Exercise limits the production of endothelin in the coronary vasculature

Beer, Vincent J. de; Bender, Shawn B.; Taverne, Yannick J.H.J.; Gao, Fen; Duncker, Dirk J.; Laughlin, M. H.; Merkus, Daphne

doi:10.1152/ajpheart.00954.2010

Cited by 23 publications

(15 citation statements)

References 38 publications

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“…distribution of blood flow over the coronary vascular bed. 36,37 We observed an increase in coronary flow velocity during Ex1, where MR continued to fall, after an initial slight increase at the start, suggesting progressive vasodilation of the coronary vascular bed with increasing workload. It has been shown that persistent vasomotor tone is present throughout the coronary microcirculation even during ischemia, with substantial vasodilator reserve remaining within the exercising vascular bed of a hypo-perfused region.…”

Section: Persistent Decrease In Coronary Microvascular Resistance Indmentioning

confidence: 70%

Synergistic Adaptations to Exercise in the Systemic and Coronary Circulations That Underlie the Warm-Up Angina Phenomenon

et al. 2012

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Background-The mechanisms of reduced angina on second exertion in patients with coronary arterial disease, also known as the warm-up angina phenomenon, are poorly understood. Adaptations within the coronary and systemic circulations have been suggested but never demonstrated in vivo. In this study we measured central and coronary hemodynamics during serial exercise. Methods and Results-Sixteen patients (15 male, 61Ϯ4.3 years) with a positive exercise ECG and exertional angina completed the protocol. During cardiac catheterization via radial access, they performed 2 consecutive exertions (Ex1, Ex2) using a supine cycle ergometer. Throughout exertions, distal coronary pressure and flow velocity were recorded in the culprit vessel using a dual sensor wire while central aortic pressure was recorded using a second wire. Patients achieved a similar workload in Ex2 but with less ischemia than in Ex1 (PϽ0.01). A 33% decline in aortic pressure augmentation in Ex2 (PϽ0.0001) coincided with a reduction in tension time index, a major determinant of left ventricular afterload (PϽ0.001). Coronary stenosis resistance was unchanged. A sustained reduction in coronary microvascular resistance resulted in augmented coronary flow velocity on second exertion (both PϽ0.001). These changes were accompanied by a 21% increase in the energy of the early diastolic coronary backward-traveling expansion, or suction, wave on second exercise (PϽ0.05), indicating improved microvascular conductance and enhanced left ventricular relaxation. Conclusions-On repeat exercise in patients with effort angina, synergistic changes in the systemic and coronary circulations combine to improve vascular-ventricular coupling and enhance myocardial perfusion, thereby potentially contributing to the warm-up angina phenomenon. (Circulation. 2012;126:2565-2574.)

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Section: Persistent Decrease In Coronary Microvascular Resistance Indmentioning

confidence: 70%

Synergistic Adaptations to Exercise in the Systemic and Coronary Circulations That Underlie the Warm-Up Angina Phenomenon

et al. 2012

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“…Enhanced ventricular relaxation reduces microvascular compression,28 which helps lower MVR. Despite vasoconstriction of the epicardial stenosed segment during exercise29 (evidenced by increased stenosis severity in our study), parallel intense vasodilatation of resistance vessels during exercise30 overcomes this, resulting in further adaptive reduction of MVR.…”

Section: Discussionmentioning

confidence: 55%

Deleterious Effects of Cold Air Inhalation on Coronary Physiological Indices in Patients With Obstructive Coronary Artery Disease

Williams

Asrress

Lumley

et al. 2018

JAHA

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BackgroundCold air inhalation during exercise increases cardiac mortality, but the pathophysiology is unclear. During cold and exercise, dual‐sensor intracoronary wires measured coronary microvascular resistance (MVR) and blood flow velocity (CBF), and cardiac magnetic resonance measured subendocardial perfusion.Methods and ResultsForty‐two patients (62±9 years) undergoing cardiac catheterization, 32 with obstructive coronary stenoses and 10 without, performed either (1) 5 minutes of cold air inhalation (5°F) or (2) two 5‐minute supine‐cycling periods: 1 at room temperature and 1 during cold air inhalation (5°F) (randomized order). We compared rest and peak stress MVR, CBF, and subendocardial perfusion measurements. In patients with unobstructed coronary arteries (n=10), cold air inhalation at rest decreased MVR by 6% (P=0.41), increasing CBF by 20% (P<0.01). However, in patients with obstructive stenoses (n=10), cold air inhalation at rest increased MVR by 17% (P<0.01), reducing CBF by 3% (P=0.85). Consequently, in patients with obstructive stenoses undergoing the cardiac magnetic resonance protocol (n=10), cold air inhalation reduced subendocardial perfusion (P<0.05). Only patients with obstructive stenoses performed this protocol (n=12). Cycling at room temperature decreased MVR by 29% (P<0.001) and increased CBF by 61% (P<0.001). However, cold air inhalation during cycling blunted these adaptations in MVR (P=0.12) and CBF (P<0.05), an effect attributable to defective early diastolic CBF acceleration (P<0.05) and associated with greater ST‐segment depression (P<0.05).ConclusionsIn patients with obstructive coronary stenoses, cold air inhalation causes deleterious changes in MVR and CBF. These diminish or abolish the normal adaptations during exertion that ordinarily match myocardial blood supply to demand.

