Angiogenesis in the Heart and Skeletal Muscle — Models for Capillary Growth

Hudlická, O; Egginton, Stuart; Brown, Margaret D.

doi:10.1007/978-1-4757-9185-3_3

Cited by 11 publications

(11 citation statements)

References 38 publications

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“…However, we believe that surgeons should be aware causes the size and number of arterioles to decrease [19]. These results have suggested that shear stress of this kind of mechanism, because many treatment modalities to improve wound healing have been based may also play an important physiological role in muscle angiogenesis, but actual stress levels have not been on the empirical concept that local blood flow is vital to wound healing, without taking into consideration estimated in vivo.…”

Section: Direct Effect Of Prazosin On Endothelial Cell Growthmentioning

confidence: 82%

“…Although the events in the microcirculation provoked by prazosin are recognized as being chiefly due to changes in hemodynamic stress resulting from increased blood flow [19], several influences other than the hemodynamic change should be considered. First, there is the direct chemical effect of prazosin on vascular proliferation.…”

Section: Direct Effect Of Prazosin On Endothelial Cell Growthmentioning

confidence: 98%

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Effects of Shear Stress on Wound-Healing Angiogenesis in the Rabbit Ear Chamber

Ichioka¹,

Shibata²,

Kosaki³

et al. 1997

Journal of Surgical Research

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Section: Direct Effect Of Prazosin On Endothelial Cell Growthmentioning

confidence: 82%

Section: Direct Effect Of Prazosin On Endothelial Cell Growthmentioning

confidence: 98%

Effects of Shear Stress on Wound-Healing Angiogenesis in the Rabbit Ear Chamber

Ichioka¹,

Shibata²,

Kosaki³

et al. 1997

Journal of Surgical Research

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“…On the basis of the evidence that prolonged bradycardia stimulates coronary angiogenesis in nonischemic (6,16,42) and postinfarcted (22) hearts of adult animals, we hypothesized that chronic reduction in heart rate induced by the ␤ 1 -blocker AT can promote growth of coronary vessels in middle-aged (1-yr-old) post-MI rats. Our data support this hypothesis by showing that, after 4 wk of chronic bradycardia in post-MI rats, coronary conductance and coronary reserve are markedly improved.…”

Section: Discussionmentioning

confidence: 99%

Reduction of heart rate by chronic β₁-adrenoceptor blockade promotes growth of arterioles and preserves coronary perfusion reserve in postinfarcted heart

Dedkov¹,

Christensen²,

Weiß³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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Dedkov, Eduard I., Lance P. Christensen, Robert M. Weiss, and Robert J. Tomanek. Reduction of heart rate by chronic ␤1-adrenoceptor blockade promotes growth of arterioles and preserves coronary perfusion reserve in postinfarcted heart. Am J Physiol Heart Circ Physiol 288: H2684 -H2693, 2005. First published January 28, 2005 doi:10.1152/ajpheart.01047.2004.-Adequate growth of coronary vasculature in the remaining left ventricular (LV) myocardium after myocardial infarction (post-MI) is a crucial factor for myocyte survival and performance. We previously demonstrated that post-MI coronary angiogenesis can be stimulated by bradycardia induced with the ATP-sensitive K ϩ channel antagonist alinidine. In this study, we tested the hypothesis that heart rate reduction with ␤-blockade may also induce coronary growth in the post-MI heart. Transmural MI was induced in 12-mo-old male Sprague-Dawley rats by occlusion of the left anterior descending coronary artery. Bradycardia was induced by administration of the ␤-adrenoceptor blocker atenolol (AT) via drinking water (30 mg/day). Three groups of rats were compared: 1) control/sham (C/SH), 2) MI, and 3) MI ϩ AT. In the MI ϩ AT rats, heart rate was consistently reduced by 25-28% compared with C/SH rats. At 4 wk after left anterior descending coronary ligation, infarct size was similar in MI and MI ϩ AT rats (67.1 and 61.5%, respectively), whereas a greater ventricular hypertrophy occurred in bradycardic rats, as indicated by a higher ventricular weight-to-body weight ratio (3.4 Ϯ 0.1 vs. 2.8 Ϯ 0.1 mg/g in MI rats). Analysis of LV function revealed a smaller drop in ejection fraction in the MI ϩ AT than in the MI group (ϳ24 vs. ϳ35%). Furthermore, in MI ϩ AT rats, maximal coronary conductance and coronary perfusion reserve were significantly improved compared with the MI group. The better myocardial perfusion indexes in MI ϩ AT rats were associated with a greater increase in arteriolar length density than in the MI group. Thus chronic reduction of heart rate induced with ␤-selective blockade promotes growth of coronary arterioles and, thereby, facilitates regional myocardial perfusion in post-MI hearts. myocardial infarction; angiogenesis; coronary circulation; resistance vessels; capillaries A LARGE TRANSMURAL MYOCARDIAL infarction (MI) of the left ventricle (LV) causes the sudden loss of a substantial number of cardiac myocytes, which leads to increased diastolic wall stress and chronic functional overload of the remaining portion of LV myocardium. As a result, the LV undergoes progressive structural remodeling, consisting of thinning and scarring of the infarcted region, chamber dilation, and eccentric hypertrophy of the surviving portion of the LV myocardium (1,27,30).Because scar tissue is not capable of contracting, LV function after MI is entirely dependent on the hypertrophied portion of the surviving LV myocardium. However, to accommodate an increased O 2 demand in the surviving overloaded cardiac myocytes, an adaptation of the vascular bed is necessary. Two basic me...

