ASPIRIN INHIBITS THE EARLY MYOCARDIAL RELEASE OF THROMBOXANE B<sub>2</sub> AND VENTRICULAR ECTOPIC ACTIVITY FOLLOWING ACUTE CORONARY ARTERY OCCLUSION IN DOGS

Coker, Susan J.; Ledingham, I. McA.; Parratt, J. R.; Zeitlin, I. J.

doi:10.1111/j.1476-5381.1981.tb09138.x

Cited by 53 publications

(13 citation statements)

References 4 publications

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“…Several reports have suggested that TXA2 contributes to myocardial ischemic injury and arrhythmias (1,6,13,17,34). The lack of an effect of platelet depletion may be due to the inability of such depletion to depress circulating TXB~ levels.…”

Section: Discussionmentioning

confidence: 95%

Platelet depletion in experimental myocardial infarction

et al. 1985

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Accumulation of platelets in the microvasculature after acute myocardial ischemia may exacerbate tissue injury through the formation of microthrombi and by the release of vasoactive substances. To assess the role of platelets in myocardial ischemic injury and infarction, circulating platelets were reduced by 94 +/- 2% (mean +/- S.E.M.) with sheep antiserum to canine platelets. Regional myocardial ischemia was produced by occlusion of the left circumflex coronary artery (LCCA) for 90 min followed by reperfusion for 5 hours. Infarct size did not differ significantly between antiplatelet serum and nonimmune serum groups: 36 +/- 8 vs. 43 +/- 4% of the area at risk, determined by a post-mortem dual staining technique (p greater than 0.05). A second occlusion-reperfusion control group, sacrificed at 24 hours, did not differ from 5 hr reperfused groups with regard to infarct size. Coronary sinus thromboxane B2 (TXB2) concentrations were not altered significantly by platelet depletion. Histopathologic examination confirmed the presence of necrosis in the infarcted myocardium and revealed substantial leukocytic infiltration in both groups. The results suggest that circulating platelets are not required for the full expression of myocardial ischemic injury resulting from temporary coronary artery occlusion followed by reperfusion.

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Section: Discussionmentioning

confidence: 95%

Platelet depletion in experimental myocardial infarction

et al. 1985

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“…TXA 2 release may be responsible for cardiac arrhythmias and may precede ventricular ectopic activity. In addition, TXA 2 causes local coronary vasoconstriction with platelet aggregation [15]. Therefore, inhibition of TXA 2 counteracts these effects.…”

Section: Discussionmentioning

confidence: 99%

Effect of Cyclooxygenase-2 Inhibitor (Celecoxib) on the Infarcted Heart in situ

Yamamoto¹,

Kakar²,

Vina³

et al. 2001

Pharmacology

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Several attempts have been made to replace aspirin with compounds without gastric toxicity; a cyclooxygenase-2 (COX-2) inhibitor, celecoxib, and a nitric oxide-aspirin, NCX-4016, have been developed for this purpose. This paper compares effects of celecoxib, NCX-4016 and aspirin on production of prostacyclin (PGI₂) and thromboxane A₂ (TXA₂) and activation of the inducible form of nitric oxide synthase (iNOS) in infarcted heart in situ. Aspirin was most effective in reducing myocardial PGI₂ synthesis and formation of TXA₂. Myocardial effects of celecoxib resemble those of NCX-4016, although the two compounds have different modes of action.

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“…In the present study, we have found that macrocortin, a 15 k fraction of the supernatant of dexamethasonetreated isolated peritoneal cells of the rat offers a beneficial effect in the early phase of acute myocardial infarction. As macrocortin, like lipomodulin (Hirata et al, 1980), has anti-phospholipase activity (thereby preventing AA release from the cell membrane) it appears likely that the cardioprotective effects of glucocorticoids are related to inhibition of early TxA2 release due to ischaemia (Coker et al, 1981). …”

mentioning

confidence: 99%

The possible mechanism of protection induced by dexamethasone against sudden death due to coronary ligation in conscious rats

Koltai¹,

Leprán²,

Nemecz³

et al. 1983

British J Pharmacology

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Rat isolated peritoneal cells (107 cells ml−1) incubated in the presence of dexamethasone (3 × 10−9 m, for 90 min) were shown to release some factor(s), having a mol. wt. of 15 k, as determined by size exclusion chromatography, which inhibited phospholipase A2 activity and offered significant protection against sudden death due to post‐infarction arrhythmias in conscious rats pre‐treated with actinomycin D (0.5 mg kg−1 i.v. 4 h before coronary ligation). This observation suggests that the cardioprotective effect of glucocorticoids in acute myocardial infarction may result from the de novo synthesis of macrocortin, an antiphospholipase protein.

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ASPIRIN INHIBITS THE EARLY MYOCARDIAL RELEASE OF THROMBOXANE B₂ AND VENTRICULAR ECTOPIC ACTIVITY FOLLOWING ACUTE CORONARY ARTERY OCCLUSION IN DOGS

Cited by 53 publications

References 4 publications

Platelet depletion in experimental myocardial infarction

Platelet depletion in experimental myocardial infarction

Effect of Cyclooxygenase-2 Inhibitor (Celecoxib) on the Infarcted Heart in situ

The possible mechanism of protection induced by dexamethasone against sudden death due to coronary ligation in conscious rats

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ASPIRIN INHIBITS THE EARLY MYOCARDIAL RELEASE OF THROMBOXANE B2 AND VENTRICULAR ECTOPIC ACTIVITY FOLLOWING ACUTE CORONARY ARTERY OCCLUSION IN DOGS

Cited by 53 publications

References 4 publications

Platelet depletion in experimental myocardial infarction

Platelet depletion in experimental myocardial infarction

Effect of Cyclooxygenase-2 Inhibitor (Celecoxib) on the Infarcted Heart in situ

The possible mechanism of protection induced by dexamethasone against sudden death due to coronary ligation in conscious rats

Contact Info

Product

Resources

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ASPIRIN INHIBITS THE EARLY MYOCARDIAL RELEASE OF THROMBOXANE B₂ AND VENTRICULAR ECTOPIC ACTIVITY FOLLOWING ACUTE CORONARY ARTERY OCCLUSION IN DOGS