Eicosanoids and myocardial ischaemia

Schrör, Karsten

doi:10.1007/978-3-662-08390-1_27

Cited by 12 publications

(8 citation statements)

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“…26 Although the mechanism of these cytoprotective effects of prostaglandins has been elusive, these cytoprotective effects have been suggested to contribute to or account for the protection of certain organs or tissues, including the heart, by prostaglandins against a variety of different noxious stimuli. 12,26 Thus, cytoprotection is the protection of a tissue by prostaglandins in the absence of alterations in blood flow, inhibition of platelet function, or inhibition of polymorphonuclear cell activation mediated by EP 2 receptors. Activation of EP 3 receptors leads to protection of the myocardium against ischemia, without causing alterations in systemic hemodynamics (vide infra) and presumably, inhibition of the function of blood-borne cells.…”

Section: Discussionmentioning

confidence: 99%

“…The mechanism(s) or the prostanoid receptor(s) mediating this effect is unknown. 12 In 1995 through 1996, we discovered that the cardioprotective effects of EPs are due, at least in part, to activation of EP 1 or EP 3 receptors, which in turn leads to the opening of ATP-sensitive potassium (K ATP ) channels. 10,13 This hypothesis is supported by the following findings: (1) The cardioprotective effects of PGE 1 (nonselective agonist for all EP receptors) and sulprostone (selective agonist of EP 1 and EP 3 receptors) are abolished by inhibition of K ATP channels with glibenclamide or 5-hydroxydecanoate (5-HD).…”

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confidence: 99%

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Selective Activation of the Prostanoid EP ₃ Receptor Reduces Myocardial Infarct Size in Rodents

Zacharowski

Olbrich²,

Piper³

et al. 1999

ATVB

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Abstract-The cardioprotective effects of E-type prostaglandins (EPs) have been attributed to vasodilatation, inhibition of platelet and neutrophil function (EP 2 mediated), and an unknown "cytoprotective effect." We have hypothesized that selective activation of EP 3 receptors may cause cardioprotection. The prostanoid derivative ONO-AE-248 selectively binds to murine EP 3␣ receptors expressed in Chinese hamster ovary (CHO) cells (K i , 15 nmol/L) and prevents the rise in cAMP caused by forskolin in CHO cells (IC 50 Ϸ1 nmol/L) in which the EP 3␣ receptor had been expressed. In anesthetized rats subjected to regional myocardial ischemia for 25 or 45 minutes and 2 hours of reperfusion, infusion of ONO-AE-248 (5 g ⅐ kg Ϫ1 ⅐ min Ϫ1 IV) caused a significant reduction in infarct size, from 60Ϯ3% (nϭ8) to 36Ϯ6% (nϭ7) and from 78Ϯ2% (nϭ11) to 58Ϯ4% (nϭ9), respectively. The reduction in infarct size caused by ONO-AE-248 in rats subjected to 25 minutes of ischemia and reperfusion was abolished by a selective inhibitor of ATP-sensitive potassium (K ATP ) channels, 5-hydroxydecanoate (nϭ6), and the protein kinase C inhibitors staurosporine (nϭ6) and chelerythrine (nϭ6). In anesthetized rabbits subjected to coronary artery occlusion for 45 or 60 minutes and 2 hours of reperfusion, infusion of ONO-AE-248 (5 g ⅐ kg Ϫ1 ⅐ min Ϫ1 IV) caused a significant reduction in infarct size, from 61Ϯ2% (nϭ10) to 36Ϯ4% (nϭ8) and from 63Ϯ4% (nϭ7) to 42Ϯ4% (nϭ7), respectively. The reduction in infarct size caused by ONO-AE-248 in the rabbit was also abolished by 5-hydroxydecanoate. The cardioprotective effect of ONO-AE-248 in rats or rabbits was not associated with any hemodynamic effects. Selective activation of the prostanoid EP 3 receptor reduces myocardial infarct size in rodents by a mechanism(s) that may involve the activation of protein kinase C and the opening of K ATP channels.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Selective Activation of the Prostanoid EP ₃ Receptor Reduces Myocardial Infarct Size in Rodents

Zacharowski

Olbrich²,

Piper³

et al. 1999

ATVB

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“…Early studies suggested that this cardioprotection was mediated via replacement of ω-6 with ω-3. Thereby an increased ratio of ω-3/ω-6 in cell membranes diminished the detrimental effects of pro-inflammatory AA-derived eicosanoids, prostaglandins and leukotrienes [95,96,97]. …”

