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Biomedical subjects

F D Maul

Publications and source records attributed to F D Maul.

81 records · Page 5Linked to original sources
PubMed1980

[Transluminal angioplasty: control of efficiency by nuclear medical methods after non-operative dilatation of critical coronary artery stenoses (author's transl)].

Preliminary results are reported using 201Tl-myocardial scintigraphy (MSC) with quantitated analysis of redistribution kinetics immediately after ergometry (climbing step test) two to four hours later respectively and (Dual-ROI-) Equilibrium-Radionuclide-Ventriculography (ERNVG) with 99mTc-in vivo-labeled erythrocytes during bicycle exercise prior to and after nonoperative transluminal angioplasty (TAP) in nine patients with critical coronary artery stenosis. ERNVG showed a good reproducibility (r = 0,972, n:20 double check) of LVEF. Successful TAP was associated with 1. increase of LVEF from 41,8 (before) to 49,8% (after TAP), 2. increase of mean normalized systolic ejection rate (MNSER = LVEF/ET) from 1,30 (before TAP) to 1,66 (after TAP), 3. increase of maximal volume change during systole (dV/dtmax/EDV) from 2,12 (before TAP) to 3,03 s-1 (after TAP). Parameters of 201Tl-redistribution kinetics (in MSC) were normalized. Ischemic reaction index increased from 62,9 +/- 5,5 (before) to 79,1 +/- 6,9% (after TAP). The degree of 201Tl-redistribution was normalized from 10,3 +/- 7,4 (before TAP) to 2,1 +/- 1,9 (after TAP, between three and four hours after exercise) as a sign of disappearance of exercise-inducible regional myocardia ischemia after successful TAP. These preliminary results underline the effectiveness of non-operative TAP in selected cases of critical coronary artery stenosis.

Cardiac Output↗
PubMed1976

In vivo behaviour of homologous urea-soluble 131I-fibrin and 125I-fibrinogen in rabbits: the effect of fibrinolysis inhibition.

The in vivo behaviour of urea-soluble fibrin monomer (FM) was compared with that of fibrinogen in rabbits. Purified rabbit 125I-fibrinogen was injected into 36 unanaesthetized rabbits. Three days later the rabbits received either purified rabbit 131I-FM I mg/kg body weight, which corresponds to cI% of the circulating plasma fibrinogen pool 131I-fibrinogen, or buffered urea only. The distribution volume of FM was 43.4 +/- 6.9 ml/kg and of fibrinogen 43.5 +/- 7.7 ml/kg (mean +/- SD). The elimination curve of urea-soluble FM as represented by the clottable 131I-radioactivity. plotted on a semi-logarithmic paper, consisted of an initial steep decay within the first 6 h and a slow flattening of the slope 6 to 24 h after injection of FM. Although a terminal single-exponential slope, as observed in fibrinogen elimination, could not be computed for the 24 h following FM injection the mean half-life time of the last segment of the clottable-radioactivity curve, between 12 h and 24 h, was 12 h. Within 24 h a mean of 83-5% of the injected FM were removed from the circulating blood. The elimination characteristics of fibrinogen were not influenced by the injected FM. Control experiments showed that buffered 3.0 M urea, the solvent of FM, does not influence distribution volume and elimination of 125I-fibrinogen. The distribution of 131I as well as 125I-radioactivities in organs representing FM and fibrinogen respectively did not differ from each other. Elevated levels of 131I-radioactivity, however, were found in the urine after FM injection suggesting an accelerated elimination of FM in comparison to fibrinogen. Fibrinolysis inhibition with high doses of aprotinin did not significantly reduce the urinary excretion of 131I-radioactivity representing breakdown of FM. Furthermore, inhibition of the fibrinolytic system had no influence on the elimination characteristics of either fibrinogen or FM. In order to explain the results obtained in this study the following theory is proposed. Intravenously injected FM forms complexes with fibrinogen and fibrinolytic degradation products. The complexes continuously increase in size until they dissociate into fibrin oligomers and carrier proteins. The oligomers are eliminated whereas the carrier proteins recycle.