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“…ET-mediated coronary vasoconstriction is reduced with increasing exercise intensity, and decreased ET production during exercise likely contributes to the metabolic coronary vasodilation (24). Moreover, ET-1 contributes to the progression of cardiopulmonary pathology in rats (25).…”

Section: Discussionmentioning

confidence: 99%

Endothelin-1 and type III collagen alterations in the heart of rats following cisplatin-induced toxicity

Huang

Liu

2011

Mol Med Report

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Abstract. Cisplatin-induced heart damage is associated with enzymes and protein alterations. The purpose of this study was to investigate cisplatin-induced alterations in cardiac endothelin (ET)-1 and type III collagen following administration of cisplatin. Male Wistar rats were randomly divided into two groups: a control and a cisplatin group. The cisplatin group received cisplatin intraperitoneally (i.p.) at a single dose of 7 mg/kg on day 6, while the controls were given the same amount of saline via the same route. On day 11, the rats were anesthetized and a thoracotomy was performed on all animals. Immunohistochemical analysis was performed to evaluate the protein expression of ET-1 and type III collagen. Sections were analyzed by digital image analysis. Results showed that the cardiac protein expression of ET-1 and type III collagen was altered following cisplatin-induced toxicity in rats. The expression of ET-1 and type III collagen was significantly increased after cisplatin treatment, supported by integrated optical density, when compared to the control group (P<0.05). The present findings indicate that such alterations may be reflected in abnormal cardiac function. Additionally, the proteins identified in this study may benefit investigations into the mechanisms underlying cisplatin-induced toxicity, thereby providing the necessary evidence for further research. IntroductionCisplatin is a chemotherapeutic agent widely used to treat a variety of solid tumors (1,2). It is also an antineoplastic drug that causes an array of adverse effects on various organs and tissues (3). Nephrotoxicity is one of the major side-effects of cisplatin chemotherapy (4) limiting the promising efficacy of cisplatin (5). Cisplatin-based chemotherapy also has a variety of vascular side-effects (6). Acute administration of cisplatin induces nausea/emesis and diarrhea (7). Chronic cisplatin may induce an enteric neuropathy characterized by changes in myenteric neurons associated with marked gastrointestinal motor dysfunction (7). Dysfunction in immune surveillance during anticancer chemotherapy of patients often causes weakness of the host defense system and a subsequent increase in microbial infections (8).Cisplatin-induced toxicity is known to be involved in the changes of antioxidant enzymes (GST, SOD, CAT, GSH-Px and GSH), serum superoxide dismutase (SOD), glutathione (GSH), malondiethylaldehyde (MDA), nitric oxide (NO) (9) and DNA (2,10). However, little is known about the changes in endothelin (ET)-1 and type III collagen expression in the heart following cisplatin-induced toxicity.The present study used immunohistochemical analysis to evaluate the expression of ET-1 and type III collagen in the heart, and to determine whether or not the protein expression is altered with cisplatin-induced toxicity. Materials and methodsAnimals and study design. Sixteen healthy adult male Wistar rats, weighing 210-250 g, were used in this study. The animals were housed individually in stainless-steel wire-bottomed cages in an air-conditione...

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Exercise limits the production of endothelin in the coronary vasculature

Cited by 23 publications

References 38 publications

Synergistic Adaptations to Exercise in the Systemic and Coronary Circulations That Underlie the Warm-Up Angina Phenomenon

Synergistic Adaptations to Exercise in the Systemic and Coronary Circulations That Underlie the Warm-Up Angina Phenomenon

Deleterious Effects of Cold Air Inhalation on Coronary Physiological Indices in Patients With Obstructive Coronary Artery Disease

Endothelin-1 and type III collagen alterations in the heart of rats following cisplatin-induced toxicity

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