In vivo production of prostacyclin and thromboxane in patients with acute myocardial infarction.

Henriksson, Peter; Wennmalm, Åke; Edhag, O; Vesterqvist, O.; Green, K

doi:10.1136/hrt.55.6.543

Cited by 60 publications

(9 citation statements)

References 15 publications

(2 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One study [41] has also shown that these large platelets are denser. In addition, patients with acute MI show a shortening of the bleeding time when compared to controls [27,44,45], an increase in thromboxane B2 excretion [46,47,48] and an increase in the bleeding time sensitivity to aspirin ( Fig. 2) [45], suggesting that the platelets of these patients may have an elevated activity of the cyclo-oxygenase pathway.…”

Section: Hyperfunctional Platelets In Coronary Artery Thrombosis and mentioning

confidence: 99%

The regulation of megakaryocyte polyploidization and its implications for coronary artery occlusion

Martin¹

1993

Eur J Clin Investigation

View full text Add to dashboard Cite

Abstract. Polyploidization is a distinctive feature of megakaryocyte differentiation. The physiological meaning and the regulation of this process are obscure. Megakaryocyte ploidy varies in normal biology and in disease. Here we review the evidence suggesting that ploidy changes may have a role in the determination of platelet reactivity and in the aetiology of coronary artery occlusion. We also present a hypothesis that may serve as a framework to explore the regulation of megakaryocyte polyploidization at the molecular level and also may provide a rational basis to explain the occurrence of ploidy changes in ischaemic heart disease.

show abstract

Section: Hyperfunctional Platelets In Coronary Artery Thrombosis and mentioning

confidence: 99%

The regulation of megakaryocyte polyploidization and its implications for coronary artery occlusion

Martin¹

1993

Eur J Clin Investigation

View full text Add to dashboard Cite

show abstract

“…In the canine model of coronary stenosis associated with endothelial injury, Golino et al (18) have described that one of the TXA2 receptor antagonists, SQ29548, abolishes cyclic flow variations and results in an increase in the left anterior descending artery cross-sectional area. It is also known that TXA2 formation increases in patients with acute MI (19). Therefore, the role of TXA2 in our MI model is clear and seems similar to the canine model and patients with acute MI.…”

Section: Discussionmentioning

confidence: 63%

An Experimental Myocardial Infarction Model in the Rat and Its Properties

Hirata

Umemura

Nakashima

1995

Japanese Journal of Pharmacology

View full text Add to dashboard Cite

ABSTRACT-The photochemical reaction between rose bengal and light (540 nm) produces thrombotic occlusion in rat coronary artery. We have now developed an experimental myocardial infarction (MI) model by photochemically induced thrombosis (PIT) in rats and investigated the mechanisms responsible for the induction of MI. PIT in the coronary artery induced myocardial ischemia, which was determined by tissue oxygen tension (tpO2), and resulted in MI. Pretreatment with a thromboxane (TX) A2-receptor antagonist, vapiprost, prevented a decrease in myocardial tpO2 and markedly reduced the MI area, although vapiprost inhibited collagen-induced platelet aggregation by 30% ex vivo. An ADP-induced platelet aggregation inhibitor, clopidogrel, also reduced the MI area. In contrast to vapiprost, clopidogrel inhibited collagen-induced platelet aggregation by 90% ex vivo. Pretreatment with a 5-HT2-receptor antagonist, ketanserin, which did not inhibit collagen-induced platelet aggregation ex vivo, prevented the decrease in myocardial tpO2 and reduced the MI area. These results suggest that TXA2, 5-HT and ADP play a role in the induction of MI and that platelet aggregation and other factors induce ischemia in this model. (1), insertion of copper coil into an artery (2) and endothelial injury by electrical current (3). The model is selected for use according to the aim of the study; e.g., ischemia-reperfusion, thrombogenesis or arrhythmias. However, an MI model caused by thrombus in rats has not been reported. Thus, mediators involved in the MI model produced by thrombus in rats remain unclear.Recently, we have reported some photochemically induced thrombosis (PIT) models in rats (4) and guinea pigs (5, 6). In these PIT models, endothelial injury is induced by singlet oxygen generated by a photochemical reaction (7,8). Fukuchi et al. (9) have previously demonstrated that the photochemically induced thrombus in the coronary artery consisted of platelets, and ventricular arrhythmias were induced. Since their model had high mortality within a few hours, they failed to detect MI in rats. Therefore, we attempted to make an MI model by thrombus in the rat coronary artery and investigate representative mediators, thromboxane (TX) A2, 5-HT and ADP, involved in MI using antagonists. MATERIALS AND METHODS Photochemically induced thrombosis (PIT) in rat coronary arteryThirty-four male Sprague-Dawly rats (Charles River Japan, Atsugi) weighing about 400 g were anesthetized by i.p. injection of 50 mg/kg of sodium pentobarbital. The jugular vein was cannulated for rose bengal and drug delivery. Tracheal intubation was performed for artificial respiration. The chest was opened by a left thoracotomy. Transillumination with green light (540 nm) was achieved by use of a xenon lamp with a heat absorbing filter and a green filter (Hamamatsu Photonics, Hamamatsu). The head (3 mm in diameter) of the green light source was fixed 5-mm-apart from the surface of the myocardium between the conoventricular vein and branches of the ventricular cordis magna in...

