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Biomedical subjects

K Silberbauer

Publications and source records attributed to K Silberbauer.

At least 37 records · Page 2Linked to original sources
PubMed1986

Bicyclo-prostaglandin E2 metabolite in congestive heart failure and relation to vasoconstrictor neurohumoral principles.

Vasodilator prostaglandins may play a role in maintaining circulatory homeostasis in patients with congestive heart failure (CHF). Plasma levels of bicyclo-prostaglandin E2 metabolite (PGEm), a chemically stabilized degradation product of the vasodilator prostaglandin E2, were determined in 45 patients with chronic CHF (New York Heart Association class II, III or IV). Mean circulating levels of bicyclo-PGEm were significantly elevated in patients with functional class III (72 +/- 8 pg/ml) or IV CHF (77 +/- 10 pg/ml) compared with control subjects (49 +/- 3 pg/ml) and patients with functional class II CHF (49 +/- 4 pg/ml). Bicyclo-PGEm concentrations correlated with plasma renin activity (r = 0.68, p less than 0.001) and plasma angiotensin II (r = 0.56, p less than 0.001) and plasma noradrenalin levels (r = 0.34, p less than 0.05). An inverse correlation was found between serum sodium concentrations and levels of bicyclo-PGEm (r = 0.46, p less than 0.01) as well as plasma renin activity (r = 0.66, p less than 0.001). Thus, prostaglandin E2 levels in plasma are increased in patients with severe CHF.

Adult↗
PubMed1986

Left ventricular function in well-controlled insulin-dependent (type I) diabetics--an echophonocardiographic study.

A high prevalence of left ventricular dysfunction in insulin-dependent (type-I) diabetics has been reported. However, the exact influence of metabolic control and/or the coexistence of early diabetic microangiopathy is unknown. Thus, we assessed left ventricular function by echophonocardiography in 50 type-I diabetics (mean age 26 +/- 7.9 years), who showed a fairly good metabolic long-term control (mean hemoglobin A1: 8.8%) after the introduction to intensified insulin therapy in comparison with 50 age- and sex-matched controls. Type-I diabetics did not differ from controls in their left ventricular internal diameters, mean wall thickness, ratio of pre-ejection period to left ventricular ejection time and systolic shortening fraction. Isovolumetric relaxation period reflecting an early diastolic event was slightly but significantly prolonged in diabetic subjects, independent of metabolic control status or existence of early microangiopathy. Isovolumetric relaxation period showed a statistically significant correlation to age in type-I diabetics, but not in controls. Possibly, the diabetic status--although well-controlled, but not normalized--may biochemically alter the myocardium and might influence its diastolic properties.

Adult↗
PubMed1986

Acute and chronic effects of captopril on bicyclo-PGEm, the stable bicyclic end product of prostaglandin E2 in essential hypertension.

Hemodynamic and hormonal actions of acute (50 mg) and chronic (150 mg/day) captopril were tested in 10 patients with essential hypertension. Under short-term conditions blood pressure was reduced, heart rate and plasma adrenaline did not change, plasma angiotensin II and plasma aldosterone decreased. Plasma renin activity, basal plasma noradrenaline and bicyclo-PGEm, a novel stable metabolite of prostaglandin E2, increased after captopril. With chronic captopril treatment blood pressure was reduced after 4 weeks before readministration of captopril, heart rate did not change, plasma renin activity and bicyclo-PGEm remained elevated for 12 h after the last captopril dose. Angiotensin II remained suppressed, aldosterone and plasma catecholamines did not change between doses. Readministration of captopril led to a further reduction in blood pressure. Angiotensin II and aldosterone were further suppressed, bicyclo-PGEm levels increased from a higher baseline. Heart rate and plasma catecholamines did not change. Taken together, the results suggest that prostaglandin E2 is involved in the acute and chronic hypotensive response of captopril in patients with essential hypertension.

Blood Pressure↗
PubMed1986

Inhibition of acetylcholine-induced bronchoconstriction in asthmatics by nifedipine.

The calcium-dependent constriction of bronchial smooth muscle cells and release of mediators derived from mast cells is important in the pathophysiology of asthma. We hypothesized that nifedipine, a slow calcium channel blocker, would inhibit or attenuate acetylcholine-induced bronchoconstriction in asthmatics. Because one consequence of mast cell activation is the release of platelet-activating factor, we wondered whether thromboxane levels would be increased during acute bronchial constriction in asthmatics. Bronchoconstriction was induced in 8 asthmatics (6 men, 2 women) by acetylcholine; each subject was pretreated either with placebo or nifedipine (20 mg sublingually) on 2 separate days. Vital capacity, forced expiratory volume in 1 s, peak expiratory flow rates and oscillatory resistance were measured prior to and after the intake of placebo or nifedipine as well as after an acetylcholine challenge. Pretreatment with nifedipine significantly attenuated acetylcholine-induced changes in all four lung function parameters studied, but did not significantly influence the increase in thromboxane B2 plasma concentrations observed after the acetylcholine challenge. From these data we conclude that nifedipine inhibits the acetylcholine-induced bronchoconstriction in asthmatics. This effect may be either a direct action on bronchial smooth muscle or may be due to the inhibition of mediators other than thromboxane.

