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.

Parasympathetic control of transmural coronary blood flow in dogs

1985 ◽  
Vol 249 (2) ◽  
pp. H337-H343 ◽  
Author(s):  
J. V. Reid ◽  
B. R. Ito ◽  
A. H. Huang ◽  
C. W. Buffington ◽  
E. O. Feigl
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Vagal Stimulation ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Regional Myocardial Blood Flow ◽  
Ventricular Wall ◽  
Flow Ratio ◽  
Outer Flow

The transmural distribution of coronary blood flow was studied during vagal stimulation in closed-chest, morphine- and alpha-chloralose-anesthetized dogs. The left main coronary artery was cannulated and perfused at constant pressure. Bradycardia during vagal stimulation was prevented by atrioventricular heart block and ventricular pacing. Beta-adrenergic receptors were blocked with propranolol (1 mg/kg iv), and aortic pressure was stabilized by means of a pressure reservoir. Regional myocardial blood flow was measured with 9-micron radioactive microspheres during vagal stimulation and during intracoronary acetylcholine infusion. Vagal stimulation increased coronary blood flow uniformly across the left ventricular wall. In contrast, intracoronary acetylcholine infusion, at a rate selected to increase total flow to the same degree, vasodilated the subendocardium more than the subepicardium, increasing the inner/outer blood flow ratio. It is concluded that both vagal activation and acetylcholine produce coronary vasodilation that is independent of left ventricular preload, afterload, and heart rate. Acetylcholine vasodilation preferentially vasodilates the subendocardium, increasing the inner/outer flow ratio, but vagal stimulation produces uniform vasodilation across the left ventricular wall.

The effect of graded coronary stenosis on myocardial blood flow and left ventricular wall motion

1977 ◽  
Vol 72 (5) ◽  
pp. 479-491 ◽  
Author(s):  
M. Nakamura ◽  
H. Matsuguchi ◽  
A. Mitsutake ◽  
Y. Kikuchi ◽  
A. Takeshita ◽  
...  
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Coronary Stenosis ◽  
Wall Motion ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Left Ventricular Wall Motion ◽  
Ventricular Wall Motion

Redistribution of myocardial fiber strain and blood flow by asynchronous activation

1990 ◽  
Vol 259 (2) ◽  
pp. H300-H308 ◽  
Author(s):  
F. W. Prinzen ◽  
C. H. Augustijn ◽  
T. Arts ◽  
M. A. Allessie ◽  
R. S. Reneman
Keyword(s):  
Blood Flow ◽  
Right Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Electrical Activation ◽  
Ventricular Wall ◽  
Activation Time ◽  
The Right ◽  
Ejection Phase

Hearts of 11 anesthetized open-chest dogs were paced from the right atrium (RA), right ventricular outflow tract (RVOT), and left ventricular apex (LVA). Maps of the sequence of electrical activation (192 electrodes), fiber strain (video technique), and blood flow (microsphere technique) in the epicardial layers were obtained from a 15- to 20-cm2 area of the anterior left ventricular wall. Electrical asynchrony in this area was 10 +/- 5 (RA), 52 +/- 12 (RVOT), and 30 +/- 16 ms (LVA, mean +/- SD, P less than 0.05 for RVOT and LVA compared with RA). Epicardial fiber strain during the ejection phase was uniformly distributed during RA pacing. However, during ventricular pacing it ranged from 13 +/- 33% (RVOT) and 23 +/- 29% (LVA) of the value during RA pacing in early-activated regions to 268 +/- 127% (RVOT) and 250 +/- 130% (LVA) of this value in late-activated regions. Epicardial blood flow ranged from 81 +/- 22% (RVOT) and 79 +/- 23% (LVA) in early-activated regions to 142 +/- 42% (RVOT) and 126 +/- 22% (LVA) in late activated regions. In all above values P less than 0.05 compared with RA. During RVOT pacing, gradients of epicardial electrical activation time, fiber strain, and blood flow pointed in the same direction. Compared with RVOT pacing, during LVA pacing all gradients were opposite in direction, and the gradients of electrical activation time and blood flow appeared to be smaller. These results indicate that timing of electrical activation is an important determinant for the distribution of fiber strain and blood flow in the left ventricular wall.

Regulation of coronary flow

2021 ◽  
pp. 11-13
Author(s):  
Nico Bruining ◽  
Eric Boersma ◽  
Dirk J. Duncker
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Arterial Blood ◽  
Arterial Inflow ◽  
Systolic Phase ◽  
Vascular Beds

This chapter describes the regulation of coronary blood flow. The left ventricle generates the systemic arterial blood pressure that is required to maintain coronary blood flow. The coronary circulation is unique among regional vascular beds in that its perfusion is impeded during the systolic phase of the cardiac cycle by the surrounding contracting cardiac muscle. Systolic contraction increases left ventricular wall tension and compresses the intramyocardial microvessels, thereby impeding coronary arterial inflow. This compression is not uniformly distributed across the left ventricular wall, resulting in a redistribution of blood flow from the subendocardium to subepicardium.

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