Ischemic preconditioning attenuates postischemic coronary artery endothelial dysfunction in a model of minimally invasive direct coronary artery bypass grafting

Thourani, Vinod H.; Nakamura, Masanori; Duarte, Ignacio; Bufkin, Bradley L.; Zhao, Zhi‐Qing; Jordan, James; Shearer, Steven T; Guyton, Robert A.; Vinten‐Johansen, Jakob

doi:10.1016/s0022-5223(99)70437-x

Cited by 39 publications

(21 citation statements)

References 26 publications

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“…129 Another study in dogs with 60-minute coronary occlusion and reperfusion also reported no improvement in the coronary vasodilator response to acetylcholine but improved reflow with ischemic preconditioning by 2 cycles of 5-minute myocardial ischemia/5-minute reperfusion. 130 However, the majority of subsequent studies reported protection by ischemic preconditioning on endothelial function, as assessed by endotheliumdependent coronary vasodilation in response to acetylcholine, serotonin, or ADP in rats, [131][132][133] guinea pigs, 134 dogs, 135,136 pigs, 137 and goats. 138 Mechanistically, the preservation of endothelial function by ischemic preconditioning was related to adenosine, 132,136 bradykinin, 133 and nitric oxide.…”

Section: Coronary Vascular Protection By Ischemic Preconditioningmentioning

confidence: 99%

“…138,139 The preservation of endothelial function by ischemic preconditioning became apparent not only as improved endothelium-dependent coronary vasodilation but also as reduced leukocyte adherence. 134,135,139 Coronary endothelial function recovers only slowly after myocardial ischemia/reperfusion and is still depressed after 1 month, but ischemic preconditioning also improves endothelium-dependent coronary vasodilation in response to acetylcholine and endothelial ultrastructure after 1 month. 140 Vice versa, delayed ischemic preconditioning 24 hours before the sustained myocardial ischemia/reperfusion increases the activity of endothelial nitric oxide synthase, which mediates preservation of coronary vasodilator response to acetylcholine, carbachol, and bradykinin.…”

Section: Coronary Vascular Protection By Ischemic Preconditioningmentioning

confidence: 99%

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The Coronary Circulation as a Target of Cardioprotection

Heusch

2016

Circulation Research

206

160

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Abstract:The atherosclerotic coronary vasculature is not only the culprit but also a victim of myocardial ischemia/ reperfusion injury. Manifestations of such injury are increased vascular permeability and edema, endothelial dysfunction and impaired vasomotion, microembolization of atherothrombotic debris, stasis with intravascular cell aggregates, and finally, in its most severe form, capillary destruction with hemorrhage. In animal experiments, local and remote ischemic pre-and postconditioning not only reduce infarct size but also these manifestations of coronary vascular injury, as do drugs which recruit signal transduction steps of conditioning. Clinically, no-reflow is frequently seen after interventional reperfusion, and it carries an adverse prognosis. The translation of cardioprotective interventions to clinical practice has been difficult to date. Only 4 drugs (brain natriuretic peptide, exenatide, metoprolol, and esmolol) stand unchallenged to date in reducing infarct size in patients with reperfused acute myocardial infarction; unfortunately, for these drugs, no information on their impact on the ischemic/reperfused coronary circulation is available. (Circ Res.

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Section: Coronary Vascular Protection By Ischemic Preconditioningmentioning

confidence: 99%

Section: Coronary Vascular Protection By Ischemic Preconditioningmentioning

confidence: 99%

The Coronary Circulation as a Target of Cardioprotection

Heusch

2016

Circulation Research

206

160

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“…Therefore, IP might be an ideal and effective method in achieving additional myocardial protection. There are nevertheless controversial data in various studies [1,[98][99][100]. During minimal invasive CABG operation, Jacobsohn described the protective effect of IP, even no change in ST-T segment and T-wave during IP has an IP effect of improved contractility [40].…”