Section: Pufa and Their Derivatives Against MImentioning

confidence: 99%

Mediterranean diet and cardioprotection: The role of nitrite, polyunsaturated fatty acids, and polyphenols

2011

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The continually increasing rate of myocardial infarction (MI) in the Western world at least partly can be explained by a poor diet lacking in green vegetables, fruits, and fish, and enriched in food that contains saturated fat. In contrast, a number of epidemiological studies provide strong evidence highlighting the cardioprotective benefits of the Mediterranean diet enriched in green vegetables, fruits, fish and grape wine. Regular consumption of these products leads to an accumulation of nitrate/nitrite/NO • , polyunsaturated fatty acids (PUFA), and polyphenolic compounds, such as resveratrol, in the human body. Studies have confirmed that these constituents are bioactive exogenous mediators, which induce strong protection against MI. The aim of this review is to provide a critical, in-depth analysis of the cardioprotective pathways mediated by nitrite/NO • , PUFA, and phenolic compounds of grape wines discovered in the recent years, including cross-talk between different mechanisms and compounds. Overall, these findings may facilitate the design and synthesis of novel therapeutic tools for the treatment of MI.

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“…Ischemia and reperfusion are associated with an increase in arachidonic acid levels in cell membranes and induce profound alterations in myocardial eicosanoid generation (6,37). Arachidonic acid is converted by cyclooxygenase (COX) to prostaglandin H 2 (PGH 2 ), which in turn is the precursor of further prostaglandins and thromboxanes.…”

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confidence: 99%

COX-2-dependent and potentially cardioprotective effects of negative inotropic substances released after ischemia

Birkenmeier

Staudt²,

Schunck³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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During reperfusion, cardiodepressive factors are released from isolated rat hearts after ischemia. The present study analyzes the mechanisms by which these substances mediate their cardiodepressive effect. After 10 min of global stop-flow ischemia, rat hearts were reperfused and coronary effluent was collected over a period of 30 s. We tested the effect of this postischemic effluent on systolic cell shortening and Ca2+ metabolism by application of fluorescence microscopy of field-stimulated rat cardiomyocytes stained with fura-2 AM. Cells were preincubated with various inhibitors, e.g., the cyclooxygenase (COX) inhibitor indomethacin, the COX-2 inhibitors NS-398 and lumiracoxib, the COX-1 inhibitor SC-560, and the potassium (ATP) channel blocker glibenclamide. Lysates of cardiomyocytes and extracts from whole rat hearts were tested for expression of COX-2 with Western blot analysis. As a result, in contrast to nonischemic effluent (control), postischemic effluent induced a reduction of Ca2+ transient and systolic cell shortening in the rat cardiomyocytes ( P < 0.001 vs. control). After preincubation of cells with indomethacin, NS-398, and lumiracoxib, the negative inotropic effect was attenuated. SC-560 did not influence the effect of postischemic effluent. The inducibly expressed COX-2 was detected in cardiomyocytes prepared for fluorescence microscopy. The effect of postischemic effluent was eliminated with applications of glibenclamide. Furthermore, postischemic effluent significantly reduced the intracellular diastolic and systolic Ca2+ increase ( P < 0.01 vs. control). In conclusion, the cardiodepressive effect of postischemic effluent is COX-2 dependent and protective against Ca2+ overload in the cells.

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Eicosanoids and myocardial ischaemia

Cited by 12 publications

References 50 publications

Selective Activation of the Prostanoid EP ₃ Receptor Reduces Myocardial Infarct Size in Rodents

Selective Activation of the Prostanoid EP ₃ Receptor Reduces Myocardial Infarct Size in Rodents

Mediterranean diet and cardioprotection: The role of nitrite, polyunsaturated fatty acids, and polyphenols

COX-2-dependent and potentially cardioprotective effects of negative inotropic substances released after ischemia

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Eicosanoids and myocardial ischaemia

Cited by 12 publications

References 50 publications

Selective Activation of the Prostanoid EP 3 Receptor Reduces Myocardial Infarct Size in Rodents

Selective Activation of the Prostanoid EP 3 Receptor Reduces Myocardial Infarct Size in Rodents

Mediterranean diet and cardioprotection: The role of nitrite, polyunsaturated fatty acids, and polyphenols

COX-2-dependent and potentially cardioprotective effects of negative inotropic substances released after ischemia

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Selective Activation of the Prostanoid EP ₃ Receptor Reduces Myocardial Infarct Size in Rodents

Selective Activation of the Prostanoid EP ₃ Receptor Reduces Myocardial Infarct Size in Rodents