ANP and renin/aldosterone secretion. Some patients with essential hypertension with highly elevated plasma ANP levels (10-20-fold above the normal range) showed an only moderate decrease of ANP and a slight increase of renin under a low sodium diet. Plasma ANP levels were significantly correlated with the heart volume (r = 0.54; p less than 0.05; radiologically determined), the electrocardiographic signs of left ventricular hypertrophy (Sokolow-Lyon index; r = 0.62; p less than 0.05) and with the left atrial diameter (r = 0.34; p less than 0.05; determined by 2-D-echocardiography). We speculate that high levels of plasma ANP in patients with essential hypertension might be interpreted as a compensatory mechanism either for an insufficient excretion of sodium or for myocardial dysfunction.

Adult↗
PubMed1987

Studies of pharmacokinetics and therapeutic effects of glucocorticoids entrapped in liposomes after intraarticular application in healthy rabbits and in rabbits with antigen-induced arthritis.

Dexamethasone palmitate (DMP) entrapped in liposomes of defined sizes was administered intraarticularly in healthy rabbits and in rabbits with antigen-induced arthritis. The pharmacokinetics and therapeutic effect of liposomal DMP were measured and compared with corresponding experiments using microcrystalline triamcinolone acetonide (TAC). The small DMP liposomes (diameter 160 nm) showed a greater decrease in joint circumference than the 3-times-higher dose of microcrystalline TAC. Moreover, about 98% of administered TAC had already disappeared from the joint 6 h after injection, whereas about 36% of liposomal DMP was still measured in synovial fluid and synovium at the same time. Increasing the vesicle diameter from 160 to 750 nm (large liposomes) improved the retention of DMP by a factor of 2.6 within 48 h after injection in healthy rabbits. In addition, none of the liposomal glucocorticoid preparations ever suppressed the endogenous plasma cortisol level, which is in contrast to the suppression measured after administration of the microcrystalline preparation.

Animals↗