Microcirculation and tolerability following i.v. infusion of PGE1 and iloprost: a randomized cross-over study in patients with critical limb ischemia.

In a randomized cross-over study, the effect of PGE(1) and iloprost on microcirculation as well as the tolerability was investigated in 36 patients with peripheral arterial occlusive disease stage III and IV according to Fontaine. Patients received PGE(1) and iloprost by single 3-h i.v.

[DRG-based cost analysis of inpatient conservative treatment of stage III/IV peripheral arterial occlusive disease].

Unlabelled: DRG-based cost analysis of inpatient conservative treatment of PAD stage III/IV BACKGROUND: In a prospective study carried out by the German Society of Angiology and the DRG Competence Center, Munich, the question was investigated whether the costs of conservative treatment of patients with PAOD stage III/IV (DRG F65) are adequately represented within the current G-DRG system. METHODS UND PATIENTS: Between September 1 and December 16, 2002, a total of 704 patients with DRG F65 (peripheral vascular diseases) were evaluated at 8 angiologic centers in Germany. Apart from the length of hospital stay, the total costs (cost equivalents) were calculated using a method developed by the DRG Research Group at the University of Münster.

Improvement of peripheral and cardiopulmonary performance after a short-term exercise program with additive prostaglandin E1.

In patients with intermittent claudication, the walking distance can be increased, both by means of several months of intensive training and administration of IV prostaglandin E1 (PGE1) for 4 weeks. The aim of this study was, therefore, to investigate whether the combination of intensive training and PGE1 infusions during pedalergometry can increase peripheral and cardiopulmonary performance after 2 weeks. Ten patients with intermittent claudication received a once-daily intravenous infusion of 60 microg PGE1 over 2 hours during pedalergometry.

Randomized reliability study evaluating constant-load and graded-exercise treadmill test for intermittent claudication.

The aim of this randomized study was to compare the reliability of the treadmill test at constant-load (C-test, 3 km/hr; fixed grade of 12%) recommended in Germany with that of the graded-exercise test (G-test, 3 km/hr; increase in grade of 3.5% every 3 minutes) propagated in the United States. In 50 patients with an absolute claudication distance (ACD) in the C-test of between 50 and 400 m, the two treadmill tests were carried out in randomized order on one and the same day, and repeated on 3 days within 1 week.

Effects of prostaglandin E1 metabolites on the induction of arterial thromboresistance.

Prostaglandin (PG) E1 has been shown to induce arterial thromboresistance in experimental animals and in man. It is known to be degraded in vivo to metabolites which have comparable (13,14-dihydro-PGE1) or no (15-keto-PGE1, 15-keto-13,14-dihydro-PGE1) biological activity. It was the goal of this study to examine whether 13,14-dihydro-PGE1 and its derivatives might share biological activity in rendering the arterial wall less thrombogenic.

Treadmill testing for evaluation of claudication: comparison of constant-load and graded-exercise tests.

Objectives: To compare the correlation and practicability of single-stage vs. graded treadmill protocols in the assessment of the absolute claudication distance (ACD).

Design: Randomized open study.

Improvement in the quality of life after i.v. PGE1 therapy for intermittent claudication.

Background: Increasingly and justifiably, clinical studies are now being expected to investigate the influence of therapeutic measures also on the quality of life of the patient.

Patients And Methods: Since no data on the variability of changes in the quality of life of the patient following PGE1 treatment are so far available, the initial investigation was designed as an uncontrolled pilot study. 104 patients (median age 64.

PGE1-induced arterial thromboresistance is a vascular property as identified by cross-perfusion technique.

Prostaglandin (PG) E1 has been shown to improve thromboresistance. This experiment was designed to examine whether an effect on the arterial wall or the platelets is responsible for this phenomenon. Using a cross-perfusion model, the aortic and iliac artery endothelium of rabbits was removed by a balloon catheter before being perfused with blood of donor rabbits.

