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Biomedical subjects

K Silberbauer

Publications and source records attributed to K Silberbauer.

At least 55 records · Page 3Linked to original sources
PubMed1984

Right ventricular performance in chronic air flow obstruction.

Right ventricular pump performances were assessed in 14 patients with chronic obstructive pulmonary disease by means of radionuclide angiocardiography using krypton-81m as a tracer. Right ventricular ejection fraction (RVEF) was significantly lower in the patients than in normal volunteers. Additionally there was a striking difference in RVEF between patients with normal pulmonary artery pressure (PAP) and those with pathologically elevated PAP. A linear negative correlation between RVEF and mean PAP could be demonstrated. From this data we suggest that radionuclide angiocardiography using krypton-81m allows non invasive assessment of right heart afterload and thus indirectly PAP.

Adult↗
PubMed1984

Pulmonary and antiaggregatory effects of prostacyclin after inhalation and intravenous infusion.

Prostacyclin (PGI2) was administered by inhalation (50 micrograms/min) and intravenous infusion (15 ng/kg/min) in 5 healthy male volunteers. Irrespective of the route of administration this substance was shown to have no effects on respiratory indices studied, whereas a significant inhibition of ADP-induced platelet aggregation and a fall in vascular resistance could be demonstrated. Mainly because of the latter action it is suggested that PGI2, or a stable synthetic analogue, might become a potent drug in various pathological conditions, in which hypertension of various causes is a problem.

Adult↗
PubMed1984

[Age dependence of the response of blood pressure, heart rate and plasma renin activity to captopril in essential hypertension].

The acute effects of the converting enzyme inhibitor captopril on blood pressure, heart rate and plasma renin activity were assessed in 53 patients (aged 20-80 years) with mild to moderate essential hypertension under basal conditions. The systolic blood pressure before captopril was elevated in patients in the forties (p less than 0,01) when compared to the younger patients and was positively correlated to the age before (r = 0.32, p less than 0.05) and after (r = 0.32, p less than 0,05) angiotensin converting enzyme inhibition with captopril 25 mg. the drop in systolic (-13%) and diastolic (-10%) blood pressure was significantly greater in patients in the fifties (p less than 0,025 and p less than 0,05 respectively) when compared to younger and older (p less than 0,1) patients. The response of plasma renin activity paralleled the blood pressure response, while heart rate after captopril was not significantly changed in any group. The lack of age dependence of the blood pressure response to captopril and of reflex tachycardia suggests converting enzyme inhibition to be a valuable adjunct for the treatment of essential hypertension in the elderly.

Adult↗
PubMed1983

Endogenous prostaglandin E2 metabolite levels, renin-angiotensin system and catecholamines versus acute hemodynamic response to captopril in chronic congestive heart failure.

Hemodynamic and hormonal responses to captopril were measured in 10 patients with severe chronic heart failure poorly controlled by digitalis and diuretics. After administration of a 25-mg dose, stroke volume (SV) increased from 53 +/- 7 to 63 +/- 9 ml (p less than 0.05), while pulmonary wedge pressure (PWP) decreased from 20 +/- 2 to 14 +/- 2 mm Hg (p less than 0.01). The hemodynamic changes were associated with increases in plasma renin activity (PRA; p less than 0.05) and in plasma levels of a novel bicyclo-prostaglandin E2 metabolite (bicyclo-PGE-m; p less than 0.01), whereas norepinephrine (NE) showed a falling tendency. In general, basal hemodynamic and basal hormonal levels did not correlate. Captopril-induced changes in mean artery pressure (MAP) and mean pulmonary artery pressure (mPAP) were positively correlated to pre-captopril PRA (r = 0.74, p less than 0.01; r = 0.64, p less than 0.05) and to changes in PRA (r = 0.85, p less than 0.01; r = 0.80, p less than 0.01) with a similar trend for angiotensin II (AII); decreases of systemic vascular resistance were more pronounced in patients with higher control NE levels (r = 0.62, p less than 0.05), the reduction of NE levels being highest in patients with higher basal concentrations (p less than 0.001); the captopril-induced decreases of mPAP and PWP were inversely related to basal bicyclo-PGE-m levels (r = 0.60, p less than 0.05; r = 0.61, p less than 0.05), and changes in mPAP were closely related to basal ratios of AII/bicyclo-PGE-m (r = 0.67, p less than 0.01). Thus, captopril exerts its acute beneficial hemodynamic effect by inhibiting the generation of AII, associated with toning down of sympathetic stimulation and increased production of vasodilating prostaglandins, such as PGE2. The relation between AII and PGE2-counteracting substances-might determine the hemodynamic response to captopril in the patients.

