Endogenous and Exogenous Nitric Oxide Protect Against Intracoronary Thrombosis and Reocclusion After Thrombolysis

Yao, Sheng-Kun; Akhtar, Salman; Scott‐Burden, Timothy; Ober, J. C.; Golino, Paolo; Buja, L. Maximilian; Casscells, Ward; Willerson, James T.

doi:10.1161/01.cir.92.4.1005

Cited by 46 publications

(33 citation statements)

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“…Exogenous delivery of nitric oxide, by administration of a nitric oxide donor, has been shown to reduce thrombus formation. 34,35,54 The suppression of PAI-1 released by platelets 36,37 and by VSMCs (current report) may contribute to this nitric oxide effect by promoting fibrinolysis. Consistent with this hypothesis, nitric oxide synthase inhibition has been reported to increase plasma PAI activity in environmentally stressed rats.…”

Section: Discussionmentioning

confidence: 63%

“…In addition to regulating vascular tone, atrial natriuretic factor (ANF), C-type natriuretic peptide (CNP), and nitric oxide-generating compounds inhibit VSMC growth and migration in vitro [27][28][29][30] and reduce neointimal formation after balloon catheter-induced vascular injury. 31,32 Nitric oxide has also been shown to provide antithrombotic activity [33][34][35] and reduce PAI-1 released from platelets. 36,37 As such, exogenous local delivery of nitric oxide synthase and CNP has been proposed as a treatment to reduce restenosis.…”

mentioning

confidence: 99%

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Natriuretic Factors and Nitric Oxide Suppress Plasminogen Activator Inhibitor-1 Expression in Vascular Smooth Muscle Cells

Bouchie

Hansen

Feener

1998

ATVB

105

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Abstract-Increased expression of plasminogen activator inhibitor-1 (PAI-1) has been reported in atherosclerotic and balloon-injured vessels. Little is known regarding the factors and mechanisms that may negatively regulate PAI-1 expression. In this report, the effect of cGMP-coupled vasoactive hormones, including natriuretic factors and nitric oxide, on the regulation of PAI-1 expression in vascular smooth muscle cells was examined. Atrial natriuretic factor 1-28 (ANF) and C-type natriuretic factor-22 (CNP) reduced angiotensin II (Ang II)-and platelet-derived growth factor-stimulated PAI-1 mRNA expression in rat aortic smooth muscle cells by 50% to 70%, with corresponding reductions in PAI-1 protein release. Treatment of human aortic smooth muscle cells with CNP similarly inhibited both platelet-derived growth factor-induced PAI-1 mRNA expression and PAI-1 protein release by 50%. Dose-response studies revealed that the inhibitory effects of CNP and ANF on PAI-1 expression were concentration dependent, with IC 50 s of Ϸ1 nmol/L for both natriuretic peptides. Ang II-stimulated PAI-1 expression was also inhibited by the nitric oxide donor S-nitroso-N-acetylpenicillamine.

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Section: Discussionmentioning

confidence: 63%

mentioning

confidence: 99%

Natriuretic Factors and Nitric Oxide Suppress Plasminogen Activator Inhibitor-1 Expression in Vascular Smooth Muscle Cells

Bouchie

Hansen

Feener

1998

ATVB

105

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“…Previous findings showed that NO release was increased in coronary artery myocardial ischemia (19)(20)(21). By contrast, other authors found that NO release was decreased (22,23). The function of endothelium plays an important role in maintaining stability and normal blood flow dynamics.…”

Section: Discussionmentioning

confidence: 87%

Effects of propofol on myocardial ischemia-reperfusion injury in rats with type-2 diabetes mellitus

