Distribution of maximum coronary blood flow in the left ventricular wall of anesthetized dogs

1978 ◽  
Vol 104 (1) ◽  
pp. 48-60 ◽  
Author(s):  
Henning Bagger
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Anesthetized Dogs

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.

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.

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

Effect of endogenous natriuretic peptide system on ventricular and coronary function in failing heart

1997 ◽  
Vol 273 (5) ◽  
pp. H2406-H2414 ◽  
Author(s):  
Kazuhiro Yamamoto ◽  
John C. Burnett ◽  
Margaret M. Redfield
Keyword(s):  
Blood Flow ◽  
Natriuretic Peptide ◽  
Coronary Blood Flow ◽  
Vascular Function ◽  
Ventricular Myocytes ◽  
Left Ventricular ◽  
Anesthetized Dogs ◽  
Peptide System ◽  
Natriuretic Peptide System

Ventricular concentrations of atrial, brain (BNP) and C-type natriuretic peptide are enhanced in congestive heart failure (CHF). Natriuretic peptide receptors are present on ventricular myocytes and stimulate guanosine 3′,5′-cyclic monophosphate (cGMP) production. cGMP has been demonstrated to affect myocyte function in vitro. Thus we hypothesized that the intracardiac natriuretic peptide system may modulate myocardial and coronary function in CHF. To test this hypothesis, the effects of an intracoronary infusion of the natriuretic peptide receptor antagonist HS-142–1 on ventricular and coronary function were examined in anesthetized dogs with chronic CHF. To determine whether receptor stimulation had contrasting effects to those of receptor blockade, intracoronary BNP was infused in anesthetized normal and CHF dogs. Low-dose HS-142–1 delayed and slowed left ventricular (LV) relaxation and decreased coronary blood flow without changes in LV pressures. Higher doses further impaired LV relaxation without further decreases in coronary blood flow. In normal and CHF dogs, exogenous BNP produced the opposite effect with a quicker onset and faster rate of LV relaxation without effects on LV pressures or coronary blood flow. The endogenous natriuretic peptide system has an autocrine-paracrine role to modulate LV and coronary vascular function in CHF.

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.

Peptide 6A, a fibrin(ogen) degradation product, increases coronary blood flow

1985 ◽  
Vol 249 (3) ◽  
pp. H457-H462 ◽  
Author(s):  
J. Mehta ◽  
T. Wargovich ◽  
W. W. Nichols ◽  
K. Saldeen ◽  
R. Wallin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Plasma Concentrations ◽  
Hydrolysis Product ◽  
Left Ventricular ◽  
Receptor Blocker ◽  
H2 Receptor ◽  
Potent Vasodilator ◽  
Anesthetized Dogs ◽  
Arterial Tone

The coronary hemodynamic effects of intracoronary administration of a fibrin(ogen)-derived pentapeptide, Ala-Arg-Pro-Ala-Lys (peptide 6A), were evaluated in open-chest anesthetized dogs. With administration of peptide 6A (2.5-30 mumol), coronary blood flow increased and coronary vascular resistance decreased promptly in a dose-related manner. Increase in coronary blood flow was independent of any change in indexes of myocardial O2 demand, indicating the peptide 6A exerts direct effects on coronary arterial tone. Systemic arterial and left ventricular end-diastolic pressures remained unchanged with smaller doses but decreased when higher doses of peptide 6A (greater than or equal to 20 mumol) were administered. Plasma concentrations of 6-ketoprostaglandin F1 alpha, stable hydrolysis product of prostacyclin, increased in coronary sinus blood samples in conjunction with increase in coronary blood flow. Administration of indomethacin (5 mg/kg iv) inhibited peptide 6A-induced release of prostacyclin and significantly attenuated the effects of peptide 6A on coronary hemodynamics. Pretreatment of animals with H2-receptor blocker cimetidine (500 mg iv) or with H1-and H2-receptor blocker diphenhydramine (50 mg iv) had no significant effects on peptide 6A-induced increase in coronary blood flow. This study suggests that this fibrin(ogen)-derived peptide has potent vasodilator effects on the coronary vascular bed of the dog, and these effects are in part mediated by stimulation of prostacyclin release.

Sign in / Sign up

Export Citation Format

Share Document