Different Roles for Thromboxane Synthetase Inhibitors and Prostacyclin Mimetics in Myocardial Reperfusion Damage*

2015 ◽  
pp. 316-321
Author(s):  
Ch. Thiemermann ◽  
K. Schr�r
Keyword(s):  
Myocardial Reperfusion ◽  
Reperfusion Damage ◽  
Thromboxane Synthetase

Role of A2A Receptor in the Modulation of Myocardial Reperfusion Damage

1999 ◽  
Vol 33 (6) ◽  
pp. 883-893 ◽  
Author(s):  
Anna Cargnoni ◽  
Claudio Ceconi ◽  
Antonella Boraso ◽  
Palmira Bernocchi ◽  
Angela Monopoli ◽  
...  
Keyword(s):  
Myocardial Reperfusion ◽  
Reperfusion Damage ◽  
A2a Receptor

Pharmacological Strategies to Contend Against Myocardial Reperfusion Damage: Diverse Chemicals for Multiple Targets

2010 ◽  
Vol 17 (21) ◽  
pp. 2261-2273 ◽  
Author(s):  
F. Correa ◽  
E. Martinez-Abundis ◽  
S. Hernandez-Resendiz ◽  
N. Garcia ◽  
M. Buelna-Chontal ◽  
...  
Keyword(s):  
Myocardial Reperfusion ◽  
Multiple Targets ◽  
Reperfusion Damage

scholarly journals Myocardial reperfusion syndrome. Pathogenesis, clinic, diagnosis

2020 ◽  
Vol 22 (1) ◽  
pp. 196-200
Author(s):  
G G Khubulava ◽  
A N Shishkevich ◽  
S S Mikhailov ◽  
E Yu Bessonov
Keyword(s):  
Myocardial Infarction ◽  
Clinical Picture ◽  
Myocardial Dysfunction ◽  
Heart Rhythm ◽  
Myocardial Reperfusion ◽  
Irreversible Damage ◽  
Pathological Physiology ◽  
No Reflow ◽  
Reperfusion Damage ◽  
No Reflow Phenomenon

The basics of pathogenesis, clinic and diagnosis of myocardial reperfusion syndrome are considered. Myocardial reperfusion syndrome is defined. Its relevance as one of the most poorly studied and formidable complications of cardiac reperfusion in myocardial infarction with elevation of the S-T segment has been explained. A brief review of the historical review of this problem and such types of manifestations of myocardial reperfusion syndrome as: diastolic myocardial dysfunction, post-reperfusion disturbances of the heart rhythm, the phenomenon of no-reflow and irreversible damage to the myocardium are briefly reviewed. The modern views on the pathological physiology of diastolic myocardial dysfunction, post-reperfusion damage to the myocardium, and the no-reflow phenomenon are analyzed. A review of current views on the pathological physiology of the development of post-reperfusion disturbances in heart rhythm is carried out. The clinical picture and the effect on the hemodynamics of such a manifestation of myocardial reperfusion syndrome as diastolic myocardial dysfunction are described. A brief description of the clinical picture of irreversible post-reperfusion damage to the myocardium is given. The clinical picture and types of post-reperfusion rhythm disturbances are described. The diagnostics of the no-reflow phenomenon has been analyzed in detail, the coronary angiographic scales for assessing thrombolysis in myocardial infarction and for assessing myocardial perfusion are graphically shown. A description of the basics of diagnosing post-reperfusion disturbances in heart rhythm, diastolic myocardial dysfunction, and post-reperfusion irreversible damage to the myocardium is given. A brief description of the known in the world literature predictors of the development of myocardial reperfusion syndrome is presented.

PathophysioSogy of Myocardial Reperfusion

1987 ◽  
Vol 5 (1) ◽  
pp. 31-48 ◽  
Author(s):  
Keith A.A. Fox ◽  
Jeffrey E. Saffitz ◽  
Peter B. Corr
Keyword(s):  
Myocardial Reperfusion

The Interrelationship between Thromboxane Biosynthesis, Aggregation and 5-Hydroxytryptamine Secretion in Human Platelets in Vitro

1980 ◽  
Vol 43 (01) ◽  
pp. 038-040 ◽  
Author(s):  
L C Best ◽  
T K Holland ◽  
P B B Jones ◽  
R G G Russell
Keyword(s):  
Human Platelet ◽  
Human Platelets ◽  
Dense Granule ◽  
Thromboxane B2 ◽  
Essential Requirement ◽  
Direct Mechanism ◽  
Thromboxane Synthetase ◽  
Thromboxane Production ◽  
Higher Doses

