Nitric Oxide Inhibition Impairs Blood Flow During Exercise in Hearts With a Collateral-Dependent Myocardial Region

Traverse, Jay H.; Kinn, James W.; Klassen, Chris; Duncker, Dirk J.; Bache, Robert J.

doi:10.1016/s0735-1097(97)00437-3

Cited by 30 publications

(28 citation statements)

References 21 publications

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“…20,29 Furthermore, NO could positively affect latent collaterals or collateral blood flow by eliciting vasodilatation or inhibiting platelet aggregation in the vascular bed distal to the target lesion. 22,30 These mechanisms 15,16,[19][20][21][22][28][29][30] can explain why NTP was more effective than NTG in improving the final angiographic results. Second, recent studies have demonstrated that HBTF 4 and lipid pool-like content 31 in large IRAs are predictors of slow-flow or no-reflow, because distal macro-and microembolism of thrombi and plaque material frequently occurs in these vessels during balloon dilatation or stenting, which, in turn, induces severe microvascular dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Impact of PercuSurge Device Conjugative With Intracoronary Administration of Nitroprusside on No-Reflow Phenomenon Following Primary Percutaneous Coronary Intervention

Youssef

Hang

et al. 2006

Circ J

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Section: Discussionmentioning

confidence: 99%

Impact of PercuSurge Device Conjugative With Intracoronary Administration of Nitroprusside on No-Reflow Phenomenon Following Primary Percutaneous Coronary Intervention

Youssef

Hang

et al. 2006

Circ J

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“…Finally, a contribution from impaired microvascular dilation, especially in cases of steal, is suggested by results of experimental studies in laboratory animals. [17][18][19][20] Maximal blood flow and conductance in collateral supply myocardium also were abnormal even in segments with normal contraction at rest (Tables 4 and 5). Because supply vessels had either no or only mild stenosis, reduced maximal blood flow may reflect a contribution from microvascular dysfunction in collateral supply myocardium.…”

Section: Discussion Principal Findingsmentioning

confidence: 98%

“…Because supply vessels had either no or only mild stenosis, reduced maximal blood flow may reflect a contribution from microvascular dysfunction in collateral supply myocardium. [17][18][19] It is possible, however, that abnormal flow reserve in collateral supply myocardium reflects the fact that a single conduit vessel must serve the needs of Ն2 vascular beds. 12,13 Under such conditions and in the presence of either diffuse atherosclerosis or even mild focal stenosis, impedance to flow in the conduit supply artery may be increased substantially and could contribute importantly to reduced maximal blood flow and conductance in the collateral supply bed.…”

Section: Discussion Principal Findingsmentioning

confidence: 99%

Relation Between Coronary “Steal” and Contractile Function at Rest in Collateral-Dependent Myocardium of Humans With Ischemic Heart Disease

et al. 1999

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Background-We tested the hypothesis that rest asynergy in collateral-dependent myocardium correlates with coronary steal. Methods and Results-PET with [13 N]ammonia measured myocardial blood flow and flow reserve in 15 patients with symptomatic chronic ischemic heart disease. Coronary angiography assessed stenosis severity and collateral blood supply. Echocardiography or contrast ventriculography evaluated regional wall motion. Collateral-dependent segments with normal flow at rest and supplied by coronary vessels having Յ50% diameter stenosis were studied. Steal was defined as a decline in myocardial blood flow with adenosine Ն0.15 mL ⅐ min Ϫ1 ⅐ g Ϫ1 versus rest. Blood flow at rest in asynergic, collateral-dependent segments with steal (1.15Ϯ0.35 mL ⅐ min Ϫ1 ⅐ g Ϫ1 ) exceeded (PϽ0.0001) that of asynergic segments without steal (0.81Ϯ0.24) and those with normal contraction (0.77Ϯ0.18). Although the flow reserve ratio of segments with normal contraction (1.8Ϯ0.8) exceeded that of asynergic ones with (0.6Ϯ0.1) or without (1.3Ϯ0.4) steal, overlap was great. Correlation between basal contraction and flow reserve ratio in collateral-dependent myocardium was significant but weak (rϭ0.45, PϽ0.001). However, segments demonstrating "steal" with adenosine manifested asynergy in 22 of 23 collateral-dependent segments versus 24 of 39 nonsteal segments ( 2 ϭ7.10, PϽ0.01). Conclusions-Although myocardial flow reserve in collateral-dependent segments with normal contraction exceeded that of asynergic segments, overlap was great. However, in patients with angina or congestive heart failure, left ventricular segments demonstrating steal with adenosine almost always exhibit asynergy at rest. Thus, coronary steal may play an important role in the pathogenesis of chronic contractile impairment at rest, whereas simple reduction of flow reserve may be less important in selected patients. (Circulation. 1999;99:2510-2516.)

