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Biomedical subjects

G Neugebauer

Publications and source records attributed to G Neugebauer.

45 records · Page 3Linked to original sources
PubMed1977

[Influence of high intravenous doses of D-penicillamine on toxic actions of cardiac glycosides in the guinea pig. Short communication (author's transl)].

Intravenous infusions of arrhythmogenic and lethal doses of ouabain and digoxin in anesthetized guinea pigs were not influenced by pretreatment with 1 g/kg D-penicillamine. The respective doses of proscillaridin and digitoxin, however, were significantly decreased by D-penicillamine. As could be demonstrated with proscillaridin this effect of D-penicillamine was dose-dependent between 0.25 and 1.0 g/kg. Obviously the strong plasma-protein binding of D-penicillamine leads to a displacement from binding sites of such cardiac glycosides which are also strongly bound to plasma proteins and thus reduces toxic doses of cardiac glycosides. Because of the extremely different doses of D-penicillamine in the animal experiments compared to those used therapeutically in man the present findings are irrelevant for clinical practice.

Animals↗
PubMed1976

[Splenectomy for traumatic rupture of the spleen in childhood and its sequaelae].

This study was undertaken in order to assess the clinical and immunological consequences of splenectomy for traumatic reasons in childhood. Immunological testing of 22 persons 1 to 20 years subsequent to removal of the spleen for traumatic rupture between the ages of 3 and 6 revealed diminished or absent agglutinins in 10 cases and diminished or absent opsonins to E. coli in 16 cases. All patients were in good health and no clinical evidence of increased susceptibility to severe infections was found postoperatively. It is, therefore, assumed that the diagnosed defects had been compensated for by other immunological mechanisms. In contrast to the opinions of other authors, it is concluded that splenectomy in childhood between the ages of 3 and 6 does not appear to carry greater risks than in later years.

Antibodies, Bacterial↗
PubMed1976

Quantification of collateral resistance in acute and chronic experimental coronary occlusion in the dog.

The resistance to coronary blood flow in various parts of the myocardium was studied with the tracer microspheres technique before and immediately after an acute coronary occlusion and several weeks after a more slowly occurring coronary occlusion by Ameroid constrictor. All experiments were carried out in the isolated, metabolically supported, empty, beating dog heart at maximal coronary vasodilation induced with adenosine. Coronary resistance of the normal empty beating heart at maximal coronary vasodilation was 0.20 mm mm Hg/(ml/min) per 100 g of tissue (subepicardium) and 0.16 mm Hg/(ml/min) per 100 g of tissue (subendocardium). After acute coronary occlusion the perfusion of the subtended myocardium was maintained at a much lower level by way of collateral vessels, which showed a resistance to flow of 3.52 mm Hg/(ml/min) per 100 g. If coronary artery occlusion proceeded more slowly the collateral vessels became more functional and myocardial infarction was avoided. During collateral enlargement collateral resistance fell from 3.52 to 0.22 mm Hg/(ml/min) per 100 g within a period of 8 weeks after implantation of the constricting device. The degree of compensation by collaterals for the loss of the occluded native coronary artery was 33% of its former conductance.

Acute Disease↗
PubMed1976

[Improvement of flow properties using Arwin in acute experimental infarct].

Reduction of blood viscosity by arwin in the acute experimental infarction. The effect of 1 unit/kg arwin on the extent of the ischemic area following ligation of a branch of the left descending coronary artery (LAD) was studied in 13 anesthetized open-chest dogs. 10 min infusion of Arwin veginning simultaneously with coronary occlusion lead to a decrease in plasma fibrinogen concentration by 69% 60 min after the end of the infusion, whereas in the control group (NaCl-infusion, 13 dogs) no equivalent decrease occurred. The average ST-segment elevation (ST) and the number of sites exhibiting ST-segment elevation (NST) in the epicardial Ecg were 9 mV and 5.0 15 min after the end of the infusion (25 min after coronary occlusion) in the Arwin-treated group and 11 mV resp. 5.9 in the control group. In the following 105 min no alteration in the electrocardiographic evidence of infarction occurred in both groups. 15 min reperfusion (after release of coronary ligation) decreased the ischemic injury in both groups significantly: arwin -group ST 4.1 mV, NST 3.0, control 3.9 mV resp. 3.5. During coronary occlusion ST-elevation was significantly less in borderline areas than in the center of the infarction, a reduction of the ischemic injury by arwin in these different zones, however, could also not be established. Hemodynamic alterations were similar in both groups. Systolic, mean and diastolic aortic pressure, left ventricular systolic pressure and heart rate remained nearly constant during 130 min of coronary occlusion, left ventricular dp/dtmax declined by 17%. 25 min after occlusion of the branch coronary flow in the LAD decreased by 38%, after 130 min by 48%. After 15 min reperfusion the reactive hyperemic response had declined to preocclusion levels. A statistically significant difference in the occurence of reperfusion arrhythmias between the arwin -treated group (25%) and control group (39%) could not be evaluated. There was no evidence that a decrease in blood viscosity produced by lowering of fibrinogen concentration concomitantly with coronary occlusion could reduce electrocardiographic assessment of myocardial injury. Conversely, the effects of arwin on impending infarction and severe angina pectoris cannot be predicted from these results. An increase in infarct size, however, which could have occurred after infusion of arwin leading to microembolization by fibrinogen degradation products was never observed.

Angina Pectoris↗
PubMedDate not supplied

Metabolism of carvedilol in man.

The metabolism of carvedilol was investigated in plasma and urine of 3 healthy male volunteers after administration of 50 mg of [14C]-labelled drug. Rapid and extensive biotransformation occurred. After 1.5 h 9% of total radioactivity in plasma consisted of unchanged drug, 22% of carvedilol-glucuronide and another 20% of oxidative cleavage products of the beta-blocking side chain. Urinary excretion of radioactivity amounted to 16% of which 2% represented unchanged drug, 32% carvedilol-glucuronide and about 25% side chain oxidation products. Ring-hydroxylated metabolites of carvedilol accounted for 18% of the radioactive compounds in the urine.

Antihypertensive Agents↗