SummaryPlatelet aggregation, secretion of 5-hydroxy tryptamine and production of thromboxane B2 were monitored simultaneously in human platelet suspensions in the absence and presence of cyclooxygenase or thromboxane synthetase inhibitors. Aggregation, secretion and thromboxane B2 formation in response to either sodium arachidonate or epinephrine were blocked by aspirin or by 1-N-butyl imidazole suggesting that thromboxane biosynthesis was an essential requirement for platelet activation by these agents. In contrast, thrombin and collagen could apparently induce aggregation and secretion via two pathways: at low doses involving thromboxane production, but at higher doses by a direct mechanism independent of thromboxane biosynthesis. In the case of ADP, inhibition of thromboxane production blocked secretion but had little effect on aggregation, indicating that secretion was probably dependent on thromboxane biosynthesis which probably occurred as a result of aggregation. Thus it appears that although the processes of thromboxane production, release of dense granule constituents and aggregation may often be intimately linked, each process can occur independently of the other, depending upon the stimulus used.

Inhibition of Platelet Aggregation by Human Placenta

1985 ◽  
Vol 54 (02) ◽  
pp. 431-437 ◽  
Author(s):  
M J Dembélé-Duchesne ◽  
A Laghchim Lahlou ◽  
H Thaler-Dao ◽  
A Crastes de Paulet
Keyword(s):  
Fatty Acid ◽  
Platelet Aggregation ◽  
Human Placenta ◽  
Cyclooxygenase Inhibitor ◽  
Synthetase Inhibitor ◽  
Inhibition Of Platelet Aggregation ◽  
Thromboxane Synthetase ◽  
Rabbit Platelets ◽  
High Doses ◽  
Induced Aggregation

SummaryHuman placental cytosol inhibits platelet aggregation induced by high doses of collagen. The aim of this study was to investigate whether this anti-aggregating activity was caused only by the presence of various activities already described in the placenta (an ADP-consuming enzyme, a fatty acid cyclooxygenase inhibitor, and a thromboxane synthetase inhibitor) or whether another factor was present.Heating the cytosol at 50° C for 6 min destroyed the inhibitor of collagen-induced aggregation. ADPase and the AA pathway inhibitors were not modified by this treatment. We therefore show the presence of an additional anti-aggregating factor: it is destroyed by heating at 50° C.We also tested for the presence of an inhibitor of AA release in the placental cytosol using three different methods (rabbit platelets in PRP, washed rabbit platelets, and NRK fibroblasts) but no inhibition could be evidenced.We conclude that this new anti-aggregating factor, which is probably a protein, acts neither through AA release inhibition nor AA cascade inhibition.

Selective Inhibition of Thromboxane Synthetase with Dazoxiben - Basis of Its Inhibitory Effect on Platelet Adhesion

1983 ◽  
Vol 49 (02) ◽  
pp. 096-101 ◽  
Author(s):  
V C Menys ◽  
J A Davies
Keyword(s):  
Arachidonic Acid ◽  
Platelet Adhesion ◽  
Fold Increase ◽  
Selective Inhibition ◽  
Inhibitory Effect ◽  
Selective Inhibitor ◽  
Coated Glass ◽  
Thromboxane Synthetase ◽  
Pre Treatment

SummaryPlatelet adhesion to rabbit aortic subendothelium or collagen-coated glass was quantitated in a rotating probe device by uptake of radio-labelled platelets. Under conditions in which aspirin had no effect, dazoxiben, a selective inhibitor of thromboxane synthetase, reduced platelet adhesion to aortic subendothelium by about 40% but did not affect adhesion to collagen-coated glass. Pre-treatment of aortic segments with 15-HPETE, a selective inhibitor of PGI2-synthetase, abolished the inhibitory effect of dazoxiben on adhesion. Concentrations of 6-oxo-PGFlα in the perfusate were raised in the presence of dazoxiben alone, and following addition of thrombin (10 units/ml) there was a 2-3 fold increase in concentration. Perfusion of damaged aorta with platelets labelled with (14C)-arachidonic acid in the presence of thrombin and dazoxiben resulted in the appearance of (14C)-labelled-6-oxo-PGFiα. Inhibition of thromboxane synthetase limits platelet adhesion probably by promoting vascular synthesis of PGI2 from endoperoxides liberated from adherent platelets, which subsequently promotes detachment of cells from the surface.

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