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“…After occlusions had been performed for 3 wk, the artery was permanently occluded. We previously observed that this degree of collateralization is sufficient to allow permanent coronary occlusion without producing infarct (31). Studies were performed after permanent occlusion had been in place for 3 days.…”

Section: Methodsmentioning

confidence: 99%

“…VEGF has been shown to upregulate eNOS expression in vascular endothelial cells but can also induce iNOS expression (4,26,30). Vascular NO effects are increased in collateralized hearts, since nonselective inhibition of NO production with N G -nitro-L-arginine (LNA) significantly decreased blood flow in collateral-dependent myocardium but did not decrease blood flow in normal hearts (22,31). Whether this increased NO effect in collateralized hearts results from constitutive NOS or from inducible NO synthase (iNOS) is unknown.…”

mentioning

confidence: 99%

Inducible nitric oxide synthase inhibits oxygen consumption in collateral-dependent myocardium

Chen

Zhang

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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RJ. Inducible nitric oxide synthase inhibits oxygen consumption in collateral-dependent myocardium. Am J Physiol Heart Circ Physiol 306: H356 -H362, 2014. First published December 6, 2013 doi:10.1152/ajpheart.00308.2013.-Following coronary artery occlusion growth of collateral vessels can provide an effective blood supply to the dependent myocardium. The ischemia, which results in growth of collateral vessels, recruits an inflammatory response with expression of cytokines and growth factors, upregulation of endothelial nitric oxide (NO) synthase (eNOS) in vascular endothelial cells, and expression of inducible nitric oxide synthase (iNOS) in both vessels and cardiac myocytes. Because NO is a potent collateral vessel dilator, this study examined whether NO derived from iNOS or constitutive NOS regulates myocardial blood flow (MBF) in the collateral region. Nonselective NOS inhibition with N G -nitro-L-arginine (LNA) caused vasoconstriction with a significant decrease in MBF to the collateral region during exercise. In contrast, the highly selective iNOS inhibitor 1400W caused a 21 Ϯ 5% increase of MBF in the collateral region. This increase in MBF following selective iNOS blockade was proportionate to an increase in myocardial O2 consumption (MV O2). The results suggest that NO produced by iNOS inhibits MV O2 in the collateralized region, so that the increase in MBF following iNOS blockade was the result of metabolic vasodilation secondary to an increase in MV O2. Thus the coordinated expression of iNOS to restrain MV O2 and eNOS to maintain collateral vasodilation act to optimize the O2 supplydemand relationship and protect the collateralized myocardium from ischemia. collateral vessel; coronary artery NITRIC OXIDE (NO) produced by constitutively expressed endothelial NO synthase (eNOS) is known to mediate the vasodilator responses to endothelium-dependent agonists such as acetylcholine and bradykinin, and is responsible for the flowmediated coronary artery dilation that occurs in response to increased endothelial shear stress (27). In addition to effects on coronary vascular smooth muscle, NO within the cardiac myocytes can compete with oxygen at cytochrome c oxidase in the mitochondrial respiratory chain to inhibit oxygen consumption (MV O 2 ) (3, 6).Coronary artery occlusion results in growth of native interarterial anastomotic channels to develop an effective collateral circulation that provides an alternative blood supply to the dependent myocardium. Developed collateral vessels have an organized smooth muscle media and are responsive to both vasodilator and vasoconstrictor influences (1, 9, 18). The ischemia, which results in growth of collateral vessels, recruits an inflammatory response with expression of cytokines in the vessel wall and a dramatic release of growth factors such as VEGF into the myocardial interstitial fluid (33). VEGF has been shown to upregulate eNOS expression in vascular endothelial cells but can also induce iNOS expression (4, 26, 30). Vascular NO effects are increased in collatera...

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Nitric Oxide Inhibition Impairs Blood Flow During Exercise in Hearts With a Collateral-Dependent Myocardial Region

Cited by 30 publications

References 21 publications

Impact of PercuSurge Device Conjugative With Intracoronary Administration of Nitroprusside on No-Reflow Phenomenon Following Primary Percutaneous Coronary Intervention

Impact of PercuSurge Device Conjugative With Intracoronary Administration of Nitroprusside on No-Reflow Phenomenon Following Primary Percutaneous Coronary Intervention

Relation Between Coronary “Steal” and Contractile Function at Rest in Collateral-Dependent Myocardium of Humans With Ischemic Heart Disease

Inducible nitric oxide synthase inhibits oxygen consumption in collateral-dependent myocardium

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