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Biomedical subjects

G Wambach

Publications and source records attributed to G Wambach.

At least 37 records · Page 2Linked to original sources
PubMed1990

Isradipine: a new calcium antagonist with strong vasodilatory but negligible cardiodepressive effects.

To assess the effects of intravenous isradipine (0.5 mg) on left ventricular function in patients pretreated with the beta-blocker propranolol (0.1 mg/kg i.v.), 10 patients were studied during cardiac catheterization for suspected coronary artery disease (confirmed in 6). All patients had normal ejection fractions at rest. Following propranolol, isradipine significantly reduced mean aortic pressure (baseline: 112 mm Hg; propranolol: 107 mm Hg; isradipine: 92 mm Hg) and left ventricular systolic pressure (149 vs. 144 vs. 117 mm Hg, respectively). Propranolol alone significantly decreased heart rate, which then increased after isradipine (75 vs. 66 vs. 70 beats/min, respectively). Cardiac index was depressed with propranolol but normalized with isradipine (3.8 vs. 3.0 vs. 3.7 L/min/m2, respectively) as was mean pulmonary artery pressure (16 vs. 18 vs. 16 mm Hg, respectively). Left ventricular contractility decreased significantly during beta-blocker infusion and reached baseline values with isradipine (2,270 vs. 2,080 vs. 2,320 mm Hg/s, respectively). Parallel to dP/dtmax, systolic wall tension decreased as a consequence of the reduction of left ventricular volume and afterload (1,223 vs. 1,332 vs. 905 units, respectively). It is concluded that isradipine effectively reduces cardiac afterload with no sign of intrinsic cardiodepression.

Adrenergic beta-Antagonists↗
PubMed1989

Interference of different ACE-inhibitors with the diuretic action of furosemide and hydrochlorothiazide.

In healthy volunteers the acute effect of furosemide (40 mg i.v.) and hydrochlorothiazide (100 mg p.o.) on diuresis, natriuresis and renal kallikrein and kinin excretion was investigated. Furosemide stimulated markedly diuresis and natriuresis as well as urinary kallikrein and kinin excretion. Pretreatment by captopril (C) reduced the diuretic and natriuretic effect of furosemide significantly probably due to a diminished (about 50%) proximal-tubular secretion of furosemide. Captopril did not alter significantly the furosemide induced changes in urinary kallikrein and kinin excretion. After captopril there was a clear dissociation between aldosterone, which was diminished by captopril continuously, and renal kallikrein and kinins, which were still stimulated by furosemide. These results suggest that renal kallikrein-kinin system is stimulated by furosemide directly and independently of aldosterone secretion. Other ACE-inhibitors like ramipril (5 mg) or enalapril (20 mg) did not influence the stimulatory effects of furosemide on diuresis or kallikrein-kinin excretion. Ramipril at a dose of 10 mg, however, enhanced the initial diuretic effect of furosemide by increased furosemide secretion and increased relative sodium excretion. Hydrochlorothiazide induced a prolonged diuresis which was not changed by either captopril or ramipril. Urinary kallikrein excretion was not stimulated by hydrochlorothiazide. Our results show an important drug interference between captopril and furosemide, which is independent of ACE-inhibition and probably only due to an interference in proximal-tubular secretion of both drugs. Between captopril and hydrochlorothiazide no such interaction could be observed.

Adult↗
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

[Status of the captopril test in the diagnosis of hypertension].

The place of captopril (C) testing in the screening for renovascular hypertension is still controversial. Baseline and C-stimulated plasma renin concentrations (PRC) were measured in 113 hypertensives, who where referred for the exclusion of secondary hypertension. In addition intravenous digital subtraction angiography (DSA) and a renal scintigraphy were performed. When renal artery disease was revealed by DSA or renin was stimulated the renal arteries were visualized by direct arteriography (and treated by angioplasty if possible). 86 patients underwent each diagnostic test: 21% had renovascular hypertension. Unilateral renal artery stenosis (n = 10) was detected by the captopril test (cutoff values: baseline greater than 40 microU/ml, after C greater than 180 microU/ml, sensitivity 100%). Bilateral renal artery stenosis (n = 8) was missed when the disease was equally severe on either side (sensitivity 50%). The specificity of C testing was 82%, overall sensitivity (uni- and bilateral disease 78%, prevalence 21%, predictive value of the positive test 0.56, predictive value of the negative test 0.93). With i.v.-DSA the renal arteries were technically evaluable in 91% (82/92) of cases. The sensitivity for the detection of all renal artery stenoses was 79% (uni-lateral 100%, bilateral 40%, specificity 97%). The sensitivity of renal scintigraphy for the detection of unilateral renal artery stenoses was 50%, for the detection of bilateral renal artery stenoses 43%, specificity 81%. The present study demonstrates the usefulness of captopril for the detection of unilateral renal artery stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