Acetylcholine↗
PubMed1986

Platelet sensitivity to prostacyclin in smokers and non-smokers.

Platelet activating effect of cigarette smoking appears to be important in the development of atherosclerosis. We previously demonstrated a reduced sensitivity of platelets to exogenous prostacyclin (PGI2) in vitro from patients with proven atherosclerotic disease, indicating a possible role of altered platelet function in the development of atherosclerosis. We now hypothesize that cigarette smoking might be an important cause of altered platelet sensitivity to PGI2 observed in patients with atherosclerosis. To test this hypothesis, the response of platelets to exogenous PGI2 was tested in chronic smokers and non-smokers, prior to and after smoking two cigarettes (active smoking) and prior to and after exposure to a tobacco smoke-contaminated atmosphere (passive smoking). This study indicates that platelets of chronic smokers are less sensitive to exogenous PGI2 than platelets of non-smokers. In addition, active as well as passive smoking decreases platelet sensitivity to PGI2 in non-smokers, whereas chronic smokers exhibit no further decline. We conclude that decreased platelet sensitivity to PGI2 might be an important contributing factor to the altered platelet function observed in patients with atherosclerosis.

Adult↗
PubMed1986

[Hemodynamic effects of nitroglycerin following acute inhibition of prostaglandin synthesis].

The mechanism of action by which nitrates produce vasodilation has not been fully clarified so far. Experimental studies indicate a possible relationship to the prostaglandin system. This study describes the consequences of acute prostaglandin synthesis inhibition on the hemodynamic effects of nitroglycerin in patients with stable angina pectoris. Intravenous application of 1 g acetylsalicylic acid was associated with a small but significant blunting of the pressure decline in the pulmonary and systemic circulation following the sublingual administration of 0.8 mg nitroglycerin. Premedication with 75 mg indomethacin i.m. was followed by a decrease in pressure decline in the pulmonary artery during intravenous nitroglycerin infusion. Significant inhibition of prostaglandin synthesis was shown by a substantial decline in plasma levels of circulating prostaglandin metabolites in both experiments. These results indicate that the mechanism of action of nitroglycerin may be partially mediated by vasodilatory prostaglandins.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Plasma vasopressin as influenced by acute and chronic blockade of the renin-angiotensin system.

The activation of the renin-angiotensin system that occurs during the development of congestive heart failure (CHF) may be accompanied by continued secretion of vasopressin (AVP) in response to non-osmotic stimuli. Increased supine plasma AVP levels (by radio-immunoassay) were found in 31 patients with moderate to severe CHF (11.49 +/- 1.00 pg/ml s.e.m.) 24 h after the last diuretic dose, which correlated with plasma renin activity (PRA) (r = 0.37, P less than 0.05). However, acute inhibition of converting enzyme with captopril did not decrease plasma AVP levels (14.9 +/- 3.9 versus 14.0 +/- 2.8 pg/ml, n = 8). Indeed, in six out of eight patients, plasma AVP actually increased following captopril - presumably secondary to haemodynamic changes. Readministration of captopril after 4 months of captopril treatment, 12 h after the last dose, again did not change AVP levels (9.58 +/- 1.2 versus 13.1 +/- 1.9 pg/ml), whereas changes in haemodynamics, PRA and angiotensin II were as expected and similar to the first test. These results suggest that the acute haemodynamic action of captopril in CHF is not mediated via suppression of vasopressin, although in some patients with non-osmotic vasopressin, excess activation of the renin-angiotensin-aldosterone system might constitute a factor.

Adult↗
PubMed1985

[Hemofiltration and the neurohumoral system in patients with severe heart failure].

6 fluid overloaded patients with congestive heart failure, NYHA classification IV, resistant to drug therapy, were treated by pump driven venovenous hemofiltration. The sympathetic nervous system measured by plasma norepinephrine concentration was stimulated in all patients. 4 of 6 patients had a markedly enhanced plasma renin activity. Between 7 and 20 l of fluid were removed by hemofiltration. The expected increase of plasma norepinephrine did not occur in 4 out of 6 patients. The improvement of cardiac pump function by hemofiltration could be an explanation for this apparent paradoxical regulation. Patients who had almost a normal plasma renin activity prior to hemofiltration showed a marked increase after the procedure. In patients with extremely high levels of plasma renin activity we noted a decrease after hemofiltration. Almost in every patient with a serum sodium concentration lower or equal 132 mmol/l the plasma renin activity was markedly elevated. Patients with normal serum sodium concentrations exhibited only slightly elevated plasma renin activity. Therefore, a hyponatremia in patients with heart failure can be used as a marker for high plasma renin activity. All patients had a significant improvement of the clinical state after hemofiltration. 3 patients, however, showed deterioration within a few weeks, due to the severity of the disease. Their plasma norepinephrine levels remained high or had a tendency to increase.

