Release of endothelin from the porcine heart after short term coronary artery occlusion

Tønnessen, Theis; Næss, Pål Aksel; Kirkebøen, Knut Arvid; Offstad, Jon; Ilebekk, Arnfinn; Christensen, Geir

doi:10.1093/cvr/27.8.1482

Cited by 44 publications

(19 citation statements)

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“…3) ET-1 enhances microvascular permeability with consequent oedema resulting in microvascular compression. Our findings showed a significant increase in plasma ET-1 levels during AMI and reperfusion, which is in agreement with the report of Tønnessen [23], reflecting endothelial dysfunction caused by ischemia and reperfusion. Our findings also showed that the myocardial tissue levels of ET-1 have a significant increase in the reflow and no-reflow myocardium compared to those in the non-ischaemic myocardium, further suggesting that endothelium was damaged to some different extent in the reflow and no-reflow myocardium.…”

Section: Discussionsupporting

confidence: 93%

Tirofiban Preserves Endothelial Junctions and Decreases Endothelin-1

Zhao

2008

Sci Pharm

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It has been verified that glycoprotein IIb/IIIa inhibitor tirofiban can attenuate myocardial no-reflow. Myocardial no-reflow has been associated with alterations in endothelial junctions. In addition, ET-1 is an important mechanism for myocardial no-reflow. However, the effect of tirofiban on endothelial junctions and Endothelin-1 (ET-1) is unknown. Methods: Twenty-eight mini-swines were randomized into 3 study groups: 10 in control, 10 given an intravenous infusion of tirofiban and 8 in sham-operated. Acute myocardial infarction and reperfusion model was created with three-hour occlusion of the left anterior descending coronary artery followed by one-hour reperfusion. Results: In control group, plasma ET-1 significantly increased, ET-1 or VE-cadherin level in the reflow and no-reflow myocardium was significantly higher or lower than that in normal myocardium. Compared with the control group, tirofiban significantly decreased plasma ET-1 and myocardial tissue ET-1, maintained VE-cadherin level. Conclusions: Tirofiban is effective in preserving endothelial junction. This beneficial effect of tirofiban could be partly due to its reduction of ET-1.

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Section: Discussionsupporting

confidence: 93%

Tirofiban Preserves Endothelial Junctions and Decreases Endothelin-1

Zhao

2008

Sci Pharm

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“…This view is supported by the observation that NOS inhibitor (L-NMMA) exhibited no effect on adenosine-induced dilation in the previous study. 3 It is speculated that the increased release of local endothelin, as commonly observed in myocardial ischemia, [35][36][37][38] may contribute to the selective endothelial dysfunction related to NO deficiency. In the present study, we found that the dilation of collateral-dependent arterioles to smooth muscle K ATP channel activator pinacidil was not altered (supplemental Figure IA), suggesting the lack of effect of coronary occlusion on endothelium-independent dilation of coronary arterioles to adenosine.…”

Section: Thengchaisri Et Al Exercise Restores Coronary Arteriolar Dilmentioning

confidence: 99%

Exercise Training Restores Coronary Arteriolar Dilation to NOS Activation Distal to Coronary Artery Occlusion

Thengchaisri

Shipley

Ren

et al. 2007

ATVB

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Objective-Exercise training has been shown to restore vasodilation to nitric oxide synthase (NOS) activation in arterioles distal to coronary artery occlusion. Because reactive oxygen species are generated during NOS uncoupling and the production of vasodilator H 2 O 2 is increased during exercise in patients with coronary disease, we proposed that H 2 O 2 may contribute to the restoration of vasodilation in porcine coronary occlusion model. Methods and Results-Left circumflex (LCX) coronary artery of miniature swine was progressively occluded for 8 weeks followed by exercise training (EX; 5 days/wk treadmill) or sedentary (SED) protocols for 12 weeks. Arterioles were isolated from distal LCX and nonoccluded left anterior descending (LAD) artery for in vitro study. Vasodilation to NOS activators adenosine and ionomycin was impaired in SED LCX, but not LAD, arterioles. This impairment was restored by L-arginine. NO production induced by adenosine was also reduced in SED LCX arterioles. EX had no effect on LAD arterioles but improved NO production and restored dilation of LCX arterioles. NOS blockade (L-NAME) inhibited vasodilation to NOS activators in LAD (SED & EX) arterioles but was ineffective in SED LCX arterioles. In EX LCX arterioles, vasodilation to NOS activators was slightly inhibited by L-NAME but abolished by catalase. H 2 O 2 production was markedly increased by adenosine in EX LCX arterioles. Conclusions-This study demonstrates that endothelium-dependent NO-mediated dilation is impaired in SED LCXarterioles and that EX training restores the impaired function. It appears that H 2 O 2 , in addition to NO, contributes significantly to EX-induced restoration of endothelium-dependent dilation of coronary arterioles distal to occlusion.

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“…Evidence suggests that the endothelins might be important modulators of both vascular tone and myocardial contractility following myocardial infarction (Yasuda et al, 1990;Watanabe et al, 1991;Matsuyama et al, 1991;T0nnessen et al, 1993). In addition, endothelins may be involved in the development of cardiac hypertrophy.…”

Section: Calculation Of Binding Parametersmentioning

confidence: 99%

Selectivity of [¹²⁵I]‐PD 151242 for human, rat and porcine endothelin ET_A receptors in the heart

Peter

Davenport

1995

British J Pharmacology

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1 Endothelin-1 binds with high affinity to heart where it acts as a potent positive inotropic agent. Our aim was to characterize the labelled and unlabelled ETA-selective antagonist PD151242 in heart tissues derived from man, rat and pigs by use of radioligand binding techniques. 0.37 ± 0.10 nM), whereas the ETB-selective compound, BQ3020, competed with only micromolar affinity (KD = 1.5 ± 0.26 gM).6 The novel ETA-selective radioligand ['25I]-PD151242 binds with high affinity to human, rat and porcine heart. In human tissue, binding was shown to be reversible and highly selective for the ETA-subtype making ['251]-PD151242 a useful selective radioligand for further characterization of the ETA-receptor in human tissue.

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Release of endothelin from the porcine heart after short term coronary artery occlusion

Abstract: Endothelin is released from the heart for several minutes during reperfusion following a brief coronary artery occlusion.

Cited by 44 publications

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Tirofiban Preserves Endothelial Junctions and Decreases Endothelin-1

Tirofiban Preserves Endothelial Junctions and Decreases Endothelin-1

Exercise Training Restores Coronary Arteriolar Dilation to NOS Activation Distal to Coronary Artery Occlusion

Selectivity of [¹²⁵I]‐PD 151242 for human, rat and porcine endothelin ET_A receptors in the heart

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Release of endothelin from the porcine heart after short term coronary artery occlusion

Abstract: Endothelin is released from the heart for several minutes during reperfusion following a brief coronary artery occlusion.

Cited by 44 publications

References 0 publications

Tirofiban Preserves Endothelial Junctions and Decreases Endothelin-1

Tirofiban Preserves Endothelial Junctions and Decreases Endothelin-1

Exercise Training Restores Coronary Arteriolar Dilation to NOS Activation Distal to Coronary Artery Occlusion

Selectivity of [125I]‐PD 151242 for human, rat and porcine endothelin ETA receptors in the heart

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Selectivity of [¹²⁵I]‐PD 151242 for human, rat and porcine endothelin ET_A receptors in the heart