Biomedical subjects

F Schwarz

Publications and source records attributed to F Schwarz.

At least 235 records · Page 13Linked to original sources

PubMed1975

Interaction of delta-5-androstene-3beta, 17beta-diol with estradiol and dihydrotestosterone receptors in human myometrial and mammary cancer tissue.

Specific receptor binding of estradiol (E-2) and dihydrotestosterone (DHT) was studied in human myometrial tissue and in human mammary cancer tissue. The inhibition of binding for E-2 and DHT by E-2, testosterone (T), DHT, dehydroepiandosterone (DHEA), dehydroepiandrosterone-sulfate (DHEA-S), androstendione (A) and 5-androstene-3beta, 17beta-diol (Adiol) was tested with the use of dextran-coated charcoal separation of bound and free E-2, respectively, and DHT. The percentage of binding inhibition was calculated with reference to the inhibition obtained with nafoxidine in a molar concentration ratio of 1,000 for E-2 binding, respectively, with cyproterone acetate in a molar concentration ratio of 10,000 for DHT binding. In 15 samples of myometrium tested, receptors were found for both E-2 and DHT. From 19 samples of mammary carcinoma tissue one showed no binding activity, three samples did bind E-2 only, five samples DHT only, and ten samples showed binding of both steroids. A 50% inhibition of E-2 binding, in myometrial as well as in tumor tissue, required a molar concentration ratio of 40 for Adiol, of more than 2,000 for DHEA. No significant inhibiting activity could be found for A up to a molar concentration ratio of 10,000 and for DHEA-S up to 40,000. With regard to DHT binding, Adiol is more active than E-2 and less active than T. Of the substances tested Adiol is therefore the only one which exerts a significant inhibiting influence at a molar ratio not far beyond the physiological range. This signifies that Adiol might interfere at the receptor level in the estrogenic stimulation of mammary cancer cells.

Adult↗

PubMed1975

Mechanical and electrical causes for lack of frequency potentiation in normal patients, in coronary artery disease and in left bundle branch block.

Nine atrial pacing (SP) runs and 8 ventricular pacing (VP) runs were carried out in patients without heart disease, and 10 AP runs in patients with coronary artery disease (CAD). For evaluation of myocardial contractility, the time derivative of left ventricular pressure (dpdt) was used. Comparing rest and AP at 155/min, AP in normal patients revealed a significant increase in dP/dtmax and a significant decrease in left ventricular end-diastolic pressure (LVEDP). This represents frequency potentiation. When comparing rest and VP values at 155/min in normal patients, no changes in dP/dtmax and LVEDP were seen. AP in patients with CAD demonstrated no change in dP/dtmax, but a decrease in LVEDP when compared to the rest values. dP/dtmin and left ventricular systolic pressure did not change in the 3 groups. VP, and even AP, in 2 additional patients with isolated left bundle branch block (LBBB) AND WITHOUt associated heart disease, revealed the same constellation of parameters as VP in normal patients. Our results show a lack of frequency potentiation in normal patients during VP and in patients with isolated LBBB during both AP and VP. It is concluded that the lack of frequency potentiation during AP in CAD is produced primarily by mechanical asynchrony of contraction, angiographically demonstrated as akinesia and dyskinesia. The lack of frequency potentiation in normal patients during VP and in patients with isolated LBBB due to asynchrony of activation resulting in asynchrony of contraction.

Action Potentials↗

PubMed1975

Vagal role and pacemaker indication in hypersensitive carotid sinus reflex.

The effect of carotid sinus pressure (CSP) on sinus rate was studied in 24 patients with sinoatrial pauses below 3 sec (control) and 23 patients with sinoatrial pauses above 3 sec (hypersensitive carotid sinus reflex equal to (HCSR). For registration of P waves, intraatrial electrograms were used. CSP was applied several times before and after atropine. Patients with HCSR showed inconstant response to CSP. The maximal result was considered diagnostic. No difference in the lengths of sinoatrial pauses was found between patients without dizziness or syncopes in the presence of HCSR and patients with dizziness that proved clinically to be based on the existence of HCSR. It was concluded that CSP-induced asystole can serve neither as a differential diagnostic criterion nor as an indication for pacemaker application. Sick sinus syndrome, and thereby dysfunction of the sinus node, were excluded by rapid atrial stimulation. Patients with HCSR showed overall higher age, slower resting heart rate before and after atropine and less atropine response during CSP compared to control. Hypersensitivity of the carotid sinus reflex was interpreted as a part of the physiological augmentation of vagal tone in elderly people.

Adult↗

PubMed1975

The pharmacodynamics of orally taken verapamil and verapamil retard as judged by their negative dromotropic effects.

The widely recognized, negative dromotropic effects of alpha-isopropyl-alpha-[N-methyl-N-homaveratryl)-gamma-aminopropyl]-3-4-dimethoxyphenylacetonitrile (verapamil, Isoptin) on arterio-venous (A-V) nodal conductions were studied using long-term atrial stimulation (AS) in 7 healthy volunteers whose mean age was 30 years. A control group consisting of three of the volunteers who underwent long-term atrial stimulation without medication was established. Since an isolated, well-known drug effect was studied over a long period of time, it was felt that this was an acceptable method for reaching valid pharmacodynamic conclusions. Atrial stimulation was carried out at hourly intervals up to 14-16 h and continued to the highest possible rate without the occurrence of 2nd degree A-V block before and following oral application of verapamil, 240 mg. The stimulus-Q (S-Q) prolongation at increased pace rates was compared to the control. Verapamil retard was tested in a similar course of investigation the following day. The results clearly demonstrated that both forms of verapamil are effective when taken orally. Verapamil acts 2 h after oral application. The peak effectiveness of the drug is found at 5 h and at this point A-V block can occur at low atrial stimulated rates. The effect of verapamil retard is obvious only after 6 h but is still apparent after 14 h and it remains constant with no peak in effectiveness. Characteristics of the resulting regressions allow to distinguish the effect of verapamil on A-V conduction from influences that might be mediated by the diurnal changes in tone of the autonomic nervous system only. The effect of verapamil after oral application is more pronounced with higher heart rates. The pharmacodnaymics of verapamil evaluated with regard to a single well-known pharmacological effect, have not necessarily to be identical with the pharmacokinetics and the bioavailability of the drug.

Adult↗

PubMed1975