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Biomedical subjects

G Wambach

Publications and source records attributed to G Wambach.

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↗
PubMed1991

[Determination of plasma atrial natriuretic peptide in follow-up of hypervolemic hemodilution in patients with retinal circulatory disorders].

We measured plasma levels of atrial natriuretic peptide (ANP) in 20 patients with impaired retinal circulation in order to monitor hypervolemic hemodilution. In 18 control subjects, plasma ANP levels averaged 37.4 +/- 7.3 pg/ml and 30.0 +/- 5.4 pg/ml before and after an i.v. infusion of 250 ml of HAES 6% over 3 hours. In 8 of 20 patients, plasma ANP exceeded the highest value of 87 pg/ml in the controls at the end of the first infusion. In the group B, ANP increased from 103 +/- 21.6 pg/ml to 142 +/- 12 pg/ml before and after the infusion. In the remaining 12 patients (group A), plasma levels of ANP were 41.1 +/- 8.6 and 44.8 +/- 6.3 pg/ml at the start and the end of the first infusion of HAES. All patients received 500 ml of HAES daily for 8 days. In group B, hemoglobin was significantly lower on day 8 (11.7 +/- 0.48 versus 13.2 +/- 0.38 mg/100 ml) compared to group A (p less than 0.005). Similarly, hematocrit and serum protein was reduced to a greater extent in group B compared to group A indicating intravascular volume expansion. Measuring plasma ANP-levels might be of value to identify patients with reduced tolerance to hemodilution therapy.

Aged↗
PubMed1991

[Cardiac peptides and their importance in heart failure].

Atrial natriuretic peptide (ANP) exhibits a favorable pharmacological profile in heart failure. In reduces preload and afterload by its natriuretic and vasodilatatory actions. Furthermore, it reduces the activity of the renin aldosterone system. This peptide is activated in early heart failure. Plasma levels of 1-28-hANP are elevated and they correlate with the clinical stage of heart failure, as well as with hemodynamic abnormalities. However, the efficacy of this cardiac hormone in heart failure is limited by renal resistance. Possible mechanisms are a reduced renal perfusion pressure, a receptor down-regulation or an overactivity of sodium-retaining hormones like the renin aldosterone system, and the sympathetic activity. The brain natriuretic peptide (BNP) is also stimulated in heart failure; however, its role in the pathophysiology of heart failure remains to be determined.

Animals↗
PubMed1991

[The effect of hemodynamic changes in 24-hour milrinone infusion on sympathetic activity and the renin-angiotensin-aldosterone system in patients with severe heart failure].

The hemodynamics of 18 patients (subgroup A) with severe heart failure (baseline Cl less than or equal to 1.55 l.min-1.m-2), including three patients with cardiogenic shock, and another 22 patients (subgroup B) with moderate heart failure (baseline Cl from 1.55 to 2.5 l.min-1.m-2) were investigated during a 24 h milrinone infusion, combined with investigation of the response of the sympathetic tone (plasma catecholamine levels) and the renin-angiotensin-aldosterone system to the hemodynamic improvement in both subgroups. Cl increased (p less than or equal to 0.001) to 162.7% after 5 min and further to 206.4% of baseline after 30 min of milrinone therapy in subgroup A, and in B to 139.3% and further to 146.4% after 15 min. PCWP decreased (p less than or equal to 0.001) to 83.8% and further to 65.5% of baseline after 30 min in subgroup A, and to 58.4% in subgroup B. Heart rate decreased (p less than or equal to 0.05) from 99.4 to 94.7 bpm in A and showed a decreasing tendency in B. MAP rose in A from 75.5 to 79.4 after 1 h and further to 83.3 mm Hg (p less than or equal to 0.01) after 24 h; in subgroup B, MAP did not change. Plasma noradrenaline level decreased (p less than or equal to 0.001) in A from 1419.5 (B: 782.9) to 838.2 (B: 529.6) after 1 h and further to 655.1 (B: 467.9) pg/ml after 24 h. Plasma renin decreased (p less than or equal to 0.01) in A from 1047.6 (B: 460.2) to 597.4 (B: 222.5) and further to 392.6 (B: 191.7) microU/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
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↗
PubMed1979

Acid- and cryoactivation of renin in human plasma.

Inactive renin in normal human plasma was activated in vitro either by cryoactivation (incubation at 0 degrees C/-5 degrees C up to 3 months) or acid-activation (dialysis to pH 3.0 for 48 h followed by diaylsis to pH 7.5). Plasma-renin-concentration was similar after either activation procedure (96 +/- 50 microU/ml vs 100 +/- 43 microU/ml). There was no further significant acid-activable renin after cryoactivation. These data suggest that conversion of inactive to active renin by optimized procedures is complete. The term "total renin" for activation results under these conditions seems to be valid.

Dialysis↗
PubMed1979

[The saralasin test in the diagnosis of hypertension (author's transl)].

