Release of immunoreactive endothelin from the heart during percutaneous transluminal coronary angioplasty

Malatino, Lorenzo; Grassi, Rosario; Stancanelli, Benedetta; Polizzi, Gaetano; Leonardi, Carmelo; Tamburino, Corrado; Tamburino, G

doi:10.1016/0002-8703(93)90421-5

Cited by 40 publications

(12 citation statements)

References 6 publications

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“…4,5 Increased plasma ET-1 levels are observed in patients with coronary artery diseases such as myocardial infarction 5 and angina 6 and immediately after PTCA. 7 In isolated perfused rat hearts, endogenous ET-1 is known to be released during ischemia/reperfusion. 8 In addition, coronary artery occlusion and reperfusion in pigs increased the local overflow and tissue content of ET-1-like immunoreactivity.…”

mentioning

confidence: 99%

Different Contributions of Endothelin-A and Endothelin-B Receptors in Postischemic Cardiac Dysfunction and Norepinephrine Overflow in Rat Hearts

et al. 2005

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Background-Endothelin (ET)-1 and norepinephrine (NE) are involved in myocardial ischemia/reperfusion injury. We investigated the role of ET-1 in ischemia/reperfusion-induced NE overflow and cardiac dysfunction using a selective ET A receptor antagonist (ABT-627), a selective ET B receptor antagonist (A-192621), and the spotting lethal (sl) rat, which carries a naturally occurring deletion in the ET B receptor gene. Methods and Results-According to the Langendorff technique, isolated hearts were subjected to 40-minute global ischemia followed by 30-minute reperfusion. In Sprague-Dawley rat hearts, ischemia/reperfusion-induced cardiac dysfunctions such as decreased left ventricular developed pressure and coronary flow and increased left ventricular end-diastolic pressure were worsened by treatment with A-192621. This agent enhanced excessive NE overflow in the coronary effluent from the postischemic heart. In contrast, treatment with ABT-627, in the absence or presence of A-192621, significantly improved postischemic cardiac dysfunction and markedly suppressed NE overflow to the same extent. Postischemic cardiac dysfunction and NE overflow in the heart of ET B receptor-deficient homozygous (sl/sl) rats were highly observed compared with cases in wild-type rats, and exaggerated responses to ischemia/reperfusion in sl/sl rats were abolished by ABT-627 treatment. Exogenously applied ET-1 produced severe cardiac dysfunction and a significant increase in NE overflow in a dose-dependent manner, but these responses were markedly suppressed in the presence of 5-N-ethyl-N-isopropyl-amiloride, an inhibitor of the Na ϩ /H ϩ exchanger (NHE). Conclusions-Pharmacological blockade or genetic deficiency of ET B receptors is detrimental to the postischemic heart, and exaggerated cardiac pathology under the above conditions is mediated by ET A receptor activation. ET A /NHEmediated excessive NE overflow is contributive, at least in part, to postischemic cardiac dysfunction in rats.

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mentioning

confidence: 99%

Different Contributions of Endothelin-A and Endothelin-B Receptors in Postischemic Cardiac Dysfunction and Norepinephrine Overflow in Rat Hearts

et al. 2005

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“…Moreover, elevation of plasma ET-1 levels and myocardial ET-1 has been demonstrated in patients with chronic heart failure and myocardial infarction [5,15]. Stimulation of cardiac ET-1 production has been shown in patients undergoing reperfusion procedures with fibrinolytic agents [16] and angioplasty [6]. Elevated plasma ET-1 levels have also been shown to be significantly correlated with poor LV function and elevated creatine kinase levels after reperfusion with fibrinolytic agents, suggesting an important role of ET in the pathogenesis of myocardial infarction [16].…”

Section: Discussionmentioning

confidence: 99%

“…Endothelin-1 (ET-1), a potent vasoconstrictor, is a 21 amino acid peptide and has been implicated as a detrimental agent adversely affecting the outcome of myocardial ischemia and reperfusion [4]. Increased plasma ET-1 levels are present in patients with coronary artery disease such as myocardial infarction [5] and immediately after percutaneous transluminal coronary angioplasty [6]. High circulating levels of ET-1 after myocardial infarction have been shown to be associated with increased morbidity and mortality [7].…”

Section: Introductionmentioning

confidence: 99%

Endothelin-1 Release during the Early Phase of Reperfusion Is a Mediator of Myocardial Reperfusion Injury