Section: Off-pump Cabg Patientsmentioning

confidence: 99%

Ischemic Preconditioning in Cardiac Surgery

Tarkka

2011

Int J Angiol

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Murry and colleagues in 1986 described a paradoxical phenomenon that exposure of the heart to repeated brief ischemic episodes delayed the severity of myocardial infarction of a following prolonged myocardial ischemia and termed it myocardial ischemic preconditioning (IP). From then on, IP had been extensively studied in various kinds of experimental models as well as in humans. Besides delaying myocardial infarction, IP has been proved to be a potent endogenous factor in preserving high energy phosphates, suppressing arrhythmias and improving postischemic functional recovery. Delaying myocardial ultrastructure damage, reducing lactate, reducing the utilization of myocardial glycogen and protecting coronary endothelium after IP has also been found. Different experimental models and conditions resembling cardiac surgery have also been investigated. The mechanism of IP is not yet clear, however. The conclusions derived from animal studies could not totally stand for the situation in open heart surgery. IP was found effective in preserving high energy phosphate, improving heart performance and decreasing cardiac troponin T release during open heart surgery. Controversial exists because in same reports there were no effects of IP. The difference in IP protocol, myocardial protective method and study object might be the reason of the controversial results. Several clinical factors may affect IP effects during clinical practice. The purpose of the present study was to review the recent literature on IP, especially the IP mechanism, IP phenomenon in cardiac surgery and the possible influential factors, to summarize whether IP might prefer additional protection of current protective strategy in cardiac surgery.

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“…This can be explained by an upregulation of coronary vascular NO production, potentially involved in the mechanism of the delayed window of preconditioning [51]. Thourani et al using the left circumflex artery as a control found that in the previously ischemic vascular bed of the anterior vascular descending artery the vasodilatory response to acetylcholine is impaired [52]. If the occlusion is preceded by the ischemic preconditioning no significant difference in the response is observed between the vascular beds of the two arteries.…”

Section: Shear Stress and Endothelial Cell Dys-functionmentioning

confidence: 99%

Preconditioning and Shear Stress in the Microcirculation in Ischemia-Reperfusion Injury

Bertuglia

2006

CCR

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Postischemic reperfusion causes microvascular endothelial cell dysfunction characterized by low shear stress, excessive oxidative stress and a reduced nitric oxide (NO) release. Recent studies have demonstrated that reduced shear forces are responsible for the impairment of endothelium-dependent vasodilation after ischemia reperfusion (I/R) injury. Preconditioning is an endogenous phenomenon whereby intermittent periods of ischemia provide protection against subsequent periods of I/R. Several models show that intermittent hypoxia (IH, brief periods of systemic hypoxia and reoxygenation), treatment with erythropoietin (EPO) and ultrasound exposure are methods of preconditioning. This chapter explores the hypothesis that these procedures that improve tolerance to subsequent I/R are directly related to shear stress. It acts as a biochemical mechanotransducer by modulating the production of vasoactive substances by endothelial cells. The adaptation of endothelial cells to high shear stress during the preconditioning period is crucial to ensure vasodilation and capillary perfusion during subsequent periods of I/R. Both IH and EPO treatment increase blood viscosity thus increasing shear stress associated with a reduced oxidative stress during postischemic reperfusion. Ultrasound treatment can also improve tolerance to I/R and normale shear stress during postischemic reperfusion by pulsatile mechanism acting on endothelial cells.

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Ischemic preconditioning attenuates postischemic coronary artery endothelial dysfunction in a model of minimally invasive direct coronary artery bypass grafting

Abstract: In this minimally invasive direct coronary artery bypass grafting model, both agonist-stimulated and basal postischemic endothelial dysfunction were attenuated by ischemic preconditioning.

Cited by 39 publications

References 26 publications

The Coronary Circulation as a Target of Cardioprotection

The Coronary Circulation as a Target of Cardioprotection

Ischemic Preconditioning in Cardiac Surgery

Preconditioning and Shear Stress in the Microcirculation in Ischemia-Reperfusion Injury

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