On the Metabolism and Pharmacokinetics of Prostaglandin E1 Administered by Intra-arterial or Intravenous Infusions

1991 ◽  
pp. 6-11
Author(s):  
B. A. Peskar ◽  
W. H. Hesse ◽  
W. Rogatti ◽  
G. Rudofsky
Keyword(s):  
Prostaglandin E1 ◽  
Intravenous Infusions

PLASMA PROSTAGLANDIN E1 CONCENTRATIONS AND HEMODYNAMICS DURING INTRAVENOUS INFUSIONS OF PROSTAGLANDIN E1 IN HUMANS AND SWINE1

1996 ◽  
Vol 61 (11) ◽  
pp. 1624-1629 ◽  
Author(s):  
Joseph A. Awad ◽  
Marinos C. Soteriou ◽  
James G. Drougas ◽  
Katherine A. Stokes ◽  
L. Jackson Roberts ◽  
...  
Keyword(s):  
Prostaglandin E1 ◽  
Intravenous Infusions

The Effect of Intravenous Adenosine Diphosphate on the Number of Circulating Platelets in Experimental Animals: Inhibition by Prostaglandin E1, Dipyridamole, SH-869 and VK-774

1977 ◽  
Vol 37 (01) ◽  
pp. 036-046 ◽  
Author(s):  
Ian B. Holmes ◽  
Gordon M. Smith ◽  
Franz Freuler
Keyword(s):  
Prostaglandin E1 ◽  
Potent Inhibitor ◽  
Adenosine Diphosphate ◽  
Dependent Manner ◽  
Response Curves ◽  
Duration Of Action ◽  
Intravenous Infusions ◽  
Long Duration ◽  
Dose Dependent ◽  
Derivatives Of

SummaryThe number of circulating platelets was monitored in anaesthetized animals by a continuous flow technique, using a Technicon Autocounter®. Intravenous infusions of adenosine diphosphate (ADP) produced transient, dose-dependent falls in circulating platelet numbers in rabbits, dogs, rats, pigs and squirrel monkeys. The rat was the most sensitive of the species investigated.In the rabbit, the effect of a submaximal dose of ADP was inhibited in a dose-dependent manner by intravenous infusions of prostaglandin E1 (PGE1), dipyridamole, and two derivatives of dipyridamole (SH-869 and VK-774). The dose-response curves for PGEl, SH-869 and VK-774 were approximately parallel, whereas that for dipyridamole was considerably less steep. PGE1 was the most potent inhibitor, but the duration of action was very short. Dipyridamole and SH-869 produced inhibition of long duration. The duration of action of VK-774 was intermediate.All inhibitors produced marked and often long-lasting hypotension. The fact that no inhibition of ADP effects could be demonstrated with dibenzyline and hexamethonium, which also produced marked hypotension of long duration, indicated that inhibition of the ADP effect by the four antagonists studied was not due to changes in blood pressure.

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

1991 ◽  
Vol 41 (3) ◽  
pp. 225-228 ◽  
Author(s):  
B.A. Peskar ◽  
W.H. Hesse ◽  
W. Rogatti ◽  
C. Diehm ◽  
G. Rudofsky ◽  
...  
Keyword(s):  
Prostaglandin E1 ◽  
Intravenous Infusions ◽  
Peripheral Arterial

The Effect on Appetite in Dogs of Pyrogenic Substances in Intravenous Infusions

1954 ◽  
Vol 27 (3) ◽  
pp. 347-352 ◽  
Author(s):  
W.M. Dale Beamer ◽  
J.E. Thomas ◽  
Beatrice Moore
Keyword(s):  
Intravenous Infusions

Ticlopidine Facilitates the Deaggregation of Human Platelets Aggregated by Thrombin

1994 ◽  
Vol 71 (01) ◽  
pp. 091-094 ◽  
Author(s):  
M Cattaneo ◽  
B Akkawat ◽  
R L Kinlough-Rathbone ◽  
M A Packham ◽  
C Cimminiello ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Platelet Aggregation ◽  
Prostaglandin E1 ◽  
Human Platelet ◽  
Adenosine Diphosphate ◽  
Human Platelets ◽  
Before And After ◽  
Normal Human ◽  
Platelet Aggregates ◽  
Induced Aggregation