[Effect of bradykinin on systemic and pulmonary hemodynamics in the human].

In our studies we investigated the vasodepressor effects of bradykinin in vivo in normotensive and hypertensive subjects. Bradykinin was injected intravenously and intraarterially (40-6050 pM/kg) respectively was infused intraarterially (40-6050 pM/kg/min). The investigations were performed in 21 normotensives and 15 hypertensives. Bradykinin injections were performed after the following pharmacological interventions: salt restriction (10 mmol Na/d), salt loading (300 mmol Na/d), captopril (50 mg), ramipril (5 mg), lisinopril (20 mg), ketotifen (2 x 1 mg), indomethacin (2 x 50 mg), and propranolol (80 mg). The results show that bradykinin lowers blood pressure dose related by marked reduction in peripheral vascular resistance. The blood pressure reduction was strongly correlated with the increase in kinin concentration. This effect of bradykinin appears to be independent of changes in sodium metabolism, of beta adrenoceptors, of histamine-1 receptors, and of prostaglandins. ACE-inhibitors potentiate the blood pressure lowering effect of bradykinin about 20- to 50-fold. In case of an intraarterial injection of bradykinin in only 2-5% o the intravenously used dose of bradykinin are needed to produce an identical fall in blood pressure. From this experiments a pulmonary clearance rate of bradykinin over 95% can be calculated. In the pulmonary arteries bradykinin has no effect on the vascular resistance. In patients suffering from primary or renovascular hypertension the blood pressure response to bradykinin was enhanced. The bradykinin potentiating effect of the ACE-inhibitors was not altered in the hypertensives. In patients suffering from bradykinin hypertension or primary hyperaldosteronism bradykinin developed the same blood pressure lowering effect as in the normotensives.

Adult↗
PubMed1989

[Diagnosis and therapy of malignant peritoneal mesothelioma].

Malignant peritoneal mesothelioma is an uncommon tumor with great diagnostic and therapeutic problems. Symptoms, clinical features and course of the disease are described in three patients which were seen at our hospital within the last years. At the beginning there are often severe weight loss, malaise and sometimes fever of unknown origin. Abdominal pain, increased abdominal girth or nausea indicate advanced tumor stages in most cases. Ultrasonography and computed tomography of the abdomen can give important information during the diagnostic approach. Nevertheless, the definite diagnosis can only be established by laparoscopy or open surgery with biopsy for a histological examination. Despite intern and extern radiotherapy as well as systemic and/or local chemotherapy the prognosis of malignant peritoneal mesothelioma remains unfavourable. Mean survival time ranges from six to 18 months.

Aged↗
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

Renal and adrenal resistance against atrial natriuretic peptide in congestive heart failure: effect of angiotensin I-converting-enzyme inhibition.