The saralasin test was performed in 68 hypertensives. A clear-cut dependence of the test results on initial plasma-renin concentration and particular sodium balance was demonstrated. Because of this dependence the saralasin test should be performed only under constant conditions. A mild stimulation of the renin-angiotension system by salt restriction to a mean sodium excretion of 50 mmol daily and 80 mg furosemide by mouth 12 hours before the test seems best. In this way essential and renovascular hypertension could be distinguished with considerable reliability (P less than 0.001). Among patients with essential hypertension one could clearly separate those with high plasma-renin concentration from those with a normal or low one. Among patients with renovascular hypertension those with haemodynamically significant renal artery stenosis could with high probability be distinguished from those with non-effective stenosis. A positive saralasin test without testing the function of the normal contralateral kidney does not provide an indication for operation.

Adult↗
PubMed1979

[Sodium-potassium-adenosine triphosphatase-activity in red cell ghosts of patients with essential hypertension (author's transl)].

Increased sodium concentration and high influx of Na22 are reported in erythrocytes of patients with essential hypertension. It was speculated, that these findings are due to a disturbed transport for sodium across red cell membranes. We found a significantly increased activity of the ouabainsensitive Na-K-ATP'ase in red cell ghosts of 27 patients with essential hypertension compaired with 32 normotensive controls. There existed no difference in Mg-ATP'ase-activity between the two groups. These findings suggest an increased activity of the Na-pump in red cell membranes of patients with essential hypertension.

Erythrocyte Membrane↗
PubMed1979

[Improved interpretation of renal-vein-renin-ratio by simultaneous determination of renal 131I-hippuric-acid-clearance-ratio in patients with renovascular hypertension (author's transl)].

In patients with unilateral vascular kidney disease and hypertension, ratio of renal-vein-renin was compared with 131I-Hippuric-acid clearance and change in blood pressure during Saralasininfusion. The ratio of renal-vein-renin was positively correlated with the ratio in renal plasma flow between the kidneys in all patients studied. The ratio of renins therefore is a result of two factors: The difference in renin secretion and the difference in blood flow in the two kidneys. In patients with angiotensin independent hypertension renin-ratios up to 2.0 were found without relevance to elevated blood pressure. When the difference in renal blood flow between both kidneys was small, even a slight difference in renal vein renin indicated hypertension related to increased renin secretion. Renin-ratios in the critical range between 1.5 and 2.5 should only be interpreted in respect to a similar ratio in renal blood flow.

Adult↗
PubMed1979

Antihypertensive effect of progesterone in rats with mineralocorticoid-induced hypertension.

Uninephrectomized, saline-fed male Sprague-Dawley rats were given DOCA 5 mg per week alone or together with progesterone 20 mg per week for 6 weeks (phase I). Subsequently, the doses of DOCA and progesterone were doubled and the rats were studied for an additional 6 wk (phase II). Progesterone prevented DOCA-induced hypertension during phase I. Phase II blood pressures were higher in DOCA-progesterone-treated animals than in controls, but remained lower than in animals treated with DOCA alone. At the end of phase II the animals were killed, and blood samples and skeletal muscle samples were taken for analysis of electrolyte content. DOCA-treated animals were found to have an increased rate of potassium excretion, an increase in muscle sodium concentration, and a decrease in muscle potassium concentration compared to the controls. Progesterone treatment significantly blunted the DOCA-induced changes in muscle electrolyte concentrations and increased the rate of sodium excretion. No hypotensive effect was observed when progesterone in doses similar to those of phase I was administered to spontaneously hypertensive rats. Thus, in experimental mineralocorticoid hypertension, the hypotensive effect of progesterone appears to correlate closely with its mineralocorticoid antagonistic properties.

Animals↗
PubMed1979

Interaction of synthetic progestagens with renal mineralocorticoid receptors.

Progesterone increases urinary sodium excretion at least in part by competition for renal mineralocorticoid receptors. In contrast, synthetic progestagens do not increase sodium excretion or even cause a slight sodium retention. We therefore compared the ability of progesterone and 12 progesterone like compounds to displace [3H]aldosterone from binding at cytoplasmic mineralocorticoid receptors in rat kidney. All synthetic progesteronelike steroids were less active than progesterone in competing with [3H]aldosterone for the receptor binding: progesterone 100%, 11 beta-OH progesterone 50%, 17 alpha OH-progesterone 24% and 16 alpha-methyl-progesterone 3%. Derivates of 17 alpha OH-progesterone (medrogestone 5%, dydrogestone 4%, medroxy progesterone-acetate 2% and chlormadinone-acetate 0.5%) were more potent than 19-nor-testosterone derivates: ethisterone 1%, norethisterone less than 1%, norethindrone less than 1%, norethyl-nodrel less than 1%, and ethynodiol-diacetate less than 1%. The decreased affinity of synthetic progestins for mineralocorticoid receptors explains in part the lack of natriuretic activity of these compounds.

Aldosterone↗