Adult↗
PubMed1985

Cardial decompensation caused by hypertension and polyglobulia associated with multiple renal oncocytomas.

A 43 year old man was referred to the Internal Department for the examination of cardial decompensation, hypertension, polyglobulia and atrophy blanche of the lower legs. Clinical and supersonic examination revealed two tumors in the left kidney (diameter 8 and 3.5 cm) and some small tumors in the right kidney. Laboratory studies disclosed erythropoietin levels up to 170 mU/ml (standard 14-61 mU/ml) and a red blood cell count of up to 8 X 10(6)/ml. After recompensation, a radical left nephrectomy and the removal of three small tumors of the right kidney four weeks later was initiated. Postoperative erythropoietin levels and red blood cell count sank to the normal range leading to the reduction of antihypertensive therapy. The clinical course indicates a strong etiological connection between hypertension as well as polyglobulia with the multiple bilateral oncocytomas. Polycythemia also led to the atrophy blanche which had resulted from disturbances of microcirculation.

Adenoma↗
PubMed1985

[Hemofiltration in chronic heart failure].

30 patients with severe congestive heart failure (NYHA IV) unresponsive to medical management were treated by continuous hemofiltration (CHF). 57% of patients received arteriovenous CHF and 43% of patients venovenous, machine assisted CHF over 95 +/- 31 hours. A reduction of body edemas was achieved. The removal of body fluid by CHF between 2 and 40 kg led to a reduction of body edemas and short-term clinical improvement. Furthermore CHF treatment induced hemodynamic improvement with a reduction of central venous pressure (18 +/- 6 cm H2O pre CHF vs 8 +/- 4 cm H2O post CHF p less than 0.01) and a reduction of left ventricular filling pressure (22 +/- 6 mm Hg vs 14 +/- 5 mm Hg, p less than 0.01), while the left ventricular ejection fraction remained unchanged. Patients with low serum sodium levels (less than 132 mval/l) benefited most. While 28/30 of patients has short-term clinical improvement between 2 and 8 weeks, 38% of patients had long-term benefits.

Adult↗
PubMed1984

Detection of aneurysms by gamma-camera imaging after injection of autologous labelled platelets.

Autologous platelet labelling was used to calculate platelet half-life in 860 patients with symptoms of coronary heart disease and/or peripheral vascular disease. Abnormal platelet deposition indicating an abdominal aortic aneurysm was found in 21 by gamma-camera imaging after reinjection of autologous indium-111 labelled platelets. Aneurysms detected by imaging were confirmed by angiography, computer tomography, and at subsequent surgery.

Adult↗
PubMed1984

[Technic of radioactive labeling of autologous human thrombocytes using 111-indium-oxine and 111-indium-oxine-sulfate and their clinical use].

Using 111indium oxine and 111indium oxine sulphate as platelet labels, maximal labelling efficiency can be achieved already after 3 minutes at an incubation temperature of 37 degrees C. Mean labelling efficiency values of about 90% are reached at a platelet count of greater than 10(9) platelets/ml, but the labelling efficiency is satisfactory also at a rather low platelet count of about 10(6) platelets/ml (71% on average). Platelet labelling with these tracers allows the calculation of platelet half-life in vivo, and gamma-camera imaging of platelet aggregates in thrombosis and renal transplant rejection as well. In the present study, the platelet half-life is significantly shortened in patients with coronary heart disease (n = 15), peripheral vascular disease (n = 13) and primary hyperlipoproteinaemia (n = 32) in comparison with 106 controls. No age dependence of platelet half-life was found in the different groups of patients whereas in the control group, a significant negative correlation between age and platelet half-life was observed.

Adult↗
PubMed1984

Effect on nitroglycerin and other organic nitrates on the in-vitro biosynthesis of arachidonic acid-metabolites in washed human platelets.

Organic nitrates exert well known vasodilating effects in coronary arteries, although the exact mechanism of action is not fully understood. In this study the influence of these drugs on the biosynthesis of eicosanoids from labelled exogenous arachidonic acid (AA) in isolated platelets was examined. Platelet malondialdehyde (MDA)-formation in the presence of the substances tested in this system was studied too. The vasodilating drugs were found to reduce the conversion rate to TxB2, hydroxy-5,8,10-heptadecatrienoic acid (HHT) and MDA in platelets dose-dependently. Isosorbid-5-mononitrate (ISMN), nitroglycerin (NG) and SIN 1, the active metabolite of molsidomin, showed their inhibitory effects at concentrations of about 1mM, isosorbid-dinitrate (ISDN) had a much weaker effect on platelet-biosynthesis - a concentration of about 3mM was necessary to inhibit TxB2-formation significantly.

Arachidonic Acid↗