Animals↗
PubMedDate not supplied

[Initial experiences in the treatment of children with metastatic and recurrent neuroblastoma using meta-iodobenzylguanidine].

At four involved hospitals 16 children were treated with Metaiodobenzylguanidine (131J-MIBG). These children had a relapse of neuroblastoma stage III or IV or did not respond sufficiently to chemotherapy. In 10 children extreme bone pain disappeared and they became free of fever during the MIBG-treatment. 10 children responded to the therapy demonstrated either by decrease of the solid tumor part or by decrease of catecholamines in urine or plasma or by decrease of bone-marrow involvement. One patient reached a complete remission continuing up to present time (longer than 180 days). 9 patients died meanwhile of tumor progression. 131J-MIBG is an effective instrument, to get a decrease of the tumor up to a complete remission in extensively pretreated patients with tumor relapse, which are refractory to chemotherapy.

3-Iodobenzylguanidine↗
PubMedDate not supplied

[131(I)-meta-iodobenzylguanidine treatment of 32 children with therapy-refractory neuroblastoma].

The selective uptake and accumulation of 131J-Metaiodobenzylguanidine in neuroblastoma cells in vivo may be utilized for targeted irradiation. The experience with 32 neuroblastoma patients refractory to conventional high dose chemotherapy is reported. At diagnosis 8 patients had Evans stage III and 22 stage IV. 11/32 experienced recurrences after complete tumor disappearance and before mIBG treatment, 16/32 progressed from residual or nonresponding tumor and in 3/32 insufficient tumor regression by chemotherapy was observed. 2 children received one mIBG course each with no evidence of disease. Mean applied activity was 128 mCi per course (35-300 mCi), 360 mCi per patient (80-1033 mCi) and 19.2 mCi/kg per patient (3.2-37.9 mCi/kg), respectively. A total of 84 courses was given (mean 2.6 per patient). Pain relief was noticed in 14/14 patients with bone pain. Complete or very good partial remission was achieved in 5/32, partial remission in 11/32 and stable disease in 6/32 patients. In 8 children progression occurred and 2 patients were not evoluable. 20 children died, 12 are still alive (6 patients with initial stage IV, 6 with stage III disease). Main side effect was transient thrombocytopenia, which became more severe with increasing number of courses. We conclude that mIBG treatment is effective in some patients with refractory neuroblastoma and may be utilized in the future as front line therapy for patients achieving only incomplete regressions after high dose chemotherapy.

3-Iodobenzylguanidine↗
PubMedDate not supplied

Outcome of [131I]metaiodobenzylguanidine therapy of neuroblastoma: seven years after.

Beginning in 1984 and based on a total of 40 treatments with [131I]metaiodobenzylguanidine (131I-MIBG) in most cases with a follow-up of 5 years or more, it seems to be worthwhile reevaluating our clinical data and draw some final conclusions: We treated 12 children with a neuroblastoma (NB) IV and 3 with a NB III. In no case 131I-MIBG was the primary therapy. The great majority suffered from recurrence. The mean treatment interval after chemotherapy was 6 months (range 0-54). We calculated a median cumulative tumor dose of 77 Gy (range 0-259) in patients with stage III and 30 Gy (range 4-267) in stage IV NB. The tumor half-life time of 131I-MIBG does not significantly differ between stage III (3 days) and IV (2-5 days). Although the median tumor dose of stage III NB exceeded that of stage IV, we found in NB IV a significant tumor remission in 7 out of 12 cases. On the other hand, a slight reduction of tumor size was seen in only 1 case of stage III NB. This indicates a lower radiation sensitivity of stage III NB. Despite this fact, the two patients with stage III NB who presented a sufficient 131I-MIBG-tumor uptake turned to become operable after 131I-MIBG. Stage IV patients improved, too, even if most of them suffered from recurrence with a very poor prognosis: 3 patients of stage IV lived longer than 48-60 month or are still alive. However, no one of this group remitted completely.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Iodobenzylguanidine↗