Influence of Prostaglandin E1 on Muscular Tissue-PO2 in Patients with Diabetic Gangrene

1989 ◽  
pp. 699-704 ◽  
Author(s):  
Robert Heinrich ◽  
Hans-Werner Krawzak ◽  
Helmut Strosche
Keyword(s):  
Prostaglandin E1 ◽  
Muscular Tissue ◽  
Tissue Po2 ◽  
Diabetic Gangrene

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

Prostaglandin E1-Induced Hyperostosis: Clinicopathologic Correlations and Possible Pathogenetic Mechanisms

1996 ◽  
Vol 16 (3) ◽  
pp. 489-507 ◽  
Author(s):  
Ona Faye-Petersen ◽  
Walter Johnson ◽  
Waldemar Carlo ◽  
Gary Hedlund ◽  
Albert Pacifico ◽  
...  
Keyword(s):  
Prostaglandin E1 ◽  
Pathogenetic Mechanisms

Excess oxygen delivery during muscle contractions in spontaneously hypertensive rats

1995 ◽  
Vol 78 (1) ◽  
pp. 101-111 ◽  
Author(s):  
J. M. Lash ◽  
H. G. Bohlen
Keyword(s):  
Blood Flow ◽  
Oxygen Saturation ◽  
Oxygen Delivery ◽  
Spontaneously Hypertensive Rats ◽  
Muscle Contractions ◽  
Hypertensive Rats ◽  
Hemoglobin Oxygen Saturation ◽  
Spontaneously Hypertensive ◽  
Tissue Po2 ◽  
Wistar Kyoto

These experiments determined whether a deficit in oxygen supply relative to demand could account for the sustained decrease in tissue PO2 observed during contractions of the spinotrapezius muscle in spontaneously hypertensive rats (SHR). Relative changes in blood flow were determined from measurements of vessel diameter and red blood cell velocity. Venular hemoglobin oxygen saturation measurements were performed by using in vivo spectrophotometric techniques. The relative dilation [times control (xCT)] of arteriolar vessels during contractions was as large or greater in SHR than in normotensive rats (Wistar-Kyoto), as were the increases in blood flow (2 Hz, 3.50 +/- 0.69 vs. 3.00 +/- 1.05 xCT; 4 Hz, 10.20 +/- 3.06 vs. 9.00 +/- 1.48 xCT; 8 Hz, 16.40 +/- 3.95 vs. 10.70 +/- 2.48 xCT). Venular hemoglobin oxygen saturation was lower in the resting muscle of SHR than of Wistar-Kyoto rats (31.0 +/= 3.0 vs. 43.0 +/- 1.9%) but was higher in SHR after 4- and 8-Hz contractions (4 Hz, 52.0 +/- 4.8 vs. 43.0 +/- 3.6%; 8 Hz, 51.0 +/- 4.6 vs. 41.0 +/- 3.6%). Therefore, an excess in oxygen delivery occurs relative to oxygen use during muscle contractions in SHR. The previous and current results can be reconciled by considering the possibility that oxygen exchange is limited in SHR by a decrease in anatomic or perfused capillary density, arteriovenular shunting of blood, or decreased transit time of red blood cells through exchange vessels.

scholarly journals GLYCOLYTIC PROPERTIES OF MUSCULAR TISSUE

1917 ◽  
Vol 31 (3) ◽  
pp. 501-517
Author(s):  
Ralph Hoagland ◽  
C.M. Mansfield
Keyword(s):  
Muscular Tissue
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