Vascular prostaglandin and thromboxane production in a canine model of myocardial ischemia.

Schmitz, James M.; Apprill, P; Buja, L. Maximilian; Willerson, James T.; Campbell, William B.

doi:10.1161/01.res.57.2.223

Cited by 71 publications

(37 citation statements)

References 42 publications

(14 reference statements)

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“…Thromboxane A 2 is a potent coronary vasoconstrictor (28) and contributes to the genesis of arrhythmias (29) and cyclical reductions in coronary blood flow (30) in the ischemic myocardium. Hydroxyeicosatetraenoic acid and thromboxane A 2 appear to contribute to the no-reflow phenomenon after reperfusion of previously ischemic myocardium (31).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-(1-7) improves the post-ischemic function in isolated perfused rat hearts

Ferreira

Santos

Almeida

2002

Braz J Med Biol Res

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We evaluated the effects of angiotensin-(1-7) (Ang-(1-7)) on postischemic function in isolated hearts from adult male Wistar rats perfused according to the Langendorff technique. Local ischemia was induced by coronary ligation for 15 min. After ischemia, hearts were reperfused for 30 min. Addition of angiotensin II (Ang II) (0.20 nM, N = 10) or Ang-(1-7) (0.22 nM, N = 10) to the Krebs-Ringer perfusion solution (KRS) before the occlusion did not modify diastolic or systolic tension, heart rate or coronary flow (basal values for Ang-(1-7)-treated hearts: 0.72 ± 0.08 g, 10.50 ± 0.66 g, 216 ± 9 bpm, 5.78 ± 0.60 ml/min, respectively). During the period of occlusion, the coronary flow, heart rate and systolic tension decreased (values for Ang-(1-7)-treated hearts: 2.83 ± 0.24 ml/min, 186 ± 7 bpm, 6.95 ± 0.45 g, respectively). During reperfusion a further decrease in systolic tension was observed in control (4.95 ± 0.60 g) and Ang II-treated hearts (4.35 ± 0.62 g). However, in isolated hearts perfused with KRS containing Ang-(1-7) the further reduction of systolic tension during the reperfusion period was prevented (7.37 ± 0.68 g). The effect of Ang-(1-7) on the systolic tension was blocked by the selective Ang-(1-7) antagonist A-779 (2 nM, N = 9), by the bradykinin B 2 antagonist HOE 140 (100 nM, N = 10), and by indomethacin pretreatment (5 mg/ kg, ip, N = 8). Pretreatment with L-NAME (30 mg/kg, ip, N = 8) did not change the effect of Ang-(1-7) on systolic tension (6.85 ± 0.61 g). These results show that Ang-(1-7) at low concentration (0.22 nM) improves myocardial function (systolic tension) in ischemia/reperfusion through a receptor-mediated mechanism involving release of bradykinin and prostaglandins.

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Section: Discussionmentioning

confidence: 99%

Angiotensin-(1-7) improves the post-ischemic function in isolated perfused rat hearts

Ferreira

Santos

Almeida

2002

Braz J Med Biol Res

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“…35 Prostacyclin, a key vasodilator and inhibitor of platelet aggregation, is synthesized primarily in endothelial cells that were damaged in this model. There were aggregation of platelets and infiltration of inflammatory cells, both capable of thromboxane synthesis.…”

Section: Dynamic Coronary Obstruction Unstable Angina Pectorismentioning

confidence: 94%

“…There were aggregation of platelets and infiltration of inflammatory cells, both capable of thromboxane synthesis. 35 Serotonin tissue concentrations were also found to be elevated; platelet aggregates were considered to be the source. 36 It was hypothesized that endothelial injury in unstable lesions in humans and in the Folts et al 31 canine model caused attachment and activation of platelets, which in turn release thromboxane and serotonin.…”