Wang

et al. 2016

Biomedical Reports

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Abstract. The current study aimed to examine the effects of propofol on myocardial ischemia-reperfusion injury (MIRI) in rats with type-2 diabetes mellitus (T2DM) and to assess the role of inflammatory mediators. Fifty healthy male adult Sprague-Dawley rats were randomly divided into the sham, ischemia-reperfusion (IR), IR plus low, middle and high-dose (6, 12 and 24 mg/kg/h, intravenous) propofol groups. The rats of all the groups were fed a high-sugar and high-fat diet for 8 weeks and streptozotocin (30 mg/kg, intraperitoneally) was used to establish the T2DM model. Apart from the sham group rats, MIRI was induced by ligating the left anterior descending coronary artery for 30 min, followed by reperfusion for 2 h. Heart rate (HR), left ventricular systolic pressure (LVSP), and the rate of left ventricular pressure increase in early systole (± dp/dt max ) were recorded. Levels of cardiac troponin T (cTnT), nitric oxide (NO), endothelin-1 (ET-1), interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were also measured. Myocardial lesions were observed under light microscopy and scanning electron microscopy. Compared with levels prior to arterial occlusion, HR, LVSP, and ± dp/dt max were significantly reduced (P<0.05) following occlusion for 30 min and reper fusion for 2 h. The administration of propofol ameliorated the cardiac function of rats as reflected by the increase in HR, LVSP and ± dp/dt max . In addition, the administration of propofol increased the serum NO concentration, and reduced ET-1 and cTnT levels, as well as levels of inflammatory mediators including IL-1β, IL-6 and TNF-α. Thus, propofol exerts protective effects against MIRI in T2DM rats by increasing NO and reducing ET-1 and the inflammatory mediators.

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“…NO is reported to have many cardioprotective effects on ischemia and reperfusion injury (21)(22)(23)(24)(25)(26). Thus, enhancement of NO production during ischemia and reperfusion by ACE inhibitors may reduce ischemia and reperfusion injury (27,28).…”

Section: Effects Of Ace Inhibitors On Myocardial Infarct Sizementioning

confidence: 99%

Cellular Mechanisms of Cardioprotection Afforded by Inhibitors of Angiotensin Converting Enzyme in Ischemic Hearts: Role of Bradykinin and Nitric Oxide.

et al. 2000

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Angiotensin converting enzyme (ACE) inhibitors inhibit the degradation of bradykinin and contribute to accumulation of bradykinin and NO, both of which may be beneficial for diseased hearts. To test this idea, we administered imidaprilat and cilazaprilat, respectively to the canine ischemic myocardium. In the open chest dogs with low constant coronary perfusion pressure (CPP, from 104 ± 3 to 42 ± 3 mmHg), coronary blood flow (CBF, 91 ± 1 to 32 ± 2 mI/100 g/min), fractional shortening (FS), and lactate extraction ratio (LER) decreased. Either imidaprilat or cilazaprilat increased CBF, FS, and LER with increases in cardiac bradykinin and NO levels. The beneficial effects of ACE inhibitors were blunted by either L-NAME (an inhibitor of NO synthase) and HOE140 (an inhibitor of bradykinin receptors), respectively. ACE inhibitors, on the other hand, are reported to attenuate the severity of myocardial stunning, which effect is partially attributable to bradykinin-and NO-dependent mechanisms.Further, ACE inhibitors limited infarct size following coronary occlusion and reperfusion. This infarct size-limitation was blunted by either L-NAME and IBTX (the antagonist of KCa channels). Bradykinin is also reported to close Kca channels. Thus, we concluded that ACE inhibitors attenuate both reversible and irreversible myocardial cellular injury via bradykinin/NOdependent mechanisms. In experimental and clinical settings, the cardioprotective effects of ACE inhibitors on the diseased heart may be attributable to these mechanisms. (Hypertens Res 2000; 23: 253-259)

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Endogenous and Exogenous Nitric Oxide Protect Against Intracoronary Thrombosis and Reocclusion After Thrombolysis

Abstract: Increasing NO production or giving an NO donor may inhibit platelet aggregation and delay intracoronary thrombus formation and reocclusion after thrombolysis.

Cited by 46 publications

References 46 publications

Natriuretic Factors and Nitric Oxide Suppress Plasminogen Activator Inhibitor-1 Expression in Vascular Smooth Muscle Cells

Natriuretic Factors and Nitric Oxide Suppress Plasminogen Activator Inhibitor-1 Expression in Vascular Smooth Muscle Cells

Effects of propofol on myocardial ischemia-reperfusion injury in rats with type-2 diabetes mellitus

Cellular Mechanisms of Cardioprotection Afforded by Inhibitors of Angiotensin Converting Enzyme in Ischemic Hearts: Role of Bradykinin and Nitric Oxide.

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