Efficacy of a new prostaglandin E1 regimen in outpatients with severe intermittent claudication: results of a multicenter placebo-controlled double-blind trial.

For the first time efficacy and safety of a new prostaglandin E1 (PGE1) regimen in the treatment of intermittent claudication were evaluated in a randomized, double-blind, placebo-controlled multicenter clinical trial. The study involved 213 outpatients with a maximum walking distance of 50 to 200 m measured on the treadmill (3 km/hr, 12% grade). After a 2-week run-in phase they received a 2-hour intravenous infusion of 60 micrograms PGE1 or placebo 5 days a week for 4 weeks.

Prostaglandin E1 decreases circulating endothelial cells.

Prostaglandin E1 (PGE1) has been claimed to have cytoprotective effects and also to decrease thrombogenicity. The effect of intraarterial (i.a.

[Development of an illness-specific instrument for assessment of quality of life in patients with arterial occlusive disease (Peripheral Arterial Occlusive Disease 86 Questionnaire)].

Impairment in health-related quality of life in patients with peripheral arterial occlusive disease (PAOD) are well-known to clinicians, but due to the lack of disease specific assessment instruments, have not been systematically investigated. We describe the development and psychometric testing of a 86-items patient-based questionnaire for the assessment of the quality of life in PAOD containing 7 dimensions: functional status, pain, symptoms, mood, disease related anxiety, social life and treatment evaluation. The questionnaire was included along with standard questionnaires in a prospective study with 308 patients suffering from PAOD in Fontaine stages I to IV before and one week into treatment.

Prostaglandin E1 increases binding of 123I-low-density lipoprotein to the human liver in vivo.

Previous in vitro radioligand binding data have shown that prostaglandin E1 (PGE1) increases the number and the binding affinity of low-density lipoprotein (LDL) receptors of the human liver. Experimental data in normo- and hypercholesterolaemic rabbits have confirmed these findings, showing a significant increase in LDL-binding to the liver in vivo after prolonged PGE1 therapy. METHODS.

[Quality of life in peripheral arterial occlusive disease. Multicenter study of quality of life characteristics with a newly developed disease-specific questionnaire].

Aim: Owing to a lack of disease-specific measuring instruments, no systematic investigations of the impairment of the quality of life in patients with peripheral arterial occlusive disease (PAOD) have so far been possible. The aim of the present study, therefore, was to develop an appropriate questionnaire and to submit it to a psychometric test in a sufficiently large number of patients.

Patients And Method: A disease-specific questionnaire comprising 86 individual items was developed (PAVK 86) and was tested in a longitudinal study involving 308 patients with confirmed peripheral arterial occlusive disease, Fontaines's stages I to IV.

PGE0 inhibits collagen and glycosaminoglycan-synthesis in the rabbit arterial wall.

The influence of 13,14-dihydro-PGE1 (PGE0), a biologically active metabolite of PGE1, on collagen and glycosaminoglycan synthesis by the rabbit arterial wall was assessed and compared with the effect of PGE1. Collagen (COL) and glycosaminoglycan (GAG) synthesis was measured using 14C proline- and 35S-incorporation respectively and both were subsequently quantified by autoradiography. PGE1 decreased GAG-synthesis by 40%, while PGE0 caused a 25% decrease.

Prostaglandins and arterial wall lipid metabolism--in vitro, ex-vivo and in-vivo radioisotopic studies.

It is the aim of this paper to review our findings in vitro, in experimental animals and in human on arterial wall lipid metabolism. Radiolabelling of LDL indicates that experimentally induced lesions in hypercholesterolemic rabbits do show less lipid accumulation if treated with prostaglandins (PGI2, PGE1, 13,14-dihydro-PGE1) or stimulators of prostaglandin synthesis (isradipine, a calcium channel blocker of the dihydropyridine family). Endogenous blockade of cyclooxygenase by ASA-pretreatment results in a complete abolishing of this apparently PG-mediated benefit.