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“…Hemodynamic forces engendered in blood flow (shear stress, pressurization, and vessel wall tension) have an impact on angiogenesis. In this context, increased shear stress induced by administration of adrenoreceptor agonists results in high capillary content and increased VEGF (32;33). High and low shear stress conditions also generate capillaries with differing morphologies (34).…”

Section: The Steps Of Angiogenesismentioning

confidence: 99%

Techniques and assays for the study of angiogenesis

Irvin

Zijlstra

Wikswo

et al. 2014

Exp Biol Med (Maywood)

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The importance of studying angiogenesis, the formation of new blood vessels from pre-existing vessels, is underscored by its involvement in both normal physiology, such as embryonic growth and wound healing, and pathologies, such as diabetes and cancer. Treatments targeting the molecular drive of angiogenesis have been developed, but many of the molecular mechanisms that mediate vascularization, as well as how these mechanisms can be targeted in therapy, remain poorly understood. The limited capacity to quantify angiogenesis properly curtails our molecular understanding and development of new drugs and therapies. Although there are a number of assays for angiogenesis, many of them strip away its important components and/or limit control of the variables that direct this highly cooperative and complex process. Here we review assays commonly used in endothelial cell biology and describe the progress toward development of a physiologically realistic platform that will enable a better understanding of the molecular and physical mechanisms that govern angiogenesis.

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Angiogenesis in the Heart and Skeletal Muscle — Models for Capillary Growth

Cited by 11 publications

References 38 publications

Effects of Shear Stress on Wound-Healing Angiogenesis in the Rabbit Ear Chamber

Effects of Shear Stress on Wound-Healing Angiogenesis in the Rabbit Ear Chamber

Reduction of heart rate by chronic β₁-adrenoceptor blockade promotes growth of arterioles and preserves coronary perfusion reserve in postinfarcted heart

Techniques and assays for the study of angiogenesis

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Angiogenesis in the Heart and Skeletal Muscle — Models for Capillary Growth

Cited by 11 publications

References 38 publications

Effects of Shear Stress on Wound-Healing Angiogenesis in the Rabbit Ear Chamber

Effects of Shear Stress on Wound-Healing Angiogenesis in the Rabbit Ear Chamber

Reduction of heart rate by chronic β1-adrenoceptor blockade promotes growth of arterioles and preserves coronary perfusion reserve in postinfarcted heart

Techniques and assays for the study of angiogenesis

Contact Info

Product

Resources

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Reduction of heart rate by chronic β₁-adrenoceptor blockade promotes growth of arterioles and preserves coronary perfusion reserve in postinfarcted heart