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Biomedical subjects

P Fitscha

Publications and source records attributed to P Fitscha.

At least 91 records · Page 5Linked to original sources
PubMed1987

Prostacyclin synthesis stimulating plasma factor in patients with peripheral vascular disease.

Human plasma contains a factor capable of stimulating vascular prostacyclin generation even in atherosclerotic vessels with minimal in-vitro capacity for PGI2-synthesis. The activity of this prostacyclin stimulating plasma factor (PSPF) has been reported to be elevated in renal failure and hepatic coma. We are not aware of any data as to whether this PSPF plays a role in maintaining hemostatic balance in patients with peripheral vascular lesions. Therefore, we examined 62 patients with peripheral vascular disease (PVD). This study group was subdivided into normo- and hyperlipemic subjects, patients with and without maturity onset diabetes, and plasma beta-thromboglobulin levels higher and lower than 50 ng/ml. 10 healthy sex and age matched persons served as controls. Vascular prostacyclin formation was studied in vitro after incubation of the patients' plasma and a buffer control with various tissue samples (human femoral artery, rat abdominal and thoracic aorta of healthy and of streptozotocin induced diabetic animals, swine endothelial layer and remaining tissue (media and adventitia) and cultured endothelial (EC) and smooth muscle cells (SMC) of minipig arota. In addition, 6-oxo-PFG1 alpha formation by cultured EC and SMC (minipig aorta source) after incubation with tris HCl-buffer or plasma were estimated by means of specific radioimmunoassays. In general, tissue samples and cells incubated in plasma exhibit a marked increase of in-vitro PGI2-formation as compared to buffer. No difference could be found between PSPF of CHD-patients and healthy controls. Similar findings were obtained using incubated vascular tissue and cultured cells by means of the bioassay and specific RIA, respectively. These findings indicate that the PSPF does not seem to be of any clinical relevance in hemostatic regulation in patients with advanced atherosclerosis.

Adult↗
PubMed1987

Development of optimal infusion regimens for epoprostenol using radio labelled platelet uptake over atherosclerotic lesions in man.

1. Epoprostenol (prostacyclin, PGI2) has been evaluated in clinical trials in peripheral vascular disease and other conditions chiefly on the basis of its platelet inhibitory properties. These therapeutic evaluations have proceeded in the absence of evidence as to the optimum infusion regimen for epoprostenol and the choice of schedules of administration has been arbitrary. We have tried to establish an optimum infusion regimen in patients with peripheral vascular disease in terms of maximal inhibition of platelet deposition on atherosclerotic lesions in vivo together with maximal inhibition of platelet aggregation ex vivo. 2. One hundred and twenty three patients with atherosclerotic peripheral vascular disease and increased platelet uptake at atherosclerotic sites were selected. Epoprostenol was administered at a fixed dose of 5 mg kg-1 min-1 for 0.5-24 h daily for 3-7 days. 3. Infusion of epoprostenol for 6 h daily for up to 5 days caused maximum decrease in platelet uptake without tachyphylaxis and without loss of the inhibitory effect of epoprostenol on platelet aggregation responses. Longer daily infusion periods were associated with progressive loss of the anti-aggregatory effect of epoprostenol without any greater decrease in platelet uptake. Shorter daily infusion periods produced smaller decreases in platelet uptake.

Adenosine Diphosphate↗
PubMed1987

Effect of prostaglandin E1 on deposition of autologous labelled platelets onto human atherosclerotic lesions in vivo.

The effects of infusions of prostaglandin E1 (PGE1) on platelet deposition at atherosclerotic sites in vivo in man have been examined. Thirteen patients with atherosclerotic vascular disease received intravenous PGE1 25 mg/kg/min for 6 hours daily for 5 days. Prostaglandin E1 had no effect on platelet uptake at atherosclerotic sites but prolonged platelet half-life significantly (P less than 0.001).

Alprostadil↗
PubMed1986

Jogging causes a significant increase in platelet sensitivity to prostacyclin.

Platelet function and platelet sensitivity to PGI2 was studied before and after jogging in seven males and four females in good health. The ADP-induced (1 microM) aggregation, being always increased after physical activity, showed during the entire follow-up period of 12 months a significant decrease at rest and after exercise compared with baseline values. The change in the aggregation response was significant for t alpha at month 1 and for delta tmax at month 2 after starting the jogging. The platelet sensitivity to PGI2, being always diminished after exercise, also increased significantly during the entire follow-up period compared with baseline levels. In contrast to the ADP-induced changes, the changes in platelet sensitivity were significant already at week 2. Our findings indicate that daily physical activity causes a significant improvement in platelet function and reduces platelet activation.

Adenosine Diphosphate↗
PubMed1986

Influence of atenolol and bopindolol on circadian heart rate.

The effects of a cardioselective beta-adrenoceptor blocker without intrinsic sympathomimetic activity (ISA) (atenolol) and a noncardioselective beta-adrenoceptor blocker with ISA (bopindolol) on circadian heart rate were studied in 10 patients (2 women and 8 men) with an average age of 52 years and the following diagnoses: coronary heart disease (n = 4) and hypertension (n = 6). The patients were treated in a randomized crossover study with 100 mg atenolol p.o. and 1 mg bopindolol p.o. Atenolol lowered the averaged circadian heart rate (HR) significantly (p less than 0.001), from 70-59 beats/min. The HR decreased during the day and also at night. After bopindolol the average circadian HR decreased only slightly, from 69-64 beats/min. HR was reduced during the day but not during the night. Nine out of 10 patients receiving atenolol developed hourly HRs less than 55 beats/min compared to 3 patients on bopindolol. There was a significant increase of hourly segments (HR less than 55 beats/min) from 11-85 and also for hourly segments with HR less than 50 beats/min from 0-46 with atenolol, whereas no significant change could be detected under bopindolol. Both drugs produced similar reductions in exercise-induced increases in HR and systolic blood pressure and these effects persisted for more than 24 h.

Adrenergic beta-Antagonists↗
PubMed1986

Platelet half-life, plasma thromboxane B2 and circulating endothelial-cells in peripheral vascular disease.

We studied platelet half-life (T/2), plasma thromboxane B2-levels (TXB2) and circulating endothelial cells in 107 patients with a mean age of 63 +/- 6.8 years and angiographically proven peripheral vascular disease (PVD). Patients were divided into 4 groups according to Fontaine but also according to additional clinical manifestations of atherosclerosis like coronary heart disease (CHD) and cerebrovascular disease (CVD). Furthermore, the influence of sex and smoking was investigated. Compared to patients without atherosclerotic manifestations we could detect an enhanced platelet consumption measured as shortened platelet half-life time (79.2 +/- 9.1 vs 100.9 +/- 5.6 hours, p less than 0.001 and an increased platelet activity measured as increased TXB2-plasma levels (51.6 +/- 20.9 vs 23.2 +/- 11.2 ng/ml, p less than 0.001). Correspondingly, the amount of circulating endothelial cells was increased 45.2 +/- 25.7 vs 20.3 +/- 23.4, p less than 0.001). Patients with PVD who smoked had the shortest actual platelet half-life, the highest TXB2 plasma levels and the greatest amount of circulating endothelial cells compared to non-smoking patients and controls. Patients with clinical stage IV according to Fontaine had the shortest platelet half-life, the highest TXB2 plasma levels and the greatest amount of circulating endothelial cells compared to the other clinical stages. Analyzing the influence of additional clinical manifestations of atherosclerosis we could detect only in patients with PVD and CHD significant differences compared to the other groups.

Adult↗