Section: Dynamic Coronary Obstruction Unstable Angina Pectorismentioning

confidence: 99%

Thrombi in Acute Coronary Syndromes

2000

Circulation

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O ver the past 35 years, the view has evolved that the acute coronary syndromes, ie, unstable angina pectoris, myocardial infarction, and sudden death, are caused by plaque rupture and formation of a platelet thrombus. There is at least a transient total or subtotal coronary occlusion in all cases of acute myocardial infarction. Q-wave infarcts are thought to differ from non-Q-wave infarcts by more stable platelet thrombi causing more prolonged and/or severe ischemia, leading to more extensive infarction. The greater platelet stability in transmural infarction is attributed to more severe or extensive plaque rupture. 1-3 Unstable angina and non-Qwave infarction, in the present view, are due to less extensive, less stable platelet thrombi that cause less severe, less extensive ischemia and/or infarction.However, autopsy data and more recent clinical findings require significant refinement of this viewpoint on the basis of the following observations. The occlusive thrombi causing Q-wave myocardial infarction contain more fibrin than the thrombi found in the other acute coronary syndromes that are characterized by more platelets and less fibrin. The higher fibrin content of thrombi causing Q-wave infarction explains their greater stability. Furthermore, this higher fibrin content suggests that the coagulation cascade is activated to a greater degree during Q-wave infarction than during non-Q-wave infarction in which platelets play a more dominant role. This review analyzes our evolving concepts focusing on the growing divergence of the different mechanisms underlying the different acute coronary syndromes and their clinical and therapeutic implications. Morphological Basis for the Current Concept of Acute Coronary SyndromesBy the mid-1930s, acute myocardial infarction was shown to be caused by coronary thrombosis resulting from intimal fissuring, which is often associated with dissecting hemorrhage into the underlying plaque. 4 -7 In the late 1930s, however, intimal fissuring was questioned and subendothelial hemorrhages were ascribed to rupture of capillaries within the plaque. 8,9 The causative role of coronary thrombosis became controversial in 1956 when pathologists first reported a low prevalence of thrombi in fatal infarction. 10 -16 The pendulum began to swing back in the mid-1960s because of improved autopsy techniques. Coronary thrombi were found in Ͼ90% of fatal infarcts, most being occlusive.Plaque hemorrhages, which were usually traceable to an intimal tear within the thrombosed segment, were found in most cases. [17][18][19][20][21] These observations reaffirmed that intimal rupture was the essential mechanism causing both subendothelial hemorrhage and intraluminal thrombosis. 22 Having found that three quarters of occlusive coronary thrombi were composed of layers of different ages, Sinapius 17,21 concluded that these thrombi developed in a protracted, recurring course. The oldest portion of thrombus usually sealed the intimal fissure and was rich in platelets. The finding that mural thrombus forma...

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“…Agents specifically designed to inhibit platelet function, including serotonin receptor antagonists (9-1 1), TXA2 synthesis inhibitors (12) or receptor antagonists (13), or MAbs to the platelet glycoprotein lIb/IlIa receptor (22), prevent the occurrence of CFVs in most cases. Furthermore, histologic examination of coronary arteries obtained at the nadir ofcyclic flow variations consistently reveals an adherent platelet mass (12,14,20 Exercise protocol. After recovery from the surgical procedure was complete and dogs were able to walk comfortably, the effect of treadmill exercise on the development ofcyclic flow variations was tested in 11 dogs (Fig.…”

Section: Introductionmentioning

confidence: 99%

“…We have previously demonstrated that serotonin (9)(10)(11) and thromboxane A2 (TXA2) (12)(13)(14) are important mediators of coronary occlusion due to platelet aggregation in anesthetized dogs with coronary artery stenoses and endothelial injury. Other factors may be important in governing the process of platelet aggregation at sites of coronary artery stenosis in awake, active animals.…”

Section: Introductionmentioning

confidence: 99%

Treadmill exercise promotes cyclic alterations in coronary blood flow in dogs with coronary artery stenoses and endothelial injury

1990

Journal of Cardiothoracic Anesthesia

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Vascular prostaglandin and thromboxane production in a canine model of myocardial ischemia.

Cited by 71 publications

References 42 publications

Angiotensin-(1-7) improves the post-ischemic function in isolated perfused rat hearts

Angiotensin-(1-7) improves the post-ischemic function in isolated perfused rat hearts

Thrombi in Acute Coronary Syndromes

Treadmill exercise promotes cyclic alterations in coronary blood flow in dogs with coronary artery stenoses and endothelial injury

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