Protective Role of Nerve Growth Factor Against Postischemic Dysfunction of Sympathetic Coronary Innervation

Abe, Takuzo; Morgan, Donald A.; Gutterman, David D.

doi:10.1161/01.cir.95.1.213

Cited by 75 publications

(46 citation statements)

References 30 publications

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“…To this extent, nerve growth factor might be a therapeutic target because this endogenous compound is capable of preventing ischemic neural stunning. 114 The acid-sensing ion channel 3 is another target given its putative role in cardiac nociception. 47 This would allow patients to sense the presence of myocardial ischemia and seek attention and intervention earlier.…”

Section: Future Directionsmentioning

confidence: 99%

Silent Myocardial Ischemia

Gutterman

2009

Circ J

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Although much progress has been made in reducing mortality from ischemic cardiovascular disease, this condition remains the leading cause of death throughout the world. This might in part be due to the fact that over half of patients have a catastrophic event (heart attack or sudden death) as their initial manifestation of coronary disease. Contributing to this statistic is the observation that the majority of myocardial ischemic episodes are silent, indicating an inability or failure to sense ischemic damage or stress on the heart. This review examines the clinical characteristics of silent myocardial ischemia, and explores mechanisms involved in the generation of angina pectoris. Possible mechanisms for the more common manifestation of injurious reductions in coronary flow; namely, silent ischemia, are also explored. A new theory for the mechanism of silent ischemia is proposed. Finally, the prognostic importance of silent ischemia and potential future directions for research are discussed. (Circ J 2009; 73: 785 -797)

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Section: Future Directionsmentioning

confidence: 99%

Silent Myocardial Ischemia

Gutterman

2009

Circ J

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“…Denervation in the apex of the heart after ischemia-reperfusion can also occur as the infarct may disrupt passage of sympathetic nerves (Barber, et al, 1983). After occlusion, infusion of NGF into coronary arteries can prevent this postischemic denervation (Abe, et al, 1997). Denervation is heterogeneous however; indeed seven days after ischemia-reperfusion, sympathetic hyperinnervation foci along with denervated myocardium are also present in the peri-infarct region (Li, et al, 2004).…”

Section: Selectivity Of Post-infarct Hyperinnervationmentioning

confidence: 99%

Sympathetic hyperinnervation and inflammatory cell NGF synthesis following myocardial infarction in rats

et al. 2006

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Sympathetic hyperinnervation occurs in human ventricular tissue after myocardial infarction and may contribute to arrhythmias. Aberrant sympathetic sprouting is associated with elevated nerve growth factor (NGF) in many contexts, including ventricular hyperinnervation. However, it is unclear whether cardiomyocytes or other cell types are responsible for increased NGF synthesis. In this study, left coronary arteries were ligated and ventricular tissue examined in rats 1-28 days post-infarction. Infarct and peri-infarct tissue was essentially devoid of sensory and parasympathetic nerves at all time points. However, areas of increased sympathetic nerve density were observed in the peri-infarct zone between post-ligation days 4-14. Hyperinnervation occurred in regions containing accumulations of macrophages and myofibroblasts. To assess whether these inflammatory cells synthesize NGF, sections were processed for NGF in situ hybridization and immunohistochemistry. Both macrophage1 antigen-positive macrophages and α-smooth muscle actin immunoreactive myofibroblasts expressed NGF in areas where they were closely proximate to sympathetic nerves. To investigate whether NGF produced by peri-infarct cells induces sympathetic outgrowth, we cocultured adult sympathetic ganglia with peri-infarct explants. Neurite outgrowth from sympathetic ganglia was significantly greater at post-ligation days 7-14 as compared to control tissue. Addition of an NGF function-blocking antibody prevented the increased neurite outgrowth induced by periinfarct tissue. These findings provide evidence that inflammatory cell NGF synthesis plays a causal role in sympathetic hyperinnervation following myocardial infarction.

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“…In animal experimental studies, temporal damage to the cardiac sympathetic nerves after transient ischemia has been shown [6][7][8][9][10][11][12][13]. In humans, several imaging studies using radiolabeled norepinephrine analog tracers have confirmed sympathetic nerve alterations, which are correlated with the area of ischemia in acute coronary syndrome [14].…”

Section: Introductionmentioning

confidence: 97%

Sympathetic nerve damage and restoration after ischemia-reperfusion injury as assessed by 11C-hydroxyephedrine

Werner

Maya

Rischpler

et al. 2015

Eur J Nucl Med Mol Imaging

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Protective Role of Nerve Growth Factor Against Postischemic Dysfunction of Sympathetic Coronary Innervation

Abstract: We conclude that exogenously infused and endogenously released NGF protects against postischemic neural stunning of sympathetic cardiac innervation.

Cited by 75 publications

References 30 publications

Silent Myocardial Ischemia

Silent Myocardial Ischemia

Sympathetic hyperinnervation and inflammatory cell NGF synthesis following myocardial infarction in rats

Sympathetic nerve damage and restoration after ischemia-reperfusion injury as assessed by 11C-hydroxyephedrine

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