Blood Flow and Transcapillary Exchange in Skeletal and Cardiac Muscle

2015 ◽  
pp. 18-30 ◽  
Author(s):  
E. M. Renkin
Keyword(s):  
Blood Flow ◽  
Cardiac Muscle ◽  
Transcapillary Exchange

Ideas about control of skeletal and cardiac muscle blood flow (1876–2003): cycles of revision and new vision

2004 ◽  
Vol 97 (1) ◽  
pp. 384-392 ◽  
Author(s):  
Loring B. Rowell
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cardiac Muscle ◽  
Neural Control ◽  
Muscle Blood Flow ◽  
Dynamic Exercise ◽  
Vascular Conductance ◽  
Site Of Action ◽  
New Vision ◽  
Muscle Chemoreflex

This perspective examines origins of some key ideas central to major issues to be addressed in five subsequent mini-reviews related to Skeletal and Cardiac Muscle Blood Flow. The questions discussed are as follows. 1) What causes vasodilation in skeletal and cardiac muscle and 2) might the mechanisms be the same in both? 3) How important is muscle's mechanical contribution (via muscle pumping) to muscle blood flow, including its effect on cardiac output? 4) Is neural (vasoconstrictor) control of muscle vascular conductance and muscle blood flow significantly blunted in exercise by muscle metabolites and what might be a dominant site of action? 5) What reflexes initiate neural control of muscle vascular conductance so as to maintain arterial pressure at its baroreflex operating point during dynamic exercise, or is muscle blood flow regulated so as to prevent accumulation of metabolites and an ensuing muscle chemoreflex or both?

scholarly journals GLP-1 and Insulin Recruit Muscle Microvasculature and Dilate Conduit Artery Individually But Not Additively in Healthy Humans

2018 ◽  
Vol 2 (2) ◽  
pp. 190-206 ◽  
Author(s):  
Alvin W K Tan ◽  
Sharmila C Subaran ◽  
Matthew A Sauder ◽  
Weidong Chai ◽  
Linda A Jahn ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Muscle ◽  
Flow Velocity ◽  
Surface Area ◽  
Brachial Artery ◽  
Microvascular Perfusion ◽  
Brachial Artery Diameter ◽  
Nutrient Delivery ◽  
Conduit Artery ◽  
Endothelial Surface

Abstract Context Glucagon-like peptide-1 (GLP-1) and insulin increase muscle microvascular perfusion, thereby increasing tissue endothelial surface area and nutrient delivery. Objective To examine whether GLP-1 and insulin act additively on skeletal and cardiac microvasculature and conduit artery. Design Healthy adults underwent three study protocols in random order. Setting Clinical Research Unit at the University of Virginia. Methods Overnight-fasted participants received an intravenous infusion of GLP-1 (1.2 pmol/kg/min) or normal saline for 150 minutes with or without a 2-hour euglycemic insulin clamp (1 mU/kg/min) superimposed from 30 minutes onward. Skeletal and cardiac muscle microvascular blood volume (MBV), flow velocity, and flow; brachial artery diameter, flow velocity, and blood flow; and pulse wave velocity (PWV) were measured. Results GLP-1 significantly increased skeletal and cardiac muscle MBV and microvascular blood flow (MBF) after 30 minutes; these remained elevated at 150 minutes. Insulin also increased skeletal and cardiac muscle MBV and MBF. Addition of insulin to GLP-1 did not further increase skeletal and cardiac muscle MBV and MBF. GLP-1 and insulin increased brachial artery diameter and blood flow, but this effect was not additive. Neither GLP-1, insulin, nor GLP-1 and insulin altered PWV. Combined GLP-1 and insulin infusion did not result in higher whole-body glucose disposal. Conclusion GLP-1 and insulin at physiological concentrations acutely increase skeletal and cardiac muscle microvascular perfusion and dilate conduit artery in healthy adults; these effects are not additive. Thus, GLP-1 and insulin may regulate skeletal and cardiac muscle endothelial surface area and nutrient delivery under physiological conditions.

scholarly journals GLP-1 at physiological concentrations recruits skeletal and cardiac muscle microvasculature in healthy humans

2014 ◽  
Vol 127 (3) ◽  
pp. 163-170 ◽  
Author(s):  
Sharmila C. Subaran ◽  
Matthew A. Sauder ◽  
Weidong Chai ◽  
Linda A. Jahn ◽  
Dale E. Fowler ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Muscle ◽  
Brachial Artery ◽  
Microvascular Perfusion ◽  
Brachial Artery Diameter ◽  
Healthy Humans

GLP-1 increases microvascular perfusion in both skeletal and cardiac muscle, and brachial artery diameter and blood flow in humans. These vascular actions may contribute to the beneficial actions of the GLP-1 receptor analogues.