[The effectiveness of standardized exercise training in intermittent claudication].

In stage II peripheral arterial occlusive disease (PAOD) physical training is generally the therapy of choice if no reopening procedures are indicated. The aim of this pilot study was to ascertain the increase in claudication distance due to the exclusive implementation of an intensive exercise programme under standardized conditions, for a planned double blind placebo controlled study regarding the efficacy of pharmacotherapy in addition to physical training. 23 in-patients (median age 62 years) with an absolute claudication distance on treadmill of between 50 m and 200 m (12% inclination, 3 km/h walking speed) participated 5 days a week in the following intensive standardized physical training programme: in the morning and afternoon supervised gymnastics for about 30 minutes, followed by 2 cycles of treadmill exercise each amounting to 66% of the absolute claudication distance.

Synergism between PGE1-metabolites(13,14-dihydro-prostaglandin E1, 15-keto prostaglandin E1, 15-keto-13,14-dihydro-prostaglandin E1) and nitric oxide (NO) on platelet aggregation.

A synergistic antiplatelet effect between prostaglandins (PG), cAMP-stimulators and nitric oxide (NO), a cGMP-stimulator, has already been described. Data on a synergism between NO and the metabolites of PGE1, however, are lacking so far. We therefore tested the antiplatelet activity of the metabolites of PGE1 alone and their synergism with NO on human platelets of 8 healthy volunteers in vitro.

Prostaglandin (PG) E1 and 13,14-dihydro (DH) PGE1 are diminishing radiation-induced arterial damage.

Rabbit abdominal aorta was irradiated with single or repeated doses up to 10 Gy. The rabbits were killed at different time intervals after irradiation. 5 micrograms/kg x 6/hr PGE1 or its biologically active metabolite 13,14-DH-PGE1 were administered either 6 hours before or 6 hours after irradiation.

On the metabolism of prostaglandin E1 administered intravenously to human volunteers.

We have demonstrated recently the formation of a biologically active metabolite of prostaglandin (PG) E1, 13,14-dihydro-PGE1, during intravenous infusions of PGE1 in patients with peripheral arterial occlusive disease. We have now investigated the levels of the immediate precursor of 13,14-dihydro-PGE1, the biologically inactive 15-keto-13,14-dihydro-PGE1, during intravenous administration of 20 micrograms, 40 micrograms or 80 micrograms PGE1 over a period of 60 min to human volunteers. It was found that levels of 15-keto-13,14-dihydro-PGE1, but not those of PGE1 itself, increased in a dose-dependent manner.

Interaction between prostaglandin E1 and nitric oxide (NO).

A synergistic antiplatelet effect between prostaglandin I2 (PGI2), a cAMP-stimulator, and nitric oxide (NO), a cGMP-stimulator, has been described. Data on a PGE1-NO interaction, however, are lacking so far. We therefore examined the question in healthy volunteers, whether a similar synergism exist between PGE1 and NO on human platelets in vitro.

Formation of 13,14-dihydro-prostaglandin E1 during intravenous infusions of prostaglandin E1 in patients with peripheral arterial occlusive disease.

Formation of 13,14-dihydro-prostaglandin (PG) E1 during intravenous infusions of PGE1 in patients with peripheral arterial occlusive disease was investigated. Using both high performance liquid chromatography (h.p.

13,14-dihydro-PGE1, an in-vivo metabolite of PGE1, decreases mitotic activity induced by corticosteroid administration.

PGE1 has antimitotic activity by virtue of its effect in increasing cAMP in vascular smooth muscle cells. The present study compares the effect of 13,14-dihydro-PGE1 (13,14-DH-PGE1) with PGE1 in an experimental model of stress induced by desoxycorticosterone in the rabbit. 13,14-DH-PGE1 significantly inhibited the stress-induced increase in mitotic activity, measured by autoradiography as percentage of 3H-thymidine positive cells, in all 3 abdominal aortic wall layers.