show abstract

“…923 - 27 Thus, activation of TXA 2 formation, largely from platelets, is a consistent finding soon after the occurrence of myocardial ischemia.…”

Section: Discussionmentioning

confidence: 92%

Potentiation of myocardial salvage by tissue type plasminogen activator in combination with a thromboxane synthetase inhibitor in ischemic cat myocardium.

Lefer

Mentley

Sun

1988

Circulation Research

View full text Add to dashboard Cite

We studied the effects of a thrombolytic agent (t-PA) and a thromboxane synthetase inhibitor (CGS-13080) in a model of myocardial ischemia and reperfusion. Occlusion of the left anterior descending coronary artery for 2 hours followed by 4 hours of reperfusion in anesthetized cats results in a large washout of creatine kinase into the blood (32 ±7 lU/mg protein) and an area of necrotic tissue comprising 52±5% of the area at risk and 9±0.6% of the left ventricle. Intravenous administration of t-PA (500 IU/kg • min) for 30 minutes alone at reperfusion or infusion of CGS-13080 (500 figlkg • hr) had no effect on washout of creatine kinase or extent of necrotic tissue development. Administration of the same doses of both t-PA and CGS-13080 together markedly attenuated creatine kinase release to 10 ± 2 IU/mg protein (p<0.01) and reduced the area of necrotic tissue to 9 ± 2% of the area at risk and only 1.3 ± 0.3% of the left ventricle (/?<0.001). No significant sustained effects of these agents were observed on mean arterial blood pressure, heart rate, or the pressure rate index in these experiments. Thus, t-PA and CGS-13080 exert synergistic effects hi preserving myocardial integrity in cats subjected to acute myocardial ischemia followed by reperfusion. The mechanism of this beneficial effect does not appear to be via reduced myocardial oxygen demand, increased myocardial oxygen supply, or enhanced inhibition of thromboxane A 2 formation. The mechanism of this anti-ischemic effect is not clear but may involve a metabolic or a cytoprotective effect. (Circulation Research

show abstract

In vivo production of prostacyclin and thromboxane in patients with acute myocardial infarction.

Cited by 60 publications

References 15 publications

The regulation of megakaryocyte polyploidization and its implications for coronary artery occlusion

The regulation of megakaryocyte polyploidization and its implications for coronary artery occlusion

An Experimental Myocardial Infarction Model in the Rat and Its Properties

Potentiation of myocardial salvage by tissue type plasminogen activator in combination with a thromboxane synthetase inhibitor in ischemic cat myocardium.

Contact Info

Product

Resources

About