SummaryNormal human platelets aggregated by thrombin undergo the release reaction and are not readily deaggregated by the combination of inhibitors hirudin, prostaglandin E1 (PGE1) and chymotrypsin. Released adenosine diphosphate (ADP) plays an important role in the stabilization of thrombin-induced human platelet aggregates. Since ticlopidine inhibits the platelet responses to ADP, we studied thrombin-induced aggregation and deaggregation of 14C-serotonin-labeled platelets from 12 patients with cardiovascular disease before and 7 days after the oral administration of ticlopidine, 250 mg b.i.d. Before and after ticlopidine, platelets stimulated with 1 U/ml thrombin aggregated, released about 80–90% 14C-serotinin and did not deaggregate spontaneously within 5 min from stimulation. Before ticlopidine, hirudin (5× the activity of thrombin) and PGE1 (10 μmol/1) plus chymotrypsin (10 U/ml) or plasmin (0.06 U/ml), added at the peak of platelet aggregation, caused slight or no platelet deaggregation. After ticlopidine, the extent of platelet deaggregation caused by the same inhibitors was significantly greater than before ticlopidine. The addition of ADP (10 μmol/1) to platelet suspensions 5 s after thrombin did not prevent the deaggregation of ticlopidine-treated platelets. Thus, ticlopidine facilitates the deaggregation of thrombin-induced human platelet aggregates, most probably because it inhibits the effects of ADP on platelets.

The Filter Loop Technique as a Method of Measuring Platelet Aggregation in the Flowing Blood of the Rat; the Inhibitory Activity of 5-oxo-l-cyclopentene-l-heptanoic Acid (AY-16,804) on Platelet Aggregation

1973 ◽  
Vol 30 (01) ◽  
pp. 138-147 ◽  
Author(s):  
Christopher R. Muirhead
Keyword(s):  
Platelet Aggregation ◽  
Prostaglandin E1 ◽  
Suitable Model ◽  
Heptanoic Acid ◽  
Simple Method ◽  
Loop Technique ◽  
Flowing Blood ◽  
Filter Loop

SummaryThe filter loop technique which measures platelet aggregation in vivo in the flowing-blood of the rat was compared to the optical density technique of Born which is carried out in vitro with platelet rich plasma. Using these two experimental models the effect on platelet aggregation of three known inhibitors sulfinpyrazone, dipyridamole and prostaglandin E1, and a novel compound 5-oxo-l-cyclopentene-l-heptanoic acid (AY-16, 804) was determined.The effects on platelet aggregation of the known inhibitors were consistent with information in the literature. Prostaglandin E1 was the most potent inhibitor in both techniques; sulfinpyrazone inhibited aggregation in both models but was less potent than prostaglandin E1. AY-16, 804 exhibited activity in vitro and in vivo similar to that of sulfinpyrazone. Dipyridamole did not inhibit platelet aggregation in vivo and did not inhibit aggregation in vitro in concentrations at which it remained soluble.The filter loop technique is a suitable model for measuring platelet aggregation in the flowing blood of the rat. It is a relatively simple method of determining aggregation and easily adapted to other species.

Prostanoide in der Therapie der chronischen arteriellen Verschlußkrankheit

1993 ◽  
Vol 13 (02) ◽  
pp. 65-72 ◽  
Author(s):  
G. Rudofsky
Keyword(s):  
Prostaglandin E1

ZusammenfassungIn den fortgeschrittenen Stadien der chronischen arteriellen Verschlußkrankheit gehören die Prostanoide, hier insbesondere Prostaglandin E1 (PGE1), zum festen Therapiekonzept, wenn lumeneröffnende Verfahren nicht durchführbar oder bereits erfolglos gewesen sind.Wie zahlreiche Studien an mehr als 1000 Patienten zeigen, kommt es nach i. a. oder i.v. PGE1 lnfusion zu deutlichen Verbesserungen trophischer Läsionen, zur vollständigen oder zumindest erheblichen Reduktion des Ruheschmerzes mit gleichzeitiger Verminderung des Analgetikabedarfs sowie zur Senkung der Amputationsrate. Bei schwerer Claudicatio mit extrem kurzen Gehstrecken konnte sowohl die schmerzfreie als auch die maximale Gehstrecke signifikant und klinisch relevant gesteigert werden. Darüber hinaus wurde der Nachweis erbracht, daß das positive Behandlungsergebnis bei den meisten Patienten sogar noch nach Monaten vorgefunden werden kann. Ein erhöhtes Risiko für unerwünschte schwerwiegende Arzneimittelwirkungen konnte weder unter i.a. noch i.v. PGE1 lnfusion aufgedeckt werden.

PROSTAGLANDIN E1 ADMINISTRATION TO PATIENTS WITH THE DUCTUS-DEPENDENT CONGENITAL HEART DISEASE

1990 ◽  
Vol 40 (6) ◽  
pp. 765-771
Author(s):  
KATSUHIKO SONE ◽  
TOSHIHIRO KOBAYASHI ◽  
TOMIO KOBAYASHI ◽  
TAKASHI KOSUDA ◽  
SANAYASU ONO ◽  
...  
Keyword(s):  
Congenital Heart Disease ◽  
Heart Disease ◽  
Congenital Heart ◽  
Prostaglandin E1
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