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Biomedical subjects

M Schlepper

Publications and source records attributed to M Schlepper.

At least 199 records · Page 11Linked to original sources
PubMedDate not supplied

Down-regulated beta-adrenoceptors in severely failing human ventricles: uniform regional distribution, but no increased internalization.

In chronic heart failure cardiac beta-adrenoceptors are decreased. In this study we investigated whether a) in severely failing human ventricles beta-adrenoceptors are uniformly decreased or regional variations exist, and b) the beta-adrenoceptor decrease is caused by increased internalization or is a real loss in beta-adrenoceptors. For this purpose we assessed beta-adrenoceptor number and subtype distribution in a particulate fraction (mainly sarcolemmal plasma membranes) and a light vesicle fraction of right and left ventricular segments (obtained by cutting transversal rings of 2 cm from the midventricular regions) of explanted hearts from 2 patients with end-stage congestive dilated cardiomyopathy (DCM) and one patient with end-stage ischemic cardiomyopathy (ICM). In all three hearts ventricular beta-adrenoceptor number was very low (7.5-10 and 21-26 fmol/mg protein in DCM, 15-22 fmol/mg protein in ICM compared to 68-74 fmol/mg protein in non-failing ventricles). beta-Adrenoceptors were uniformly decreased over the whole ventricular region and no considerable regional variations existed. The same held true for beta 1- and beta 2-adrenoceptors. In ICM decrease in beta-adrenoceptors was due to a concomitant reduction in beta 1- and beta 2-adrenoceptors, in DCM it was mainly caused by beta 1-adrenoceptor down-regulation. In all ventricular segments investigated light vesicle beta-adrenoceptors amounted to about 5-7% of total ventricular beta-adrenoceptors, and this was not significantly different from non-failing left ventricles. We conclude that a) in severely failing human ventricles beta-adrenoceptors are evenly down-regulated and no regional variations exist, and b) the decrease in beta-adrenoceptors is not due to enhanced internalization but is a real loss of beta-adrenoceptors.

Adult↗
PubMedDate not supplied

Heterodromia in accessory A-V connections.

In 15 patients with WPW-syndrome the atrio-ventricular and ventriculoatrial conduction was studied by recording of intracardiac potentials during atrial and ventricular pacing. Typical differences in the patterns of normal and accessory A-V conduction identified accessory V-A conduction in 13 patients. According to the evaluation of accessory A-V and V-A conductivity by high rate pacing the patients studied can be divided into three groups: Group I (5 pat): equally good accessory A-V and V-A conductivity. Group II (5 pat): good accessory A-V and impaired accessory V-A conductivity. Group III (5 pat): impaired accessory A-V and good V-A conductivity. In group I the course of investigation was repeated after the application of Ajmaline. The distinct heterodromia in group II and III and the different behaviour of the accessory A-V and V-A conduction after Ajmaline can be explained by the in vitro experiments of Fuente (3). According to our results and to the finding that an excellent accessory V-A conduction is a presupposition for the initiation of supraventricular re-entry tachycardia, it seems mandatory to analyze accessory A-V and V-A conduction properties as well.

Adolescent↗
PubMedDate not supplied

AR-L 115 in coronary artery disease: positive inotropic effects and increase of left-ventricular pump function without inducing angina.

1. AR-L 115 improves pump function in patients with advanced and fully treated congestive cardiomyopathy. Since, in spite of such beneficial responses, the energy cost involved might be detrimental when used in advanced coronary artery disease, we monitored clinical haemodynamic and ECG responses to AR-L 115 (2 mg/kg body weight, bolus) in ten patients with coronary artery disease who had developed angina pectoris and/or pathological increases in left ventricular-end diastolic pressure (LVEDP) at the end of a 1 min pacing stress test. 2. When subjected to these stress conditions again (but this time during the peak effect of AR-L 115), there was no longer evidence of ischaemic myocardial impairment, neither clinically by ECG or haemodynamically. 3. There were (average) increase of 43% in cardiac index, 16% in heart rate, 27% in stroke index, 20% in ejection fraction, 31% in VCF and 39% in dp/dt max, while LVEDP decreased to normal values as if at resting conditions. All changes were significant (P less than 0.05). 4. LV-systolic pressure and end diastolic volume (P greater than 0.05) remained the same. Thus the AR-L 115-induced improved LV-pump function was accomplished under stress conditions in the absence of evidence for myocardial ischaemia.

Adult↗
PubMedDate not supplied

Comparative efficacy of the new cardiotonic agent DPI 201-106 versus dobutamine in dilated cardiomyopathy: analysis by serial pressure/volume relations and "on-line" MVO2 assessment.

DPI 201-106 (DPI) as a positive inotropic drug might be useful in treating dilated cardiomyopathy (DCM). In seven DCM patients with normal (group A) and eight DCM patients with abnormal (group B) left ventricular (LV) function, we analyzed serially (computer-assisted) pressure/volume (P/V) effects as P/V loops (microtip catheter/99mTc scintigraphy) using DPI (30 micrograms/kg X min i.v.) and dobutamine (DOB) (10 micrograms/kg X min i.v.) for quantitative comparison of hemodynamic effects. Contractility (dP/dtmax) improvement was greater with DPI (group A, +23%; group B, +47%) than with DOB (group A, +21%; group B, +32%), as was the simultaneous LV end-diastolic pressure decrease--DPI (group A, -39%; group B, -42%) versus DOB (group A, -21%; group B, -18%). LV efficiency increased with DPI (group A, +22%; group B, +55%), but myocardial oxygen consumption (MVO2) did not change significantly. Five of 15 patients showed an increase in dP/dtmax with DPI only; with DPI there were fewer "nonresponders" than with DOB. Thus, DPI increases contractility in DCM hearts while reducing preload rather than causing higher metabolic costs. Such beneficial hemodynamic effects appear to be stronger in the more impaired myocardium (group B patients) and quantitatively superior to those induced by DOB. This might indicate that residual myocardial reserves are more readily accessible to the influences of DPI than to those of DOB. Serial P/V loops and MVO2 assessment aided the demonstration of DPI's efficacy in a more complex way.

Adult↗
PubMedDate not supplied

The use of expanded polytetrafluoroethylene (PTFE) grafts for myocardial revascularization.

In 18 patients necessitating aorto-coronary bypass grafting procedures in whom suitable veins were not available, 22 PTFE grafts were used in combination with 47 saphenous-vein grafts. 14 patients were studied angiographically 1-26 months after operation, with a mean follow-up of 12 months. 59% of the expanded PTFE grafts and 86% saphenous vein grafts were patent. Factors affecting PTFE graft patency were similar to those of vein grafts. We conclude, that it is reasonable to use this artificial prosthesis only when sufficient veins are not available. Expanded PTFE grafts of 3-5 mm diameter can remain patent and functional for more than 2 years.

Blood Vessel Prosthesis↗