Adult↗
PubMed1982

[Dose-dependent increase in prostacyclin synthesis from various vascular tissues by dipyridamole].

Due to the more detailed knowledge of prostaglandin metabolism in the recent past increasing interest was focused onto dipyridamole acting as platelet active substance. It was the goal of this study to investigate whether dipyridamole is able to exert any effect on vascular PGI2-synthesis. It is demonstrated that dipyridamole has a dose-dependent (0.1-100 microM) increasing effect on PGI2-synthesis or 6-oxo-PGF1 alpha-levels, respectively (the stable metabolite of prostacyclin). At a dose range of more than 10 microM this increase reaches the level of significance. Assuming that PGI2 acts as a local hormone in the vascular system this effect on PGI2-synthesis stimulation might contribute to the knowledge of the in vivo action of the substance.

Animals↗
PubMed1982

[Sipple syndrome (bilateral phaeochromocytoma medullary C-cell carcinoma of the thyroid gland) with exceptionally prolonged clinical course].

The sporadic occurrence of the Sipple syndrome with bilateral phaeochromocytoma and medullary thyroid carcinoma is a well-known pathological entity. The present report refers to a patient with medullary thyroid carcinoma, initially misdiagnosed as Hurthle-cell adenoma after partial resection of the thyroid gland. 5 and 8 years later the patient underwent bilateral adrenalectomy for phaeochromocytoma. 4 years after the second phaeochromocytoma a palpable thyroid nodule developed, thyroidectomy was performed and the tumour diagnosed as a medullary thyroid carcinoma. This diagnosis was confirmed by reexamination of the histological specimens obtained during the first surgical intervention. We were prompted to report the current case history, because of the protracted course of the medullary thyroid carcinoma in this patient and to point out the value of the determination of pentagastrin stimulated calcitonin values in patients with medullary thyroid carcinoma for diagnosis, postoperative follow-up and in family screening studies.

Adrenal Gland Neoplasms↗
PubMed1982

Acute hypotensive effect of captopril in man modified by prostaglandin synthesis inhibition.

1 A study was carried out to investigate the possible contribution of prostaglandins in captopril-induced hypotension. 2 Healthy volunteers and patients with essential hypertension were given single oral doses of 25 mg and 50 mg captopril respectively before and after cyclo-oxygenase inhibition with indomethacin. 3 The acute hypotensive effect of captopril was not associated with changes in heart rate. As expected, captopril led to an increase in plasma renin activity, decrease in plasma angiotensin II, and decrease in plasma aldosterone concentration. 4 After acute indomethacin pretreatment the acute hypotensive effect of captopril was significantly blunted in volunteers and in the 14 hypertensive patients. Changes in plasma renin activity and angiotensin II were significantly lower from a lower baseline. 5 Prostaglandins may therefore be mediators of the initial captopril effect. The blunting effect of indomethacin should be taken into account under clinical conditions.

Adult↗
PubMed1982

[Molsidomine, a coronary drug with platelet-aggregating inhibitory activity].

The influence of molsidomin (4 mg i.v.) on platelet function, on the plasma concentrations of 6-oxo-PGF1 alpha, the stable metabolite of prostaglandin I2, and thromboxane B2, the stable metabolite of thromboxine A2 was determined in ten patients with coronary heart disease. Prostaglandin I2 is generated in the vessel wall and is a potent vasodilator and inhibitor of platelet aggregation, whereas thromboxane A2 is a vasoconstrictor and a proaggregatory substance. In addition, in-vitro tests were performed, too. 60 min after bolus injection a decrease of systolic and diastolic blood pressure was observed, whereas heart rate remained nearly constant. Platelet aggregation decreased significantly; the addition of PGI2 in vitro had an additive effect. The plasma concentrations of 6-oxo-PGF1 alpha increased after 60 minutes, whereas thromboxane B2 concentrations remained unchanged. In vitro, SIN1, a metabolite of molsidomin generated in the liver, led to a dose-dependent inhibition of ADP-induced platelet aggregation, whereas molsidomin was nearly inactive. Thus molsidomin shows an inhibition of platelet function besides the known antianginal properties. The vasodilatatory and platelet inhibiting effects of this compound may be due partly to a stimulation of the prostaglandin I2 synthesis in the vessel wall.

Angina Pectoris↗
PubMed1982

[Value of the detection of arteriosclerotic lesions with labeled autologous thrombocytes].