We compared the natriuretic and diuretic effect of an intravenous infusion of 1-28 human atrial natriuretic peptide (hANP) (0.1 micrograms/kg/min over 30 min) in 10 patients with congestive heart failure (CHF) and in 10 control subjects of similar age and sex. In the controls, urine volume rose from 36.8 +/- 8.55 to 115.6 +/- 34.2 ml/30 min and urinary sodium excretion from 4.55 +/- 0.8 to 11.2 +/- 2.24 mEq/30 min before and during the infusion of ANP, respectively. In patients, baseline urine volume and sodium output were similar, however, rise in urine volume and urinary sodium was greatly reduced during the infusion of hANP. In patients with CHF, baseline plasma ANP levels (604.1 +/- 135.3 vs. 39.4 +/- 5.85 pg/ml; p less than 0.005) and urinary excretion of cyclic GMP (cGMP) (41.8 +/- 5.22 vs. 15.2 +/- 4.19 nmol/30 min; p less than 0.05) were significantly elevated compared to controls. The absolute and relative rise in cGMP excretion, however, was blunted in patients with CHF. In the controls, angiotensin I-converting-enzyme (ACE) inhibition by enalapril significantly reduced the urinary output of sodium and water after ANP infusion. Plasma ANP levels and urinary cGMP remained unaltered by ACE inhibition. Furthermore, treatment with enalapril resulted in a rise in renin and a drop in aldosterone levels. The reduction of plasma renin and serum aldosterone by ANP was maintained after ACE inhibition. In the patient group, administration of enalapril (3 X 2.5 mg every 6 h) reduced ACE activity in the serum from 84.7 +/- 16.9 to 2.13 +/- 0.88 U/l. Arterial blood pressure was lowered from 114.7 +/- 6.69 to 106.1 +/- 7.25 mm Hg systolic and from 76.9 +/- 3 to 69.2 +/- 3.7 mm Hg diastolic. However, natriuresis and diuresis and creatinine clearance following infusion of ANP remained unaltered.

Adrenal Glands↗
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↗
PubMed1989

Detection of renal impairment in cases of chronic abuse of analgesics by administration of desamino-D-arginine vasopressin.

An early diagnosis of renal dysfunction is particularly important in patients with chronic abuse of analgesics. First morphological changes in cases of analgesic nephropathy are found in the renal medulla. Therefore, urinary osmolarity as well as the urinary excretion of cyclic adenosine monophosphate (AMP) and kallikrein were measured after application of desamino-D-arginine vasopressin (DDAVP) as parameters of the renal tubular function in 21 patients with normal creatinine clearance and a regular, excessive use of analgesics. The results were compared with those of 17 healthy volunteers and 8 patients with chronic renal insufficiency after analgesic nephropathy. In patients with analgesic nephropathy the urine osmolarity after 12 h of thirst was 367 +/- 28 mOsm/kg and did not increase after DDAVP. The results obtained from healthy volunteers were 781 +/- 39 mOsm/kg. Half of the patients with chronic misuse of analgesics had lower values of urine osmolarity after thirst and DDAVP compared to the reference area of healthy subjects. Similar results were found when the effect of DDAVP under conditions of water-loading was tested. The excretion of cyclic AMP as a second messenger of DDAVP and of kallikrein did not differ between patients with chronic abuse of analgesics and healthy volunteers. The excretion of kallikrein in patients with manifest analgesic nephropathy, however, was decreased. Thus the renal concentration test with DDAVP proved to be useful in early diagnosis of renal dysfunction caused by analgesics.

Adult↗
PubMed1988

Impaired renal responsiveness to human atrial natriuretic peptide (hANP) in normotensive patients with type 1 diabetes mellitus.

Potential impairment of the efficacy of human atrial natriuretic peptide (human ANF-(99-126), hANP), the most potent endogenous natriuretic agent in healthy subjects, was examined in eight male normotensive patients with uncomplicated type 1 diabetes mellitus (aged 22-37 years). After giving informed consent, patients and eight male control subjects (aged 22-28 years) received in a random double-blind study design i.v. bolus injections of 100 micrograms hANP (Bissendorf peptide) or placebo. At base-line, patients differed from controls in elevated creatinine clearance (P less than 0.05) and in mild postprandial hyperglycemia. Whereas the responses of urinary cyclic guanosine monophosphate, the second messenger of hANP, were found to be normal in patients, the diuretic and natriuretic effects of hANP were grossly impaired when compared to controls (P less than 0.01); hANP resulted in increased plasma protein concentrations only in controls (P less than 0.05 vs patients). In both groups, creatinine clearance remained uninfluenced by hANP. There were similar decreases in plasma renin activity, aldosterone, levels, and blood pressure (systolic more than diastolic) in both groups (P less than 0.05 vs placebo). Heart rate and blood glucose remained unchanged. Thus, there is evidence for a decreased responsiveness to hANP exclusively of renal fluid, sodium, and chloride excretion in uncomplicated type 1 diabetes mellitus. The mechanisms responsible for this phenomenon remain obscure, neither a down regulation at the hANP receptor sites nor an hANP-induced shift from intra- to extravascular fluid volume are likely to be involved in its probably diabetes-specific pathogenesis.

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↗