Tamareille¹,

Terwelp²,

Amirian³

et al. 2013

Cardiology

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Purpose: In acute myocardial infarction, left ventricular (LV) unloading reduces endothelin-1 (ET-1) release. We tested that endogenous ET-1 released during acute myocardial infarction might mediate ischemia/reperfusion (I/R) injury by stimulating increased intracellular calcium concentration, [Ca²⁺]_i, and apoptosis. Methods: Rabbits were subjected to 1 h of coronary artery occlusion followed by 3 h of reperfusion. Unloading was initiated 15 min prior to reperfusion and was maintained during reperfusion. The control group was subjected to reperfusion. Animals were treated with ET-1 receptor antagonist BQ123. In parallel, isolated rabbit cardiomyocytes subjected to simulated I/R with or without ET-1 or BQ123, intracellular Ca²⁺ and cell death were assessed with flow cytometry. Results: LV unloading prior to reperfusion reduced myocardial ET-1 release at 2 h of reperfusion. Infarct size was reduced in unloaded and BQ123 groups versus controls. LV unloading and BQ123 treatment reduced the percentage of apoptotic cells associated with increases in Bcl-2 protein levels in ischemic regions. BQ123 reduced both ET-1-induced [Ca²⁺]_i increase and cell death for myocytes subjected to stimulated I/R. Conclusion: We propose that components of reperfusion injury involve ET-1 release which stimulates calcium overload and apoptosis. Intravenous ET-1 receptor blockade prior to reperfusion may be a protective adjunct to reperfusion therapy in acute myocardial infarction patients.

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“…After coronary angioplasty of the left anterior descending coro nary artery, the plasma endothelin level increased in the coronary sinus in the time interval from 2 through 5 min after the procedure. The increase was highest in subjects with unsuccessful angioplasty [17], Several hours after coronary angioplasty a rise in the urinary endothelin-1 level was also observed [18], On the other hand, other authors did not find changes in endothelin concentrations in the great cardiac vein or femoral artery, even in patients in whom distal coronary vasoconstriction was observed [19],…”

Section: Discussionmentioning

confidence: 99%

Local Changes in the Plasma Endothelin Level in the Coronary Artery Immediately after Percutaneous Transluminal Coronary Angioplasty

Vojáček¹,

Lisý²,

Šimek³

et al. 1997

Cardiology

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Endothelin plays an important role in cardiovascular pathology. As one of the most important endothelium-derived vasoconstrictor substances, endothelin together with endothelium-derived vasodilating factor control vascular tone and contribute to the vasoconstrictory response if the production of endothelium-derived vasodilating factor is impaired. The aim of the study was to assess the changes of the local endothelin level in coronary circulation immediately after percutaneous transluminal coronary angioplasty (PTCA). Plasma endothelin levels were measured in blood samples from the peripheral vein and ostium of the coronary artery before the angioplasty, and from the distal coronary artery just beyond the dilated segment and the peripheral vein immediately after the procedure. The plasma endothelin level was significantly higher in the ostium of the coronary artery already prior to PTCA as compared to the peripheral vein (10.9 ± 3.4 vs. 7.2 ± 2.1 pg/ml, p < 0.005). There was no change in the endothelin level in the coronary artery distal to the dilated segment immediately after the procedure as compared to the initial level, although this level was higher than the postangioplasty venous level (9.8 ± 2.9 vs. 7.7 ± 2.0 pg/ml, p < 0.005). Individual changes in coronary-artery plasma endothelin levels as a response to coronary angioplasty were disparate. An increase and a decrease in coronary artery plasma endothelin levels by more than 2 pg/ml after coronary angioplasty were observed in 3 and 6 subjects, respectively. In conclusion, increased plasma endothelin levels were found in blood samples drawn from the coronary artery as compared to the peripheral vein. There was no further change in the plasma endothelin level in the coronary artery distal to the dilated segment after angioplasty; however, the individual responses were disparate.

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Release of immunoreactive endothelin from the heart during percutaneous transluminal coronary angioplasty

Cited by 40 publications

References 6 publications

Different Contributions of Endothelin-A and Endothelin-B Receptors in Postischemic Cardiac Dysfunction and Norepinephrine Overflow in Rat Hearts

Different Contributions of Endothelin-A and Endothelin-B Receptors in Postischemic Cardiac Dysfunction and Norepinephrine Overflow in Rat Hearts

Endothelin-1 Release during the Early Phase of Reperfusion Is a Mediator of Myocardial Reperfusion Injury

Local Changes in the Plasma Endothelin Level in the Coronary Artery Immediately after Percutaneous Transluminal Coronary Angioplasty

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