In 44 patients with clinical signs of carotid artery stenosis a positive Doppler-ultrasound was obtained. In all patients the lesions were confirmed by angiography. In the patients labelling of autologous platelets with 111Indium-oxine-sulphate was done in order to calculate the platelet half-life. In addition we tried to visualize the verified atherosclerotic lesions under a gamma-camera. In all patients the platelet half-life was significantly shortened in comparison to the controls. In none of the patients studied a visualization of the angiographically verified atherosclerotic lesions could be obtained. These findings point out, that only in recently developed and very severe atherosclerotic lesions the number of platelets deposed on the vascular surface is enough to allow gamma-camera imaging.

Aged↗
PubMed1981

[Influence of the venous wall--platelet interaction by dihydroergotamine (author's transl)].

The incubation of rabbit venous rings (vena cava) is followed by the synthesis and release of prostacyclin (prostaglandin I2, PGI2), as measured by the inhibition of ADP-induced platelet aggregation. The incubation of the venous rings in dihydroergotamine leads to a stimulation of PGI2 synthesis and/or release. This effect of dihydroergotamine, apart from the vasoactive properties of this compound, might prove advantageous as a prophylactic measure in venous thrombosis.

Adenosine Diphosphate↗
PubMed1981

[Platelet sensitivity to prostacyclin (PGI2) in patients with juvenile-onset diabetes mellitus (author's transl)].

Platelet function (ADP-induced platelet aggregation) in 20 patients with juvenile-onset diabetes mellitus was not different from that of age- and sex-matched controls. Platelet sensitivity to exogenous PGI2 was not diminished in diabetic patients. No sex differences were detected. There was no correlation between concomitant blood glucose levels and platelet sensitivity to PGI2.

Adenosine Diphosphate↗
PubMed1981

Decreased sensitivity of human platelets to PGI2 during long-term intraarterial prostacyclin infusion in patients with peripheral vascular disease--a rebound phenomenon?

During successful treatment of peripheral vascular disease with synthetic prostacyclin no alteration in platelet function was reported (1). In 8 patients infused with synthetic prostacyclin continuously for 7 days intraarterially, the platelet function was monitored. Special attention was drawn to the platelet sensitivity in vitro for PGI2, which is discussed as an important factor maintaining the hemostatic balance. In all the patients with peripheral vascular disease between 24 and 48 hours after the beginning of the infusion a sudden decrease in platelet sensitivity accompanied by an increase in platelet count could be seen. These dramatic alterations representing probably a rebound phenomenon occurring during long-term PGI2-treatment might be an explanation for a non-beneficial effect of the treatment and in some cases a limiting factor for the continuation of the infusion itself. It is not clear, if this rebound phenomenon is due to a stimulation of an endogenous inhibitor, lowering the synthesis of a naturally occurring substance acting against this inhibitor or tachyphylaxia.

Aged↗
PubMed1981

Decreased prostacyclin sensitivity of human platelets after jogging and squash.

8 healthy male volunteers performed jogging (as an example of an aerobic metabolic condition) and squash (as an example of an intermittently anaerobic metabolic condition). The platelets sensitivity to prostacyclin (PGI2) decreased after jogging. After squash, a statistically significant (p 0,001) decrease in the sensitivity of the platelets could be seen. Our findings suggest that an early alteration of platelet sensitivity might play a key role in maintaining the hemostatic balance and could be of greater importance than the vascular wall PGI2-synthesis, as the sensitivity changes immediately, whereas the PGI2-formation change is a long-term process.

Adult↗
PubMed1981

Plasma concentrations of plbatelet-specific proteins in coronary artery disease.

The plasma concentrations of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) were measured in 100 patients with documented coronary artery disease (CAD) and in 40 controls. 18 patients had had coronary artery bypass surgery (CABS), 25 patients were on therapy with beta-blocking agents and 19 were treated with oral anticoagulants. 38 patients with CAD received neither CABS nor beta-blocking or anticoagulating drugs. The highest plasma concentrations of beta-TG and PF4 were found in the patient group without medical or surgical treatment (patients versus controls: p less 0.01). Patients with CABS showed beta-TG and PF4 levels within the normal range. Patients with beta-blocking agents also had lower beta-TG and PF4 values than the patient group without therapy (p less than 0.05). By contrast, patients on oral anticoagulation therapy presented with similar plasma concentrations of beta-TG and PF4 as untreated patients. Our data indicate that surgical or medical treatment with beta-blocking agents, but not with oral anticoagulants, may have some influence on platelet function in patients with CAD. beta-TG and PF4 radioimmunoassay may be a simple method to study platelet involvement in various diseases and to evaluate possible influences of medical of surgical treatment on in vivo platelet function.

Adrenergic beta-Antagonists↗