Regional myoglobin concentration in the myocardium of the dog

1968 ◽  
Vol 46 (6) ◽  
pp. 908-910 ◽  
Author(s):  
Naomi M. Anderson ◽  
Giorgio Brandi
Keyword(s):  
Blood Flow ◽  
Right Ventricle ◽  
Cardiac Muscle ◽  
Chronic Hypoxia ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall

It has been demonstrated previously that chronic hypoxia leads to an increase in myoglobin concentration. Evidence of differences in [Formula: see text] and blood flow in deep and superficial layers of cardiac muscle suggest that there might be a corresponding difference in myoglobin concentration in the myocardium. Results showed an even distribution of myoglobin concentration in inner and outer layers of the left ventricular wall, right ventricle, and septum, suggesting that [Formula: see text] in inner layers of the left ventricular wall is not sufficiently diminished to stimulate an increase in myoglobin concentration.

scholarly journals Unusual Sign from an Unusual Cause: Wellens’ Syndrome due to Myocardial Bridging

2018 ◽  
Vol 2018 ◽  
pp. 1-3
Author(s):  
Paurush Ambesh ◽  
Dikshya Sharma ◽  
Aditya Kapoor ◽  
Aviva-Tobin Hess ◽  
Vijay Shetty ◽  
...  
Keyword(s):  
Blood Flow ◽  
Case Report ◽  
Chest Pain ◽  
Coronary Artery ◽  
Cardiac Muscle ◽  
Blood Supply ◽  
Myocardial Bridging

It is vital to recognize correctly, chest pain of cardiac etiology. Most commonly, it is because of blood supply-demand inequity in the myocardium. However, the phenomenon of myocardial bridging as a cause of cardiac chest pain has come to attention reasonably recently. Herein, a coronary artery with a normal epicardial orientation develops a transient myocardial course. If the cardiac muscle burden is substantial, the respective artery gets compressed during each cycle of systole, thereby impeding blood flow in the artery. Hence, myocardial bridging has been attributed to as a rare cause of angina. In this case report, the authors discuss a patient in whom myocardial bridging turned out to be an elusive cause of angina. We wish to underscore the importance of being clinically mindful of myocardial bridging when assessing a patient with angina.

Effects of dipyridamole on muscle blood flow in exercising miniature swine

1989 ◽  
Vol 257 (5) ◽  
pp. H1507-H1515 ◽  
Author(s):  
M. H. Laughlin ◽  
R. E. Klabunde ◽  
M. D. Delp ◽  
R. B. Armstrong
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Muscle ◽  
Respiratory Muscle ◽  
Maximal Exercise ◽  
Treadmill Exercise ◽  
Vo2 Max ◽  
Miniature Swine ◽  
Extensor Muscles ◽  
Vasodilator Reserve

The purpose of this study was to determine whether a vasodilator reserve exists in respiratory muscles and forelimb skeletal muscles in miniature swine during treadmill exercise. Blood flow (BF) was measured with radiolabeled microspheres during preexercise and before and after dipyridamole (DYP; 1 mg/kg iv) at 2 min of treadmill exercise at 11.2 (70% Vo2 max) and 17.6 km/h (Vo2 max). Muscle BFs were increased during exercise, and the relationship between exercise intensity and BF varied among the muscles. The high-oxidative extensor muscles and the flexor muscles attained peak BFs at 11.2 km/h, whereas the more superficial, lower oxidative extensor muscles showed increases in BF up to maximal exercise. During running at 11.2 km/h, DYP produced increases in BF only in cardiac muscle, respiratory muscle and the medial head of the triceps muscle (MHT), which is composed of 91% slow-twitch oxidative (SO) fibers. During maximal exercise (17.6 km/h), DYP produced a 31-mmHg decrease in mean arterial pressure (MAP) and increases in vascular conductance in all muscles studied. BF was only increased in MHT and cardiac muscle. We conclude that vasodilator reserve remains in skeletal muscle and respiratory muscle even during maximal exercise in swine. If it is assumed that DYP-induced vasodilation in a muscle sample is indicative of adenosine production, these results suggest that SO skeletal muscle (MHT) and respiratory muscle are similar to cardiac muscle in that they produce adenosine even when adequately perfused. Furthermore, during maximal exercise, all skeletal muscle appears to produce adenosine, suggesting that muscle BF is restricted under these conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

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