What is capillary density

Pathophysiology of chronic heart failure Lancet 88 Francis G. Neurohumoral activation and progression of heart failure: hypothetical and clinical considerations J.

Fishbein M. Maclean D. Maroko P. Experimental myocardial infarction in the rat: qualitative and quantitative changes during pathologic evolution Am. Van Kerckhoven R. Boomsma F. Saxena P. Schoemaker R.

Chronic administration of moxonidine suppresses sympathetic activation in a rat heart failure model Eur. Debets J. Struyker-Boudier H.

Smits J. Delayed but not immediate captopril therapy improves cardiac function in conscious rats, following myocardial infarction J. Kalkman E. Altered cardiac collagen and associated changes in diastolic function of infarcted rat hearts Cardiovasc. Low-dose aspirin improves in vivo hemodynamics in conscious, chronically infarcted rats Cardiovasc.

Bilgin Y. Determinants of coronary reserve in rats subjected to coronary artery ligation or aortic banding Cardiovasc.

Nelissen-Vrancken H. Kuizinga M. Daemen M. Early captopril treatment inhibits DNA synthesis in endothelial cells and normalization of maximal coronary flow in infarcted rat hearts Cardiovasc. Chronic aspirin treatment affects collagen deposition in non-infarcted myocardium during remodeling after coronary artery ligation in the rat J.

Patrignani P. Filabozzi P. Patrono C. Selective cumulative inhibition of platelet thromboxane production by low-dose aspirin in healthy subjects J. Pfeffer J. Pfeffer M. Braunwald E. Hemodynamic benefits and prolonged survival with long-term captopril therapy in rats with myocardial infarction and heart failure Circulation 75 I I Regionally different vascular response to vasoactive substances in the remodelled infarcted rat heart; aberrant vasculature in the infarct scar J.

Benjamin I. Jalil J. Tan L. Cho K. Weber K. Clark W. Isoproterenol-induced myocardial fibrosis in relation to myocyte necrosis Circ. Gerdes A. Callas G. Kasten F. Differences in regional capillary distribution and myocyte sizes in normal and hypertrophic rat hearts Am.

Batra S. Rakusan K. Capillary length, tortuosity, and spacing in rat myocardium during cardiac cycle Am. Myocardial infarct size and ventricular function in rats Circ.

Wallenstein S. Zucker C. Fleiss J. Some statistical methods useful in circulation research Circ. Lindenfeld J. Robertson A. Lowes B. Bristow M. Aspirin impairs reverse myocardial remodeling in patients with heart failure treated with beta-blockers J.

Ziegler D. Haxhiu M. Kaan E. Papp J. Ernsberger P. Pharmacology of moxonidine, an I1-imidazoline receptor agonist J. Motz W. Scheler S. Mox B. The potential clinical application of moxonidine in congestive heart failure Rev.

Negrao C. Moreira E. Santos M. Farah V. Krieger E. Vagal function impairment after exercise training J. Bradykinin mediates cardiac preconditioning at a distance Am.

Heart Circ. Courtney K. Colwell W. Jensen R. Prostaglandins and pacemaker activity in isolated guinea pig SA node Prostaglandins 16 Hedqvist P. Basic mechanisms of prostaglandin action on autonomic neurotransmission Annu. Haynes D. Wright P. Gadd S. Whitehouse M. Vernon-Roberts B. Is aspirin a prodrug for antioxidant and cytokine-modulating oxymetabolites? Agents Actions 39 49 Kohl P.

Noble D. Mechanosensitive connective tissue: potential influence on heart rhythm Cardiovasc. Volders P. Interstitial fibrosis and angiotensin-converting enzyme inhibition in patients with end-stage myocardial infarction J. Harmsen E. Ruzicka M. Leenen F. Sensitivity to ischaemic ATP breakdown in different models of cardiac hypertrophy in rats J.

Turek Z. Grandtner M. Kubat K. Ringnalda B. Kreuzer F. Arterial blood gases, muscle fiber diameter and intercapillary distance in cardiac hypertrophy of rats with an old myocardial infarction Pflugers Arch. Beghi C. Kikkawa Y. Olivetti G. Myocardial infarction in rats. Infarct size, myocyte hypertrophy, and capillary growth Circ. Wright A. Capillary growth and changes in heart performance induced by chronic bradycardial pacing in the rabbit Circ.

Granetzny A. Schwanke U. Schmitz C. Pharmacologic heart rate reduction: effect of a novel, specific bradycardic agent on the heart Thorac. Stewart J. Simpson I. Smith R. Callicott C. Gray H. Camm A. Left ventricular energetics: heat production by the human heart Cardiovasc. Xie Z. Gao M. Horimoto M. Togashi H. Saito H. Koyama T. Rearrangement of the ventricular capillary network in stroke-prone spontaneously hypertensive rats SHRSP following a late start of treatment with the angiotensin converting enzyme blocker temocapril Jpn.

Heart J. Tharp G. Wagner C. Chronic exercise and cardiac vascularization Eur. Arterialization of the capillary network in the left ventricular subendocardium in young rats subjected to exercise training Hokkaido Igaku Zasshi 72 Areskog N.

Effects and adverse effects of autonomic blockade in physical exercise Am. White F. McKirnan M. Breisch E. Guth B. In a study conducted at the University of Missouri-Columbia, the improved function and increased density of capillaries with exercise training was explored. While such effects of exercise were supported by researchers' findings, they also found evidence for capillary growth, or the development of new capillaries with exercise training.

Following an exercise program for an extended period of time can lead to improved capillary function, increased capillary density at your muscle sites and the growth of new capillaries, where needed. While the development of new capillaries indicates that exercise does increase your number of capillaries, such increases are marginal and may not affect all people.

Though exercise has the potential to increase your number of capillaries, the major effect of exercise on your capillaries involves improving those that you already have. By Matthew Lee. Matthew Lee. Matthew Lee has been writing professionally since Past and current research projects have explored the effect of a diagnosis of breast cancer on lifestyle and mental health and adherence to lifestyle-based i. The model assumes that oxygen consumption in maximal exercise is limited by the ability of capillaries to deliver oxygen to tissue and is therefore strongly dependent on capillary density, defined as the number of capillaries per unit cross-sectional area of muscle.

Based on an analysis of oxygen transport processes occurring at the microvascular level, the model allows estimation of the minimum number of straight, evenly spaced capillaries required to achieve a given oxygen consumption rate.

This discrepancy is partly accounted for by the fact that capillary density decreases with muscle contraction and muscle biopsy samples typically are strongly contracted.